tag:blogger.com,1999:blog-57834661109817738452024-03-13T21:26:26.147-07:00PRION CONFERENCETerry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.comBlogger5125tag:blogger.com,1999:blog-5783466110981773845.post-39371584079998817842022-09-14T14:53:00.001-07:002022-09-14T14:55:11.997-07:00PRION CONFERENCE 2022 ABSTRACTS CWD TSE PrP ZOONOSIS<p><span style="background-color: white; font-family: arial; font-size: 13.3333px;">PRION 2022 ABSTRACTS, AND A BIG THANK YOU TO </span></p><div style="background-color: white; font-family: arial; font-size: 13.3333px;">On behalf of the Prion2020/2022 Congress Organizing Committee and the NeuroPrion Association, we heartily invite you to join us for the International Conference Prion2020/2022 from 13.-16. September 2022 in Göttingen.<br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Prion 2022 Conference abstracts: pushing the boundaries<br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286</a></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white;"><span style="font-family: arial;"><span style="font-size: 13.3333px;">PRION CONFERENCE 2022 ABSTRACTS CWD TSE PrP ZOONOSIS</span></span></div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Transmission of prion infectivity from CWD-infected macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.</b></div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;">Samia Hannaoui<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Ginny Cheng<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Wiebke Wemheuer<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>, Walter J. Schulz-Schaeffer<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>, Sabine Gilch<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, and Hermann M. Schätzl<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span></div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>Department of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine & Hotchkiss Brain Institute; University of Calgary, Calgary, Canada; <span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Aims</b>: Chronic wasting disease (CWD) is a prion disease of cervids. Its rapid geographic expansion, shedding of infectivity and persistence in the environment for many years are of concern for humans. Here, we provide the first evidence by transmission experiments to different transgenic mouse models and bank voles that <i>Cynomolgus macaques</i> inoculated via different routes with CWD-positive cervid tissues harbor infectious prions that elicit clinical disease in rodents.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Material and Methods</b>: We used tissue materials from macaques inoculated with CWD to inoculate transgenic mice overexpressing cervid PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">C</span>followed by transmission into bank voles. We used RT-QuIC, immunoblot and PET blot analysis to assess brains, spinal cords, and tissues of the gastrointestinal tract (GIT) for the presence of prions.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Results</b>: Our results show that of the macaque materials that induced clinical disease in transgenic mice,73% were from the CNS (46% spinal cord and 27% brain), and 27% were from the spleen, although attack rates were low around 20%. Clinical mice did not display PK-resistant PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span>(PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">res</span>) in immunoblot, but showed low-levels of prion seeding activity. Transmission into bank voles from clinical transgenic mice led to a 100% attack rate with typical PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">res</span>signature in immunoblot, which was different from that of voles inoculated directly with CWD or scrapie prions. High-level prion seeding activity in brain and spinal cord and PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">res</span>deposition in the brain were present. Remarkably, we also found prion seeding activity in GIT tissues of inoculated voles. Second passage in bank voles led to a 100% attack rate in voles inoculated with brain, spinal cord and small intestine material from first round animals, with PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">res</span>in immunoblot, prion seeding activity, and PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">res</span>deposition in the brain. Shortened survival times indicate adaptation in the new host. This also shows that prions detected in GIT tissues are infectious and transmissible. Transmission of brain material from sick voles back to cervidized mice revealed transmission in these mice with a 100% attack rate, and interestingly, with different biochemical signature and distribution in the brain.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Conclusions</b>: Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including oral one. The disease manifested as atypical in macaques and transgenic mice, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Funded by</b>: The National Institutes of Health, USA, and the Alberta Prion Research Institute/Alberta Innovates Canada.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Grant number</b>: 1R01NS121016-01; 201,600,023</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Acknowledgement</b>: We thank Umberto Agrimi, Istituto Superiore di Sanità, Rome, Italy, and Michael Beekes, Robert-Koch Institute Berlin, Germany, for providing the bank vole model. We thank the University of Calgary animal facility staff and Dr. Stephanie Anderson for animal care.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD</b></div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;">Samia Hannaoui<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Irina Zemlyankina<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Sheng Chun Chang<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Maria Immaculata Arifin<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Vincent Béringue<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>, Debbie McKenzie<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">c</span>, Hermann M. Schatzl<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, and Sabine Gilch<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span></div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>Department of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine; Hotchkiss Brain Institute; University of Calgary, Calgary, Canada; <span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>Université Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France; <span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">c</span>Department of Biological Sciences, Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Canada</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Aims</b>: Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we aimed to determine the zoonotic potential of CWD using a mouse model for human prion diseases.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Material and Methods</b>: Transgenic mice overexpressing human PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">C</span>homozygous for methionine at codon 129 (tg650) were inoculated intracerebrally with brain homogenates of white-tailed deer infected with Wisc-1/CWD1 or 116AG CWD strains. Mice were monitored for clinical signs and were euthanized at terminal disease. Brains were tested by RT-QuIC, western blot upon PK digestion, and immunohistochemistry; fecal homogenates were analyzed by RT-QuIC. Brain/spinal cord and fecal homogenates of CWD-inoculated tg650 mice were inoculated into tg650 mice or bank voles. Brain homogenates of bank voles inoculated with fecal homogenates of CWD-infected tg650 mice were used for second passage in bank voles.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Results</b>: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">C</span>with deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650 brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650 mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;">Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Conclusions</b>: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Funded by</b>: We are grateful for financial support from the Natural Sciences and Engineering Research Council of Canada, the National Institutes of Health, Genome Canada, and the Alberta Prion Research Institute. SG is supported by the Canada Research Chairs program.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 13.3333px; margin-bottom: 1em; margin-top: 1em;"><b>Acknowledgement</b>: We thank Dr. Trent Bollinger, WCVM, University of Saskatchewan, Saskatoon, Canada, for providing brain tissue from the WTD-116AG isolate, Dr. Stéphane Haïk, ICM, Paris, France, for providing brain tissue from vCJD and sCJD cases, and Dr. Umberto Agrimi, Istituto Superiore di Sanità, Italy, for the bank vole model. We thank animal facility staff for animal care, Dr. Stephanie Anderson for veterinary oversight, and Yo-Ching Cheng for preparing recombinant PrP substrates. Thank you to Dr. Stephanie Booth and Jennifer Myskiw, Public Health Agency of Canada, Canada.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><b>The chronic wasting disease agent from white-tailed deer is infectious to humanized mice after passage through raccoons</b></div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;">Eric Cassmann<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Xu Qi<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>, Qingzhong Kong<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>, and Justin Greenlee<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span></div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>National Animal Disease Center, Agricultural Research Service, US Department of Agriculture, Ames, IA, USA</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>Departments of Pathology, Neurology, National Center for Regenerative Medicine, and National Prion Disease Pathology Surveillance Center, Case Western Reserve University, Cleveland, Ohio, USA</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><b>Aims</b>: Evaluate the zoonotic potential of the raccoon passaged chronic wasting disease (CWD) agent in humanized transgenic mice in comparison with the North American CWD agent from the original white-tailed deer host.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><b>Material and Methods</b>: Pooled brain material (GG96) from a CWD positive herd was used to oronasally inoculate two white-tailed deer with wild-type prion protein genotype and intracranially inoculate a raccoon. Brain homogenates (10% w/v) from the raccoon and the two white-tailed deer were used to intracranially inoculate separate groups of transgenic mice that express human prion protein with methionine (M) at codon 129 (Tg40h). Brains and spleens were collected from mice at experimental endpoints of clinical disease or approximately 700 days post-inoculation. Tissues were divided and homogenized or fixed in 10% buffered neutral formalin. Immunohistochemistry, enzyme immunoassay, and western blot were used to detect misfolded prion protein (PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span>) in tissue.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><b>Results</b>: Humanized transgenic mice inoculated with the raccoon passaged CWD agent from white-tailed deer exhibited a 100% (12/12) attack rate with an average incubation period of 605 days. PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span>was detected in brain tissue by enzyme immunoassay with an average optical density of 3.6/4.0 for positive brains. PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span>also was detected in brain tissue by western blot and immunohistochemistry. No PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span>was detected in the spleens of mice inoculated with the raccoon passaged CWD agent. Humanized mice inoculated with the CWD agent from white-tailed deer did not have detectable PrP<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">Sc</span>using conventional immunoassay techniques.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><b>Conclusions</b>: The host range of the CWD agent from white-tailed deer was expanded in our experimental model after one passage through raccoons.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><b>Funded by</b>: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><b>Acknowledgement</b>: We thank Quazetta Brown, Lexi Frese, Rylie Frese, Kevin Hassall, Leisa Mandell, and Trudy Tatum for providing excellent technical support to this project.</div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><div style="margin-bottom: 1em; margin-top: 1em;"><b>Stable and highly zoonotic cervid prion strain is possible</b></div><div style="margin-bottom: 1em; margin-top: 1em;">Manuel Camacho, Xu Qi, Liuting Qing, Sydney Smith, Jieji Hu, Wanyun Tao, Ignazio Cali, and Qingzhong Kong</div><div style="margin-bottom: 1em; margin-top: 1em;">Department of Pathology, Case Western Reserve University, Cleveland, USA</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Aims</b>: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in some areas. Multiple in vitro conversion experiments and in vivo animal studies suggest that the CWD-to-human transmission barrier is not unbreakable. A major public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Material and Methods</b>: We inoculated a few sCJD brain samples into cervidized transgenic mice, which were intended as negative controls for bioassays of brain tissues from sCJD cases who had hunted or consumed vension from CWD-endemic states. Some of these mice became infected and their brain tissues were further examined by serial passages in humanized or cervidized mice.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Results</b>: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a ‘cervidized’ CJD strain that we termed CJD<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">ElkPrP</span>. We observed 100% transmission of CJD<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">ElkPrP</span>in transgenic mice expressing human PrP (Tg40h). We passaged CJD<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">ElkPrP</span>two more times in the Tg12 mice. We found that such second and third passage CJD<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">ElkPrP</span>prions also led to 100% infection in the Tg40h mice. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice, despite that natural elk CWD isolates and CJD<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">ElkPrP</span>share the same elk PrP sequence.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Conclusions</b>: Our data demonstrate that highly zoonotic cervid prion strains are not only possible but also can be stably maintained in cervids and that CWD zoonosis is prion strain-dependent.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Funded by</b>: NIH</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Grant number</b>: R01NS052319, R01NS088604, R01NS109532</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Acknowledgement</b>: We want to thank the National Prion Disease Pathology Surveillance Center and Drs. Allen Jenny and Katherine O’Rourke for providing the sCJD samples and the CWD samples, respectively.</div><div style="margin-bottom: 1em; margin-top: 1em;"><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Adaptation of chronic wasting disease (CWD) prion strains in hosts with different <i style="box-sizing: border-box;">PRNP</i> genotypes</b></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;">Camilo Duque Velasquez<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,c</span>, Elizabeth Triscott<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,c</span>, Chiye Kim<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,c</span>, Diana Moreno<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,c</span>, Judd Aiken<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b,c</span>, and Debbie McKenzie<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,c</span></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>Department of Biological Science, University of Alberta, Edmonton, AB T6G 2G8, Canada; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>Department of Agriculture, Food & Nutritional Science, University of Alberta, Edmonton, AB T6G 2G8, Canada; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">c</span>Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB T6G 2M8, Canada</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Aims</b>: The contagious nature of CWD epizootics and the PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>amino acid variation of cervids (and susceptible sympatric species) guarantee the expansion of prion conformational diversity and selective landscapes where new strains can arise. CWD strains can have novel transmission properties including altered host range that may increase zoonotic risk as circulating strains diversify and evolve. We are characterizing the host adaptability of characterized CWD strains as well as CWD isolates from different cervid species in various enzootic regions.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Material and Methods</b>: Characterized CWD strains as well as a number of isolates from hunter-harvested deer were bioassayed in our rodent panel (transgenic mice expressing cervid alleles G96, S96 and H95-PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>, elk PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>, bovine PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>, and both hamsters and non-transgenic laboratory mice). Strain characteristics were compared using computer based scoring of brain pathology (e.g. PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">CWD</span>brain distribution), western blot and protein misfolding cyclic amplification (PMCA).</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Results</b>: Transmission of various isolates resulted in the selection of strain mixtures in hosts expressing similar PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>, particularly for polymorphic white-tailed deer and for Norwegian reindeer. As of the second passage, transmission of P153 moose prions from Norway has not resulted in emergence of strains with properties similar to any North American CWD strains in our taxonomic collection (Wisc-1, CWD2, H95<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">+</span>and 116AG).</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Conclusions</b>: Our data indicates polymorphic white-tailed deer can favor infection with more than one strain. Similar to transmission studies of Colorado CWD isolates from cervids expressing a single PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>primary structure, the isolate from Norway reindeer (V214) represents a strain mixture, suggesting intrinsic strain diversity in the Nordfjella epizootic. The diversity of CWD strains with distinct transmission characteristics represents a threat to wildlife, sympatric domestic animals and public health.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Funded by</b>: Genome Canada and Genome Alberta (Alberta Prion Research Institute and Alberta Agriculture & Forestry); NSERC</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Grant number</b>: #LSARP 10205; NSERC RGPIN-2017-05539</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Acknowledgement</b>: We would like to thank Margo Pybus (Alberta Environment and Parks) Trent Bollinger (University of Saskatchewan) for providing us with tissue samples from hunter-harvested deer and Sylvie Benestad for providing moose and reindeer samples.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Application of PMCA to understand CWD prion strains, species barrier and zoonotic potential</b></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;">Sandra Pritzkow<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Damian Gorski<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Frank Ramirez<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Fei Wang<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Glenn C. Telling<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>, Justin J. Greenlee<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">c</span>, Sylvie L. Benestad<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">d</span>, and Claudio Soto<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>Department of Neurology, University of Texas Medical School at Houston, Houston, Texas, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">c</span>Virus and Prion Research Unit, United States Department of Agriculture, Ames, Iowa, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">d</span>Norwegian Veterinary Institute, OIE Reference Laboratory for CWD, Ås, Norway</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Aims</b>: Chronic wasting disease (CWD) is a prion disease affecting various species of cervids that continues to spread uncontrollably across North America and has recently been detected in Scandinavia (Norway, Sweden and Finland). The mechanisms responsible for the natural transmission of CWD are largely unknown. Furthermore, the risk of CWD transmission to other species, including humans, is also unknown and remains a dangerous enigma. In this study, we investigated the potential of CWD prions to infect several other animal species (sheep, cattle, pig, hamster, and mouse) including humans, by examining their capacity to convert the normal prion protein of distinct species in a PMCA reaction. Moreover, we also investigated whether the <i style="box-sizing: border-box;">in vivo</i> passage of CWD through intermediate species alters their capacity for zoonotic transmission, which may represent a major hazard to human health.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Material and Methods</b>: For these studies, we used brain material from CWD-infected white-tailed deer (<i style="box-sizing: border-box;">Odocoileus virginianus</i>), elk (<i style="box-sizing: border-box;">Cervus canadensis</i>), and mule deer (<i style="box-sizing: border-box;">Odocoileus hemionus</i>) as species native to North America. We also used CWD-infected Moose (<i style="box-sizing: border-box;">Alces alces</i>), reindeer (<i style="box-sizing: border-box;">Rangifer tarandus</i>) and red deer (<i style="box-sizing: border-box;">Cervus elaphus</i>) as Norwegian cervids. We also used brains from cattle, sheep and pigs experimentally infected by CWD. To study interspecies-transmission and zoonotic potential, samples were tested via PMCA for the conversion of PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>into PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>using different combinations of inoculum and host species. Based on these analyses we estimated the spillover and zoonotic potential for different CWD isolates. We define and quantify spillover and zoonotic potential indices as the efficiency by which CWD prions sustain prion generation <i style="box-sizing: border-box;">in vitro</i> at the expense of normal prion proteins from various mammals and human, respectively.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Results</b>: Our results show that prions from some cervid species, especially those found in Northern Europe, have a higher potential to transmit disease characteristics to other animals. Conversely, CWD-infected cervids originated in North America appear to have a greater potential to generate human PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>. We also found that <i style="box-sizing: border-box;">in vivo</i> transmission of CWD to cattle, but not to sheep or pigs substantially increases the ability of these prions to convert human PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>by PMCA.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Conclusions</b>: Our findings support the existence of different CWD prion strains with distinct spillover and zoonotic potentials. We also conclude that transmission of CWD to other animal species may increase the risk for CWD transmission to humans. Our studies may provide a tool to predict the array of animal species that a given CWD prion could affect and may contribute to understanding the risk of CWD for human health.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Funded by</b>: National Institute of Health</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Grant number</b>: P01 AI077774</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Generation of human chronic wasting disease in transgenic mice</b></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;">Zerui Wang<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Kefeng Qin<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>, Manuel V. Camacho<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Ignazio Cali <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,c</span>, Jue Yuan<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Pingping Shen<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Tricia Gilliland<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Syed Zahid Ali Shah<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Maria Gerasimenko<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Michelle Tang<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Sarada Rajamanickam<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Anika Yadati<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, Lawrence B. Schonberger<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">d</span>, Justin Greenlee<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">e</span>, Qingzhong Kong<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,c</span>, James A. Mastrianni<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>, and Wen-Quan Zou<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,c</span></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>Department of Neurology and Center for Comprehensive Care and Research on Memory Disorders, the University of Chicago Pritzker School of Medicine, Chicago, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">c</span>National Prion Disease Pathology Surveillance Center, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">d</span>Division of High-Consequence Pathogens and Pathology, Centers for Disease Control and Prevention, 1600 Clifton Rd, Atlanta, GA, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">e</span>Virus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, 1920 Dayton Avenue, Ames, IA, USA</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Aims</b>: Chronic wasting disease (CWD) results from the accumulation of an infectious misfolded conformer (PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>) of cellular prion protein (PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>) in the brains of deer and elk. It has been spreading rapidly throughout many regions of North America, exported inadvertently to South Korea, and more recently identified in Europe. Mad cow disease has caused variant Creutzfeldt-Jakob disease (vCJD) in humans and is currently the only known zoonotic prion disease. Whether CWD is transmissible to humans remains uncertain. The aims of our study were not only to confirm whether CWD prion isolates can convert human brain PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>into PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span><i style="box-sizing: border-box;">in vitro</i> by serial protein misfolding cyclic amplification (sPMCA) but also to determine whether the sPMCA-induced CWD-derived human PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>is infectious.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Material and Methods</b>: Eight CWD prion isolates from 7 elks and 1 deer were used as the seeds while normal human brain homogenates containing either PrP-129 MM (n = 2) or PrP-129 VV (n = 1) were used as the substrates for sPMCA assay. A normal elk brain tissue sample was used as a negative control seed. Two lines of humanized transgenic (Tg) mice expressing either human PrP-129VV or −129 MM polymorphism were included for transmission studies to determine the infectivity of PMCA-amplified PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>. Wester blotting and immunohistochemistry and hematoxylin & eosin staining were used for determining PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>and neuropathological changes of inoculated animals.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Results</b>: We report here the generation of the first CWD-derived infectious human PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>using elk CWD PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>to initiate conversion of human PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>from normal human brain homogenates with PMCA <i style="box-sizing: border-box;">in vitro</i>. Western blotting with a human PrP selective antibody confirmed that the PMCA-generated protease-resistant PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>was derived from the human brain PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>substrate. Two lines of humanized transgenic mice expressing human PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>with either Val or Met at the polymorphic codon 129 developed clinical prion disease following intracerebral inoculation with the PMCA-generated CWD-derived human PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>. Diseased mice exhibited distinct PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>patterns and neuropathological changes in the brain.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Conclusions</b>: Our study, using PMCA and animal bioassays, provides the first evidence that CWD PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>has the potential to overcome the species barrier and directly convert human PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>into infectious PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">Sc</span>that can produce bona fide prion disease when inoculated into humanized transgenic mice.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Funded by</b>: CJD Foundation and NIH</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Mortality surveillance of persons potentially exposed to chronic wasting disease</b></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;">R.A. Maddox<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, R.F. Klos<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>, L.R. Will<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>, S.N. Gibbons-Burgener<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>, A. Mvilongo<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, J.Y. Abrams<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, B.S. Appleby<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">c</span>, L.B. Schonberger<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, and E.D. Belay<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>Wisconsin Department of Health Services (WDHS), Division of Public Health, Madison, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">c</span>National Prion Disease Pathology Surveillance Center (NPDPSC), Case Western Reserve University, Cleveland, USA</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Aims</b>: It is unknown whether chronic wasting disease (CWD), a prion disease of cervids, can infect people, but consumption of meat from infected animals would be the most likely route of transmission. Wisconsin Department of Health Services, Division of Public Health (WDHS) personnel maintain a database consisting of information collected from hunters who reported eating, or an intention to eat, venison from CWD-positive cervids. These data, collected since 2003, allow for the evaluation of causes of mortality in individuals potentially exposed to CWD.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Material and Methods</b>: The WDHS database contains the name, date of birth, when available, year of CWD-positive deer harvest, and city and state of residence for each potentially exposed individual. The database also includes information on how the deer was processed (self-processed or by a commercial operator) and when applicable, names of others with whom the venison was shared. Duplicate entries (i.e., those who consumed venison from CWD-positive deer in multiple hunt years) are determined by first name, last name, and date of birth. All names in the database are cross-checked with reported cases of human prion disease in Wisconsin and cases in the National Prion Disease Pathology Surveillance Center (NPDPSC) diagnostic testing database. Persons with date of birth available are also cross-checked with prion disease decedents identified through restricted-use national multiple cause-of-death data via a data use agreement with the National Center for Health Statistics (NCHS).</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Results</b>: The database currently consists of 1561 records for hunt years 2003–2017 and 87 additional records for 2018–2019. Of these, 657 records have accompanying date of birth; 15 entries were removed as duplicates leaving 642 unique individuals. Of these individuals, 278 of 426 (66%) who ate venison from a CWD-positive deer and provided processing information reported self-processing. No matches were found among any persons in the database cross-checked with WDHS human prion disease surveillance data, NPDPSC data (February 2022 update), and NCHS data through 2020.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Conclusions</b>: Because of the linkage of person and CWD-positive animal in the WDHS database, reviewing the cause of mortality in potentially exposed persons is possible. The number of individuals cross-checked so far is likely only a small percentage of those potentially exposed to CWD in Wisconsin, and many more years of vital status tracking are needed given an expected long incubation period should transmission to humans occur. Nevertheless, the findings of this ongoing review are thus far reassuring.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Prion disease incidence, United States, 2003–2020</b></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;">R.A. Maddox<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, M.K. Person<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, K. Kotobelli<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>, A. Mvilongo<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, B.S. Appleby<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>, L.B. Schonberger<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, T.A. Hammett<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, J.Y. Abrams<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>, and E.D. Belay<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, USA; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>National Prion Disease Pathology Surveillance Center (NPDPSC), Case Western Reserve University, Cleveland, USA</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Aims</b>: Mortality data, in conjunction with neuropathological and genetic testing results, are used to estimate prion disease incidence in the United States.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Material and Methods</b>: Prion disease decedents for 2003–2020 were identified from restricted-use U.S. national multiple cause-of-death data, via a data use agreement with the National Center for Health Statistics, and from the National Prion Disease Pathology Surveillance Center (NPDPSC) database. NPDPSC decedents with neuropathological or genetic test results positive for prion disease for whom no likely match was found in the NCHS multiple cause-of-death data were added as cases for incidence calculations, while those with negative neuropathology results but with cause-of-death data indicating prion disease were removed. Unmatched cases in the NPDPSC database lacking neuropathological testing but with a positive real-time quaking-induced conversion (RT-QuIC) test result were additionally assessed. Age-specific and age-adjusted average annual incidence rates were calculated from the combined data; the year 2000 as the standard population and the direct method were used for age-adjustment.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Results</b>: A total of 7,921 decedents were identified as having prion disease during 2003–2020 for an age-adjusted average annual incidence of 1.2 per million population. The age-adjusted incidence between males and females (1.3 and 1.1 per million, respectively) differed significantly (p < 0.0001). The age-specific average annual incidence among those <55 and ≥55 years of age was 0.2 and 4.8 per million, respectively; incidence among those ≥65 was 6.1 per million. Eighteen cases were <30 years of age for an age-specific incidence of 8.0 per billion; only 6 of these very young cases were sporadic (3 sporadic CJD, 3 sporadic fatal insomnia), with the rest being familial (9), variant (2), or iatrogenic (1). The age-adjusted annual incidence for the most recent year of data, 2020, was 1.3 per million. However, assessment of RT-QuIC positive cases lacking neuropathology in the NPDPSC database suggested that approximately 20% more cases may have occurred in that year; the addition of a subset of these cases that had date of death information available (n = 44) increased the 2020 rate to 1.4 per million.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Conclusions</b>: Mortality data supplemented with the results of neuropathological, CSF RT-QuIC, and genetic testing can be used to estimate prion disease incidence. However, the identification in the NPDPSC database of RT-QuIC-positive cases lacking date of death information suggests that this strategy may exclude a number of probable prion disease cases. Prion disease cases <30 years of age, especially those lacking a pathogenic mutation, continue to be very rare.</p></div><div style="margin-bottom: 1em; margin-top: 1em;"><div style="margin-bottom: 1em; margin-top: 1em;"><b>Shedding of Chronic Wasting Disease Prions in Multiple Excreta Throughout Disease Course in White-tailed Deer</b></div><div style="margin-bottom: 1em; margin-top: 1em;">Nathaniel D. Denkers<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Erin E. McNulty<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Caitlyn N. Kraft<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Amy V. Nalls<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Joseph A. Westrich<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Wilfred Goldmann<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>, Candace K. Mathiason<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, and Edward A. Hoover<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span></div><div style="margin-bottom: 1em; margin-top: 1em;"><span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>Prion Research Center, College of Veterinary Medicine and Biological Sciences, Department of Microbiology, Immunology, and Pathology; Colorado State University, Fort Collins, CO, USA; <span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>Division of Infection and Immunity, The Roslin Institute and the Royal Dick School of Veterinary Studies, University of Edinburgh, Midlothian, UK</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Aims</b>: Chronic wasting disease (CWD) now infects cervids in South Korea, North America, and Scandinavia. CWD is unique in its efficient transmission and shedding of prions in body fluids throughout long course infections. Questions remain as to the magnitude of shedding and the route of prion acquisition. As CWD continues to expand, the need to better understand these facets of disease becomes more pertinent. The purpose of the studies described was to define the longitudinal shedding profile of CWD prions in urine, saliva, and feces throughout the course of infection in white-tailed deer.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Material and Methods</b>: Twelve (12) white-tailed deer were inoculated with either 1 mg or 300ng of CWD. Urine, saliva, and feces were collected every 3-month post-inoculation (MPI) throughout the study duration. Cohorts were established based on PNRP genotype: codon 96 GG (n = 6) and alternate codons 96 GS (n = 5) & 103NT (n = 1). Urine and saliva were analyzed using iron-oxide magnetic extraction (IOME) and real-time quaking induced conversion (RT-QuIC)(IQ). Feces were subjected to IOME, followed by 4 rounds protein misfolding cyclic amplification (PMCA) with products analyzed by RT-QuIC (IPQ). To determine whether IPQ may be superior to IQ, a subset of urine and saliva were also tested by IPQ. Results were compared with clinical disease status.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Results</b>: Within the 96 GG cohort, positive seeding activity was detected in feces from all deer (100%), in saliva from 5 of 6 (83%), and in urine from 4 of 6 (66%). Shedding in all excreta occurred at, or just after, the first positive tonsil biopsy result. In the 96 GS/103NT cohort, positive seeding activity could be detected in feces from 3 of 6 (50%) deer, saliva in 2 of 6 (33%), and urine in 1 of 6 (16%). Shedding in excreta was detected >5 months after the first tonsil positive result. Four of six 96 GG deer developed clinical signs of CWD, whereas only 2 of the 96 GS/103NT did. Shedding was more frequently detected in deer with clinical disease. The IPQ protocol did not significantly improve detection in saliva or urine samples, however, it significantly augmented detection in feces by eliminating non-specific background commonly experienced with IQ. Negative control samples remained negative in samples tested.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Conclusions</b>: These studies demonstrate: (a) CWD prion excretion occurs throughout infection; (2) PRNP genotype (GG≫GS/NT) influences the excreta shedding; and (3) detection sensitivity in excreta can vary with different RT-QuIC protocols. These results provide a more complete perspective of prion shedding in deer during the course of CWD infection.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Funded by</b>: National Institutes of Health (NIH)</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Grant number</b>: RO1-NS061902-09 R to EAH, PO1-AI077774 to EAH, and R01-AI112956-06 to CKM</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Acknowledgement</b>: We abundantly thank Sallie Dahmes at WASCO and David Osborn and Gino D’Angelo at the University of Georgia Warnell School of Forestry and Natural Resources for their long-standing support of this work through provision of the hand-raised, CWD-free, white-tailed deer used in these studies</div><div style="margin-bottom: 1em; margin-top: 1em;"><div style="margin-bottom: 1em; margin-top: 1em;"><b>Large-scale PMCA screening of retropharyngeal lymph nodes and in white-tailed deer and comparisons with ELISA and IHC: the Texas CWD study</b></div><div style="margin-bottom: 1em; margin-top: 1em;">Rebeca Benavente<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Paulina Soto<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>, Mitch Lockwood<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>, and Rodrigo Morales<span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span></div><div style="margin-bottom: 1em; margin-top: 1em;"><span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">a</span>Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Texas, USA; <span style="font-size: 12px; line-height: 0; position: relative; vertical-align: baseline;">b</span>Texas Park and Wildlife Department, Texas, USA</div><div style="margin-bottom: 1em; margin-top: 1em;">Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that affects various species of cervids, and both free-ranging and captive animals. Until now, CWD has been detected in 3 continents: North America, Europe, and Asia. CWD prevalence in some states may reach 30% of total animals. In Texas, the first case of CWD was reported in a free-range mule deer in Hudspeth and now it has been detected in additional 14 counties.</div><div style="margin-bottom: 1em; margin-top: 1em;">Currently, the gold standard techniques used for CWD screening and detection are ELISA and immunohistochemistry (IHC) of obex and retropharyngeal lymph nodes (RPLN). Unfortunately, these methods are known for having a low diagnostic sensitivity. Hence, many CWD-infected animals at pre-symptomatic stages may be misdiagnosed. Two promising <i>in vitro</i> prion amplification techniques, including the real-time quaking-induced conversion (RT-QuIC) and the protein misfolding cyclic amplification (PMCA) have been used to diagnose CWD and other prion diseases in several tissues and bodily fluids. Considering the low cost and speed of RT-QuIC, two recent studies have communicated the potential of this technique to diagnose CWD prions in RPLN samples. Unfortunately, the data presented in these articles suggest that identification of CWD positive samples is comparable to the currently used ELISA and IHC protocols. Similar studies using the PMCA technique have not been reported.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Aims</b>: Compare the CWD diagnostic potential of PMCA with ELISA and IHC in RPLN samples from captive and free-range white-tailed deer.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Material and Methods</b>: In this study we analyzed 1,003 RPLN from both free-ranging and captive white-tailed deer collected in Texas. Samples were interrogated with the PMCA technique for their content of CWD prions. PMCA data was compared with the results obtained through currently approved techniques.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Results</b>: Our results show a 15-fold increase in CWD detection in free-range deer compared with ELISA. Our results unveil the presence of prion infected animals in Texas counties with no previous history of CWD. In the case of captive deer, we detected a 16% more CWD positive animals when compared with IHC. Interestingly, some of these positive samples displayed differences in their electroforetic mobilities, suggesting the presence of different prion strains within the State of Texas.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Conclusions</b>: PMCA sensitivity is significantly higher than the current gold standards techniques IHC and ELISA and would be a good tool for rapid CWD screening.</div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Funded by: USDA</b></div><div style="margin-bottom: 1em; margin-top: 1em;"><b>Grant number</b>: AP20VSSPRS00C143</div><div style="margin-bottom: 1em; margin-top: 1em;"><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">ATYPRION project: assessing the zoonotic potential of interspecies transmission of CWD isolates to livestock (preliminary results).</b></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;">Enric Vidal<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,b</span>, Juan Carlos Espinosa<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">c</span>, Samanta Giler<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,b</span>, Montserrat Ordóñez<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,b</span>, Guillermo Cantero<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a,b</span>, Vincent Béringue<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">d</span>, Justin J. Greenlee<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">e</span>, and Juan Maria Torres<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">c</span></p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">a</span>Unitat mixta d’Investigació IRTA-UAB en Sanitat Animal. Centre de Recerca en Sanitat Animal (CReSA). Campus de la Universitat Autònoma de Barcelona (UAB), Bellaterra, Catalonia; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">b</span>IRTA. Programa de Sanitat Animal. Centre de Recerca en Sanitat Animal (CReSA). Campus de la Universitat Autònoma de Barcelona (UAB), Bellaterra, Catalonia; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">c</span>Centro de Investigación en Sanidad Animal, CISA-INIA-CSIC, Valdeolmos, Madrid, Spain; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">d</span>Molecular Virology and Immunology, French National Research Institute for Agriculture, Food and Environment (INRAE), Université Paris-Saclay, Jouy-en-Josas, France; <span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">e</span>Virus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, USA</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Aims</b>: Since variant Creutzfeldt-Jackob disease was linked to the consumption of bovine spongiform encephalopathy prions, the study of the pathobiological features of animal prions, particularly their zoonotic potential, is of great concern to the scientific community and public health authorities. Furthermore, interspecies transmission of prions has been demonstrated as a putative evolutionary mechanism for prions, that can lead to the emergence of new features including the ability to infect humans. For instance, small ruminants’ atypical scrapie prions, when propagated in a bovine or porcine host, can shift to a classical BSE phenotype thus posing a potential risk in case of human exposure. So far, no hard evidence of zoonotic transmission of cervids’ chronic wasting disease (CWD) to humans has been published, however experimental transmission to bovine, ovine and caprine hosts has been achieved. Our goal is to investigate if, once passaged through these domestic species, CWD prions might become infectious to humans.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Material and Methods</b>: Different CWD isolates experimentally adapted to cattle, sheep and goat (Hamir et al, 2005, 2006, 2007, Greenlee et al 2012) have been intracerebrally inoculated to transgenic mouse models expressing the human cellular prion protein either homozygous for methionine or valine at codon 129 (Tg340-Met129 and Tg362-Val129). Additionally, inocula obtained from experimental transmission of elk CWD to ovinized (Tg501) and bovinized (BoTg110) transgenic mice, as well as white-tailed deer CWD to BoTg110 mice, are currently being bioassayed in both human PrP<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">C</span>transgenic models.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Results and conclusions</b>: No evidence of transmission has been found on first passage for bovine adapted elk and mule deer CWD to none of the humanized models. The remaining bioassays are ongoing without showing clinical signs yet, as well as second passages for the negative 1<span style="box-sizing: border-box; font-size: 13.2px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">st</span>passages.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Funded by</b>: <i style="box-sizing: border-box;">La Marató de TV3</i> foundation.</p><p style="box-sizing: border-box; font-family: "Open Sans", sans-serif; font-size: 17.6px; margin: 1em 0px; word-break: break-word;"><b style="box-sizing: border-box;">Grant number</b>: ATYPRION (201,821–30-31-32)</p></div></div></div></div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286" rel="nofollow noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286</a></div><div style="background-color: white; color: #333333; font-family: sans-serif; font-size: 16px; margin-bottom: 1em; margin-top: 1em;"><br /></div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-5783466110981773845.post-18693959570870341172021-06-28T08:23:00.004-07:002021-06-28T08:23:45.319-07:00Prion Conference 2020 and 2021 Canceled <p> <span style="background-color: white; font-family: arial; font-size: 13.3333px;">re-Prion Conference 2021?</span></p><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Prion Conference 2020 and 2021 Canceled, SEE;</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Dear Researcher,</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Finally, we decided to postpone the Prion2020 conference to 2022.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">The new dates are: 13 - 16 September 2022 (with workshops on 13 September), location: Göttingen (Germany).</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">The website prion2020 will be updated soon.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">On behalf of Professor Inga Zerr</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Am 09.06.2021 um 21:55 schrieb Terry Singeltary <flounder9@verizon.net>:</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">PRION2020 POSTPONED TO 2021 – DUE TO CORONAVIRUS (COVID-19)</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Due to the extraordinary circumstances with COVID 19, we have decided to postpone the upcoming congress Prion2020. We will circulate new dates as soon as possible. We will keep the program as it is decided so far. Please check this website for updates.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">For any questions, please contact us via email: prion2020@med.uni-goettingen.de</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">We appreciate your continued interest in our conference and you will soon hear from us again.</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Best regards,</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Inga Zerr & Prion Team</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">========</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">Greetings Dr. Inga Zerr Ma'am, and Prion Conference 2021 et al, </div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">i have been curious about what is going on with Prion Conference 2021. ...snip...end...TSS</div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><a href="https://prionconference.blogspot.com/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://prionconference.blogspot.com/</a></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;"><br /></div><div style="background-color: white; font-family: arial; font-size: 13.3333px;">terry</div>Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-5783466110981773845.post-39676523341954724752020-04-20T13:56:00.002-07:002021-06-08T13:58:30.203-07:00PRION2020 POSTPONED TO 2021 – DUE TO CORONAVIRUS (COVID-19)<div style="font-family: arial; font-size: 13.3333px;">
PRION2020 POSTPONED TO 2021 – DUE TO CORONAVIRUS (COVID-19)</div>
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Due to the extraordinary circumstances with COVID 19, we have decided to postpone the upcoming congress Prion2020.</div>
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We will circulate new dates as soon as possible. We will keep the program as it is decided so far. Please check this website for updates.</div>
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For any questions, please contact us via email: prion2020@med.uni-goettingen.de We appreciate your continued interest in our conference and you will soon hear from us again. Best regards, Inga Zerr & Prion Team</div>
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SATURDAY, APRIL 18, 2020 </div>
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Coronavirus at Smithfield pork plant: The untold story of America's biggest outbreak</div>
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Tyson Foods processing plant in rural Iowa hit hard by coronavirus with 186 positive cases</div>
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Thursday, May 23, 2019 </div>
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Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts</div>
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Sunday, February 25, 2018 </div>
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PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW</div>
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TUESDAY, JULY 04, 2017</div>
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*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***</div>
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Wednesday, May 24, 2017 </div>
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PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1</div>
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Thursday, December 1, 2016 </div>
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PRION2017 DECIPHERING NEURODEGENERATIVE DISORDERS 23 – 26 May 2017 Edinburgh </div>
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MONDAY, MAY 02, 2016 </div>
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Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo</div>
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ALSO SEE;</div>
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<a href="http://www.prions2016bcn.com/assets/abstract-book.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.prions2016bcn.com/assets/abstract-book.pdf</a></div>
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SEE WORKING LINK;</div>
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PRION 2015</div>
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PRION 2015 ORAL ABSTRACTS</div>
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Saturday, May 30, 2015</div>
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PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS</div>
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PRION 2014</div>
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Monday, June 23, 2014 </div>
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*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD </div>
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Monday, June 23, 2014 </div>
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*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD </div>
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<a href="https://www.landesbioscience.com/journals/prion/6.Poster_Topic%202_Prion%20Diseases%20in%20Animals.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.landesbioscience.com/journals/prion/6.Poster_Topic%202_Prion%20Diseases%20in%20Animals.pdf</a> </div>
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PRION 2013</div>
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<a fg_scanned="1" href="https://www.tandfonline.com/doi/abs/10.4161/pri.24864" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.tandfonline.com/doi/abs/10.4161/pri.24864</a></div>
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PRION 2012</div>
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<a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.4161/pri.20605" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.tandfonline.com/doi/abs/10.4161/pri.20605</a></div>
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<a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.4161/pri.20615?src=recsys" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.tandfonline.com/doi/abs/10.4161/pri.20615?src=recsys</a></div>
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<br /></div>
<div style="line-height: 1.22em;">
<a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.4161/pri.20615" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.tandfonline.com/doi/abs/10.4161/pri.20615</a></div>
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<br /></div>
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<a fg_scanned="1" href="https://www.tandfonline.com/doi/abs/10.4161/pri.20608?src=recsys" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.tandfonline.com/doi/abs/10.4161/pri.20608?src=recsys</a></div>
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<br /></div>
<div style="line-height: 1.22em;">
<a fg_scanned="1" href="https://www.tandfonline.com/doi/abs/10.4161/pri.20608" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.tandfonline.com/doi/abs/10.4161/pri.20608</a></div>
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PRION 2011</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Seven main threats for the future linked to prions</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
The NeuroPrion network has identified seven main threats for the future linked to prions.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
First threat</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed. Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Second threat</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Third threat</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Fourth threat</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy, whereas other countries, including the US, Brazil, and Argentine do not have these constraints. However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Fifth threat</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Sixth threat</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Seventh Threat</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
<a fg_scanned="1" href="http://www.neuroprion.org/en/np-neuroprion.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/en/np-neuroprion.html</a></div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
<a fg_scanned="1" href="http://www.neuroprion.org/en/np-news.html#63731832" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/en/np-news.html#63731832</a></div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
PRION 2010</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
<div style="line-height: 1.22em;">
WEDNESDAY, SEPTEMBER 08, 2010</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
CWD PRION CONGRESS SEPTEMBER 8-11 2010</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
PRION 2010</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html</a></div>
</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf</a></div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
<a fg_scanned="1" href="http://tandfonline.com/toc/kprn20/4/3?nav=tocList" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://tandfonline.com/toc/kprn20/4/3?nav=tocList</a></div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
PRION 2009 CONFERENCE</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
<div style="line-height: 1.22em;">
P.9.21 Molecular characterization of BSE in Canada</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle. Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. * It also suggests a similar cause or source for atypical BSE in these countries.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
*** It also suggests a similar cause or source for atypical BSE in these countries. ***</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. *** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. *** It also suggests a similar cause or source for atypical BSE in these countries. ***</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
=====</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
<div style="line-height: 1.22em;">
October 2009</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
O.11.3</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Infectivity in skeletal muscle of BASE-infected cattle</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta” Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
=====</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
<div style="line-height: 1.22em;">
P.5.3</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Differences in the expression levels of selected genes in the brain tissue of cattle naturally infected with classical and atypical BSE.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Magdalena Larska1, Miroslaw P. Polak1, Jan F. Zmudzinski1, Juan M. Torres2 1National Veterinary Institute, Poland; 2CISA/INIA</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Background: Recently cases of BSE in older cattle named BSE type L and type H were distinguished on the basis of atypical glycoprofiles of PrPres. The nature of those strains is still not fully understood but it is suspected that the atypical BSE cases are sporadic. Hitherto most BSE cases were studied in respect to the features of PrPSc. Here we propose gene expression profiling as a method to characterize and distinguish BSE strains.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Objectives: The aim of the study was to compare the activities of some factors which are known to play a role in TSE’s pathogenesis in order to distinguish the differences/similarities between all BSE types. Methods: 10 % homogenate of brain stem tissue collected from obex region of medulla oblongata from 20 naturally infected BSE cows (8 assigned as classical BSE, other 8 and 4 infected with atypical BSE L type and H type respectively) was used in the study. As negative control animals we’ve used 8 animals in the age between 2.5 and 13 years. The genes were relatively quantified using SYBR Green real time RT-PCR. Raw data of Ct values was transformed into normalized relative quantities using Qbase Plus®.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Results and Discussion: In most of the tested genes significant differences in the expression levels between the brain stem of healthy cattle and animals infected with different BSE types were observed. In c-type BSE in comparison to healthy and atypical BSE the overexpression of the gene of bcl-2, caspase 3, 14-3-3 and tylosine kinase Fyn was significant. Simultaneously in atypical BSEs type-L and type-H the levels of prion protein, Bax and LPR gene was elevated in comparison to c-BSE. Additionally L-BSE was characterized by the overexpression of STI1 and SOD genes compared to the other of BSE types. The downregulation of the gene encoding NCAM1 was observed in all BSE types in comparison to healthy cows. Different gene expression profiles of bovine brains infected with classical and atypical BSE indicates possible different pathogenesis or source of the disease.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
O.10.1</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Transmission of uncommon forms of bovine prions to transgenic mice expressing human PrP: questions and progress</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Vincent Béringue, Hubert Laude INRA, UR 892, Virologie Immunologie Moléculaires, France</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
The active, large-scale testing of livestock nervous tissues for the presence of protease-resistant prion protein (PrPres) has led to the recognition of 2 uncommon PrPres molecular signatures, termed H-type and L-type BSE. Their experimental transmission to various transgenic and inbred mouse lines unambiguously demonstrated the infectious nature of such cases and the existence of distinct prion strains in cattle. Like the classical BSE agent, H- and L-type (or BASE) prions can propagate in heterologous species. In addition L-type prions acquire molecular and neuropathologic phenotypic traits undistinguishable from BSE or BSE-related agents upon transmission to transgenic mice expressing ovine PrP (VRQ allele) or wild-type mice. An understanding of the transmission properties of these newly recognized prions when confronted with human PrP sequence was therefore needed. Toward this end, we inoculated mice expressing human PrP Met129 with several field isolates. Unlike classical BSE agent, L-type prions appeared to propagate in these mice with no obvious transmission barrier. In contrast, we repeatedly failed to infect them with Htype prions. Ongoing investigations aim to extend the knowledge on these uncommon strains: are these agents able to colonize lymphoid tissue, a potential key factor for successful transmission by peripheral route; is there any relationship between these assumedly sporadic forms of TSE in cattle and some sporadic forms of human CJD are among the issues that need to be addressed for a careful assessment of the risk for cattle-to-human transmission of H- and L-type prions.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
O.4.3</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
O.4.4</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
PrPSc distribution pattern in cattle experimentally challenged with H-type and L-type atypical BSE</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Anne Buschmann1, Ute Ziegler1, Leila McIntyre2, Markus Keller1, Ron Rogers3, Bob Hills3, Martin H. Groschup1 1Friedrich-Loeffler-Institut, INEID, Germany; 2Faculty of Veterinary Medicine, University of Calgary, Canada; 3Health Canada, Ottawa, Canada</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Background: After the detection of two novel BSE forms designated H-type and L-type BSE, the question of the pathogenesis and the agent distribution in cattle affected with these forms was fully open. From initial studies, it was already known that the PrPSc distribution in L-type BSE affected cattle differed from that known for classical BSE (C-type) where the obex region always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved. No information was available on the distribution pattern in H-type BSE.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Objectives: To analyse the PrPSc and infectivity distribution in cattle experimentally challenged with H-type and L-type BSE.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Methods: We analysed CNS and peripheral tissue samples collected from cattle that were intracranially challenged with Htype (five animals) and L-type (six animals) using a commercial BSE rapid test (IDEXX HerdChek), immunohistochemistry (IHC) and a highly sensitive Western blot protocol including a phosphotungstic acid precipitation of PrPSc (PTA-WB). Samples collected during the preclinical and the clinical stages of the disease were examined. For the detection of BSE infectivity, selected samples were also inoculated into highly sensitive Tgbov XV mice overexpressing bovine prion protein (PrPC).</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Results: Analysis of a collection of fifty samples from the peripheral nervous, lymphoreticular, digestive, reproductive, respiratory and musculo-skeletal systems by PTA-WB, IDEXXHerdChek BSE EIA and IHC revealed a general restriction of the PrPSc accumulation to the central nervous system.</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
Discussion: Our results on the PrPSc distribution in peripheral tissues of cattle affected with H-type and L-type BSE are generally in accordance with what has been known for C-type BSE. Bioassays are ongoing in highly sensitive transgenic mice in order to reveal infectivity.</div>
</div>
</div>
<div style="line-height: 1.22em;">
<br /></div>
<div style="line-height: 1.22em;">
see page 176 of 201 pages...tss</div>
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<div style="line-height: 1.22em;">
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf </div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf</a></div>
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<a fg_scanned="1" href="http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html</a></div>
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ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD</div>
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Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5 The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.</div>
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<a href="http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf</a></div>
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PRION2008 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a></div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/programme.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/programme.pdf</a></div>
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0C7.04</div>
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North American Cervids Harbor Two Distinct CWD Strains</div>
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Authors</div>
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Angers, R. Seward, T, Napier, D., Browning, S., Miller, M., Balachandran A., McKenzie, D., Hoover, E., Telling, G. 'University of Kentucky; Colorado Division of Wildlife, Canadian Food Inspection Agency; University Of Wisconsin; Colorado State University.</div>
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Despite the increasing geographic distribution and host range of CWD, little is known about the prion strain(s) responsible for distinct outbreaks of the disease. To address this we inoculated CWD-susceptible Tg(CerPrP)1536+/· mice with 29 individual prion samples from various geographic locations in North America. Upon serial passage, intrastudy incubation periods consistently diverged and clustered into two main groups with means around 210 and 290 days, with corresponding differences in neuropathology. Prion strain designations were utilized to distinguish between the two groups: Type I CWD mice succumbed to disease in the 200 day range and displayed a symmetrical pattern of vacuolation and PrPSc deposition, whereas Type II CWD mice succumbed to disease near 300 days and displayed a strikingly different pattern characterized by large local accumulations of florid plaques distributed asymmetrically. Type II CWD bears a striking resemblance to unstable parental scrapie strains such as 87A which give rise to stable, short incubation period strains such as ME7 under certain passage conditions. In agreement, the only groups of CWD-inoculated mice with unwavering incubation periods were those with Type I CWD. Additionally, following endpoint titration of a CWD sample, Type I CWD could be recovered only at the lowest dilution tested (10-1), whereas Type II CWD was detected in mice inoculated with all dilutions resulting in disease. Although strain properties are believed to be encoded in the tertiary structure of the infectious prion protein, we found no biochemical differences between Type I and Type II CWD. Our data confirm the co·existence of two distinct prion strains in CWD-infected cervids and suggest that Type II CWD is the parent strain of Type I CWD.</div>
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see page 29, and see other CWD studies ;</div>
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http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</div>
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Monday, December 1, 2008 </div>
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When Atypical Scrapie cross species barriers </div>
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Authors Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France. </div>
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Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence. The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie. Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage. Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate. (i) the unsuspected potential abilities of atypical scrapie to cross species barriers (ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a></div>
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<a fg_scanned="1" href="http://www.istitutoveneto.it/flex/cm/pages/ServeBLOB.php/L/IT/IDPagina/1" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.istitutoveneto.it/flex/cm/pages/ServeBLOB.php/L/IT/IDPagina/1</a></div>
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Sunday, November 23, 2008</div>
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PRION October 8th - 10th 2008 Book of Abstracts</div>
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<a fg_scanned="1" href="http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.html</a></div>
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PRION2007 NEWSLETTER</div>
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<a fg_scanned="1" href="http://www.neuroprion.org/en/np-event-prion-2007.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/en/np-event-prion-2007.html</a></div>
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<a href="http://www.assembly.ab.ca/lao/library/egovdocs/2007/ca6/apri/158719_07.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.assembly.ab.ca/lao/library/egovdocs/2007/ca6/apri/158719_07.pdf</a></div>
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PRION2007 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf</a> </div><div style="line-height: 1.22em;"><br /></div><div style="line-height: 1.22em;"><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">P04.27</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasm�zas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; L�wer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat � l�Energie Atomique, France; 3Instituto Superiore di Sanit�, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Background:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Aims:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Methods:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Results:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Conclusions:</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;">The work referenced was performed in partial fulfilment of the study �BSE in primates� supported by the EU (QLK1-2002-01096).</span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><br /></span></div><div><span style="color: #202020; font-family: Helvetica, Arial, sans-serif; font-size: 13px;"><a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a></span></div></div>
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FC5.5.1</div>
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BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc C-terminal Truncated Fragments</div>
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Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux, MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4; Monaco, S3 1University of Verona, of Neurological and Visual Sciences, Italy; 2CEA, IMETI/SEPIA, France; 3University of Verona, Neurological and Visual Sciences, Italy; 4IMETI/SEPIA, France; 5IZSPLVA, Italy; 6The Scripps Research Insitute, USA</div>
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The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent human prion disease, remains still unknown. The marked disease phenotype heterogeneity observed in sCJD is thought to be influenced by the type of proteinase K-resistant prion protein, or PrPSc (type 1 or type 2 according to the electrophoretic mobility of the unglycosylated backbone), and by the host polymorphic Methionine/Valine (M/V) codon 129 of the PRNP. By using a two-dimensional gel electrophoresis (2D-PAGE) and imunoblotting we previously showed that in sCJD, in addition to the PrPSc type, distinct PrPSc C-terminal truncated fragments (CTFs) correlated with different sCJD subtypes. Based on the combination of CTFs and PrPSc type, we distinguished three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1 of all genotypes,; (ii) the second was found in M/M-2 (cortical form); (iii) the third in amyloidogenic M/V- 2 and V/V-2 subtypes (Zanusso et al., JBC 2004) . Recently, we showed that sCJD subtype M/V-2 shared molecular and pathological features with an atypical form of BSE, named BASE, thus suggesting a potential link between the two conditions. This connection was further confirmed after 2D-PAGE analysis, which showed an identical PrPSc signature, including the biochemical pattern of CTFs. To pursue this issue, we obtained brain homogenates from Cynomolgus macaques intracerebrally inoculated with brain homogenates from BASE. Samples were separated by using a twodimensional electrophoresis (2D-PAGE) followed by immunoblotting. </div>
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***We here show that the PrPSc pattern obtained in infected primates is identical to BASE and sCJD MV-2 subtype. These data strongly support the link, or at least a common ancestry, between a sCJD subtype and BASE. </div>
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This work was supported by Neuroprion (FOOD-CT-2004-506579)</div>
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FC5.5.2</div>
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Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical BSE Phenotype and a Muscle Wasting Disease</div>
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Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2; Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati, M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L2 1University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA, Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta, Italy</div>
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The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecular basis, in a pre-symptomatic clinical stage. In recent years, the active surveillance system has uncovered atypical BSE cases, which are characterized by distinct conformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported two Italian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. A major limitation of transmission studies to mice is the lack of reliable information on clinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolates by i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and in experimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. </div>
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***This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle and in some subtypes of inherited and sporadic Creutzfeldt-Jakob disease.</div>
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P02.35</div>
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Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE</div>
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Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden</div>
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Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. </div>
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***The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.</div>
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<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.com/pdf_docs/conferences/prion2007/abstract_book.pdf</a> </div>
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<a fg_scanned="1" href="http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html</a></div>
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P03.141</div>
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Aspects of the Cerebellar Neuropathology in Nor98</div>
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Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,</div>
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Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
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***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.</div>
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<a href="http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf</a></div>
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PRION2006 NEWSLETTER</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/newsletters/neuroprion-newsletter-prion-2006-special-issue.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/newsletters/neuroprion-newsletter-prion-2006-special-issue.pdf</a></div>
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PRION2006 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2006/abstract_book.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2006/abstract_book.pdf</a></div>
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ORAL-04</div>
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EPIDEMIOLOGY OF CHRONIC WASTING DISEASE IN NORTH AMERICAN CERVIDS M. W. Miller</div>
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Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, Colorado, USA.</div>
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Chronic wasting disease (CWD) occurs naturally in North American deer (Odocoileus spp.), wapiti, and moose (collectively called "cervids"). CWD presently occurs in scattered foci throughout North America, both in the wild and in commercial facilities. CWD is contagious among its natural hosts, and epidemics can persist under both captive and free-ranging conditions, resulting in remarkably high infection rates. The precise mechanism of contagion remains unclear, although accumulations of disease-associated prion protein (PrPCWD) in lymphatic tissues associated with the gastrointestinal tract suggest shedding via feces and perhaps saliva. Analyses of epidemic data suggest that indirect (animal-environment-animal) transmission may be the dominant force in epidemic dynamics, and the CWD agent has been shown to persist in environments contaminated by excreta or carcass remains for years. Variation in cellular prion protein appears to influence CWD pathogenesis, and may provide a biological mechanism for emergence of variant strains within and among the four naturally susceptible species. The long-term implications of CWD for public, livestock, and wildlife health remain uncertain. Unfortunately, limitations of existing technology available to combat prion diseases make control of CWD ineffective or infeasible under most conditions. 23</div>
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ORAL-19</div>
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IINTERSPECIES PRION TRANSMISSION IS CONTROLLED BY CONFORMATIONAL COMPATIBILITY BETWEEN PRPSC AND HETEROTYPIC PRPC</div>
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K.M. Green*1, S.R. Browning*1,6, T.S. Seward2, M. Green4, E.A. Hoover5, G.C. Telling1,2,3,7</div>
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1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging,3Department of Neurology, 4UK Transgenic Facility University of Kentucky, Lexington, Ky USA. 5Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Co, USA 6Present address: Department of Infectology, Scripps Research Institute, Jupiter, Florida, USA</div>
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7To whom correspondence should be addressed:gtell2@uky.edu * These authors contributed equally</div>
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The threats to humans and livestock from interspecies prion transmission are difficult to assess because the factors controlling this process remain uncertain. To address this we have used transgenic mouse models to understand the roles played by PrP primary structure, prion strains and the species specificity of protein X in controlling interspecies prion infection in the context of cervid transmission barriers. Cervid prions are of particular concern because chronic wasting disease (CWD) of North American and South Korean cervids is the only recognized prion disease of wild animals and its increasing geographic range, contagious nature, and environmental persistence have raised concerns about prion dissemination and the potential for further interspecies transmission. We show that conformational compatibility of PrPSc in a prion strain and PrP primary structure in a new host is the most important determinant of interspecies prion transmission barriers. Although prion strains can acquire totally new host range properties following heterologous conversion of PrPP C in a new host, the strain-related biochemical properties of PrPSc may remain relatively stable. We also show that the cervid PrP polymorphism at residue 132, which is equivalent to the human PrP 129 polymorphism, is a crucial determinant of cervid prion transmission and has a profound controlling effect on PrPSc-related prion strain properties. Our transgenic approaches modeling trans-species prion susceptibility in cervids also speak to the possible origins of CWD since cervid transgenic mice are also vulnerable, to varying degrees, to sheep scrapie prions, the degree of susceptibility being strain related. One particularly well-characterized sheep scrapie isolate, SSBP/1, caused disease as efficiently as CWD prions from diseased deer or elk. Finally, while transmissions in transgenic mice based on the protein X model of prion propagation produced chimeric prions, passage of which resulted in novel cervid prions with an extended host range compared to CWD-cervid prions, the unexpected susceptibilities of such mice to CWD and mouse prions are inconsistent with the previously hypothesized role of protein X in prion propagation.</div>
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GEN-13</div>
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PRION PROTEIN GENES AFFECT SUSCEPTIBILITY OF CERVIDS TO CHRONIC WASTING DISEASE</div>
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C. Johnson1, J. Johnson1, J.P. Vanderloo1, D. Keane2, P. Bochsler2, J.M. Aiken1, D. McKenzie1</div>
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1Department of Animal Health and Biomedical Sciences and 2Wisconsin Veterinary Diagnostic Laboratory, University of Wisconsin, Madison, WI, USA mckenzie@svm.vetmed.wisc.edu</div>
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The primary sequence of the prion protein affects susceptibility to transmissible spongiform encephalopathies (TSE; prion disease) in mice, sheep and humans. The Prnp sequence of freeranging, Wisconsin white-tailed deer was determined and the Prnp genotypes of CWD-positive and - negative deer compared. Six amino acid (AA) changes were identified; two of which were located in pseudogenes. Two alleles, a glutamine to lysine polymorphism at codon 226 and a single octapeptide repeat insertion into the pseudogene, have not been previously reported. The predominant alleles, wild-type (glutamine at AA95, glycine at AA96 and glutamine at AA226) and a glycine to serine polymorphism at AA96 (G96S), comprise almost 98% of the Prnp alleles in the Wisconsin white-tailed deer population. Comparison of the allelic frequencies in the CWD-positive and -negative deer suggests that G96S and a glutamine to histidine polymorphism at AA 95 (Q95H) are linked to a reduced susceptibility to CWD. The G96S allele does not, however, provide complete resistance, as a CWD-positive G96S/G96S deer was identified. The G96S allele is also linked to slower progression of disease in CWD-positive deer based on the deposition of PrPCWD in the obex region of the medulla oblongata. To further determine the effect of variations of the cervid Prnp alleles on susceptibility, deer with known Prnp genotypes were orally dosed with CWD inocula prepared from wild-type/wild-type homozygous animals. The experimentally infected wild-type/wild-type animals have succumbed to disease, animals heterozygous for Prnp alleles have not.</div>
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PA-03</div>
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PRIONS IN SKELETEL MUSCLE OF CWD INFECTED DEER</div>
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R.C. Angers*1, S.R. Browning*1,6, T.S. Seward2, C.J. Sigurdson4, 7, M.W. Miller5, E.A. Hoover4, G.C. Telling1, 2, 3, 8 1Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky, Lexington, KY 40536, 2Sanders Brown Center on Aging, University of Kentucky, 3Department of Neurology, University of Kentucky, 4Department of Microbiology, Immunology and Pathology, Colorado State University, 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526; 6 Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458; 7 Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstr 12, 8091 Zurich, Switzerland; 8 To whom correspondence should be addressed: e-mail: gtell2@ uky.edu; * These authors contributed equally to this work</div>
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The zoonotic potential of chronic wasting disease (CWD) has become a public health concern since the transmission of bovine spongiform encephalopathy (BSE) prions to humans resulting in variant Creutzfeldt- Jakob disease (vCJD). Studies in mice, sheep and humans indicated that PrPSc could be detected in the skeletal muscles. Since the most probable route of human exposure to CWD is through consumption or handling of meat from infected animals, it is important to assess whether skeletal muscle from affected cervids harbors prions. CWD-susceptible Tg(CerPrP) mice were intracranially inoculated with brain and matched skeletal muscle homogenates from moribund as well as non-infected control deer. Tg mice inoculated with either brain or muscle homogenates from CWD-infected deer developed clinical illness with characteristic prion disease symptoms and the brains of recipients accumulated cervid PrPSc. The mean incubation times for animals inoculated with brain material ranged between 231 and 283 days, whereas mice receiving muscle tissue had average incubation periods between 360 and 492 days. Tg mice inoculated with material from CWD-negative deer did not develop prion disease or accumulate PrPSc. Brain and muscle samples used to inoculate Tg(CerPrP) mice were analyzed for the presence of PrPSc. Brain samples producing the shortest incubation times had levels of PrPP Sc detectable by Western blotting in 25 µg total protein, whereas PrPSc P was detectable only after sodium phosphotungstate (NaPTA) precipitation of 0.5 mg for isolates with the longest incubation periods. No protease-resistant material was detected in muscle when 50 mg total protein was precipitated with NaPTA and analyzed by Western blot. Although a possible role of prion strain variability cannot currently be dismissed, these results suggest variable prion titers in the CNS and skeletal muscle from different CWD-infected deer in the same phase of disease.</div>
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***PLEASE SEE FULL TEXT 234 PAGES *** ;</div>
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<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a></div>
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OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles</div>
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Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA</div>
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Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.</div>
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Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.</div>
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Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.</div>
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In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.</div>
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Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.</div>
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The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.</div>
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<a href="http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf?nocache=1216084967</a></div>
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PR-26</div>
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NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS</div>
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R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway</div>
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Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as "atypical" scrapie, as opposed to "classical scrapie". Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion.</div>
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*** Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.</div>
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<a href="http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf</a></div>
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A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes</div>
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Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations</div>
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*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway</div>
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***Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)</div>
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Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. </div>
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*** These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.</div>
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<a fg_scanned="1" href="http://www.pnas.org/content/102/44/16031.abstract" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.pnas.org/content/102/44/16031.abstract</a></div>
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PRION2005 PRESS RELEASE</div>
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PRION2005 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/abstract_book.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/abstract_book.pdf</a></div>
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PRION2004 PRESS RELEASE</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/dossier_de_presse.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/dossier_de_presse.pdf</a></div>
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<a fg_scanned="1" href="https://www.neuroprion.org/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.neuroprion.org/</a></div>
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PRION2004 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/abstract_book.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/abstract_book.pdf</a></div>
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<a fg_scanned="1" href="https://www.neuroprion.org/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.neuroprion.org/</a></div>
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<a fg_scanned="1" href="https://ec.europa.eu/commission/presscorner/detail/en/IP_04_690" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://ec.europa.eu/commission/presscorner/detail/en/IP_04_690</a></div>
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<a fg_scanned="1" href="http://tandfonline.com/loi/kprn20?open=1&year=2007&repitition=0#vol_1_2007" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://tandfonline.com/loi/kprn20?open=1&year=2007&repitition=0#vol_1_2007</a></div>
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*see archives of previous Prion Conferences, the ones that are still available, scroll down towards bottom in this link.</div>
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<a fg_scanned="1" href="http://www.neuroprion.org/en/np-news.html#42417828" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neuroprion.org/en/np-news.html#42417828</a></div>
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U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 </div>
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Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001</div>
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Date: Tue, 9 Jan 2001 16:49:00 -0800</div>
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From: "Terry S. Singeltary Sr."</div>
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Reply-To: Bovine Spongiform Encephalopathy</div>
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To: BSE-L@uni-karlsruhe.de </div>
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######### Bovine Spongiform Encephalopathy ######### </div>
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Greetings List Members,</div>
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I was lucky enough to sit in on this BSE conference call today and even managed to ask a question. that is when the trouble started.</div>
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I submitted a version of my notes to Sandra Blakeslee of the New York Times, whom seemed very upset, and rightly so.</div>
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"They tell me it is a closed meeting and they will release whatever information they deem fit. Rather infuriating."</div>
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and i would have been doing just fine, until i asked my question. i was surprised my time to ask a question so quick.</div>
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(understand, these are taken from my notes for now. the spelling of names and such could be off.)</div>
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[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.</div>
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[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?</div>
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[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]</div>
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[host Richard] could you repeat the question?</div>
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[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?</div>
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[not sure whom ask this] what group are you with?</div>
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[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.</div>
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[not sure who is speaking] could you please disconnect Mr. Singeltary</div>
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[TSS] you are not going to answer my question?</div>
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[not sure whom speaking] NO</div>
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from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;</div>
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[unknown woman] what group are you with?</div>
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[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?</div>
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at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.</div>
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IF i were another Country, I would take heed to my notes, BUT PLEASE do not depend on them. ask for transcript from;</div>
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RBARNS@ORA.FDA.GOV 301-827-6906</div>
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he would be glad to give you one ;-)</div>
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Rockville Maryland, Richard Barns Host</div>
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BSE issues in the U.S., How they were labelling ruminant feed? Revising issues.</div>
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The conference opened up with the explaining of the U.K. BSE epidemic winding down with about 30 cases a week.</div>
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although new cases in other countries were now appearing.</div>
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Look at Germany whom said NO BSE and now have BSE.</div>
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BSE increasing across Europe.</div>
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Because of Temporary Ban on certain rendered product, heightened interest in U.S.</div>
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A recent statement in Washington Post, said the New Administration (old GW) has a list of issues. BSE is one of the issues.</div>
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BSE Risk is still low, minimal in U.S. with a greater interest in MBM not to enter U.S.</div>
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HOWEVER, if BSE were to enter the U.S. it would be economically disastrous to the render, feed, cattle, industries, and for human health.</div>
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(human health-they just threw that in cause i was listening. I will now jot down some figures in which they told you, 'no need to write them down'. just hope i have them correct. hmmm, maybe i hope i don't ???)</div>
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80% inspection of rendering</div>
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*Problem-Complete coverage of rendering HAS NOT occurred.</div>
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sizeable number of 1st time FAILED INITIAL INSPECTION, have not been reinspected (70% to 80%).</div>
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Compliance critical, Compliance poor in U.K. and other European Firms.</div>
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Gloria Dunason Major Assignment 1998 goal TOTAL compliance. This _did not_ occur. Mixed level of compliance, depending on firm.</div>
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Rendering FDA license and NON FDA license</div>
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system in place for home rendering & feed 76% in compliance 79% cross contamination 21% DID NOT have system 92% record keeping less than 60% total compliance</div>
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279 inspectors 185 handling prohibited materials</div>
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Renderer at top of pyramid, significant part of compliance. 84% compliance</div>
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failed to have caution statement render 72% compliance & cross contamination caution statement on feed, 'DO NOT FEED TO CATTLE'</div>
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56 FIRMS NEVER INSPECTED</div>
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1240 FDA license feed mills 846 inspected</div>
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"close to 400 feed mills have not been inspected"</div>
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80% compliance for feed.</div>
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10% don't have system.</div>
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NON-FDA licensed mills There is NO inventory on non licensed mills. approximately 6000 to 8000 Firms ??? 4,344 ever inspected. "FDA does not have a lot of experience with"</div>
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40% do NOT have caution statement 'DO NOT FEED'.</div>
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74% Commingling compliance</div>
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"This industry needs a lot of work and only half gotten to"</div>
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"700 Firms that were falitive, and need to be re-inspected, in addition to the 8,000 Firms."</div>
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Quote to do BSE inspection in 19 states by end of January or 30 days, and other states 60 days. to change feed status??? Contract check and ask questions and pass info.</div>
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At this time, we will take questions.</div>
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[I was about the third or fourth to ask question. then all B.S.eee broke loose, and i lost my train of thought for a few minutes. picked back up here]</div>
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someone asking about nutritional supplements and sourcing, did not get name. something about inspectors not knowing of BSE risk??? the conference person assuring that Steve Follum? and the TSE advisory Committee were handling that.</div>
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Some other Dr. Vet, whom were asking questions that did not know what to do???</div>
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[Dennis Wilson] California Food Agr. Imports, are they looking at imports?</div>
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[Conference person] they are looking at imports, FDA issued imports Bulletin.</div>
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[Linda Singeltary ??? this was a another phone in question, not related i don't think] Why do we have non-licensed facilities?</div>
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(conference person) other feed mills do not handle as potent drugs???</div>
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Dennis Blank, Ken Jackson licensed 400 non FDA 4400 inspected of a total of 6000 to 8000,</div>
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(they really don't know how many non licensed Firms in U.S. they guess 6000 to 8000??? TSS)</div>
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Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not'</div>
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Warren-Maryland Dept. Agr. Prudent to re-inspect after 3 years. concerned of Firms that have changed owners.</div>
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THE END</div>
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TSS</div>
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############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############ </div>
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FROM New York TIMES </div>
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Subject: Re: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting of cut version...</div>
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Date: Thu, 11 Jan 2001 22:02:47 -0700</div>
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From: "Sandy Blakeslee"</div>
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To: "Terry S. Singeltary Sr." References: 1 </div>
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Hi terry -- thanks for all your help. I know it made a difference with the FDA getting out that release. </div>
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----- Original Message -----</div>
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From: "Terry S. Singeltary Sr."</div>
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To: Sent: Thursday, January 11, 2001 2:06 PM</div>
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Subject: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting of cut version...</div>
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hi sandy,</div>
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From the New York Times NYTimes.com, January 11, 2001</div>
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Many Makers of Feed Fail to Heed Rules on Mad Cow Disease By SANDRA BLAKESLEE</div>
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Large numbers of companies involved in manufacturing animal feed are not complying with regulations meant to prevent the emergence and spread of mad cow disease in the United States, the Food and Drug Administration said yesterday.</div>
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The widespread failure of companies to follow the regulations, adopted in August 1997, does not mean that the American food supply is unsafe, Dr. Stephen Sundlof, director of the Center for Veterinary Medicine at the F.D.A., said in an interview.</div>
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But much more needs to be done to ensure that mad cow disease does not arise in this country, Dr. Sundlof said.</div>
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The regulations state that feed manufacturers and companies that render slaughtered animals into useful products generally may not feed mammals to cud-chewing animals, or ruminants, which can carry mad cow disease.</div>
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All products that contain rendered cattle or sheep must have a label that says, "Do not feed to ruminants," Dr. Sundlof said. Manufacturers must also have a system to prevent ruminant products from being commingled with other rendered material like that from chicken, fish or pork. Finally, all companies must keep records of where their products originated and where they were sold.</div>
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Under the regulations, F.D.A. district offices and state veterinary offices were required to inspect all rendering plants and feed mills to make sure companies complied. But results issued yesterday demonstrate that more than three years later, different segments of the feed industry show varying levels of compliance.</div>
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Among 180 large companies that render cattle and another ruminant, sheep, nearly a quarter were not properly labeling their products and did not have a system to prevent commingling, the F.D.A. said. And among 347 F.D.A.-licensed feed mills that handle ruminant materials - these tend to be large operators that mix drugs into their products - 20 percent were not using labels with the required caution statement, and 25 percent did not have a system to prevent commingling.</div>
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Then there are some 6,000 to 8,000 feed mills so small they do not require F.D.A. licenses. They are nonetheless subject to the regulations, and of 1,593 small feed producers that handle ruminant material and have been inspected, 40 percent were not using approved labels and 25 percent had no system in place to prevent commingling.</div>
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On the other hand, fewer than 10 percent of companies, big and small, were failing to comply with the record-keeping regulations.</div>
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The American Feed Industry Association in Arlington, Va., did not return phone calls seeking comment.</div>
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http://www.nytimes.com/2001/01/11/science/11COW.html </div>
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Subject: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001</div>
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Date: Wed, 10 Jan 2001 14:04:21 -0500</div>
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From: "Gomez, Thomas M."</div>
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Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de </div>
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######### Bovine Spongiform Encephalopathy #########</div>
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USDA/APHIS would like to provide clarification on the following point from Mr. Singeltary's 9 Jan posting regarding the 50 state conference call.</div>
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[Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not']</div>
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Dr. Detwiler was responding to an announcement made during the call to use the FDA emergency number if anyone wanted to report a cow with signs suspect for BSE. Mr. Singeltary is correct that Dr. Detwiler asked participants to use the FDA emergency number as a last resort to report cattle suspect for BSE. What Mr. Singeltary failed to do was provide the List with Dr. Detwiler's entire statement. Surveillance for BSE in the United States is a cooperative effort between states, producers, private veterinarians, veterinary hospitals and the USDA. The system has been in place for over 10 years. Each state has a system in place wherein cases are reported to either the State Veterinarian, the federal Veterinarian in Charge or through the veterinary diagnostic laboratory system. The states also have provisions with emergency numbers. Dr. Detwiler asked participants to use the systems currently in place to avoid the possibility of a BSE-suspect report falling through the cracks. Use of the FDA emergency number has not been established as a means to report diseased cattle of any nature.</div>
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U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 </div>
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Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001</div>
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Date: Tue, 9 Jan 2001 16:49:00 -0800</div>
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<a fg_scanned="1" href="http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div>
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THURSDAY, SEPTEMBER 26, 2019 </div>
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Veterinary Biologics Guideline 3.32E: Guideline for minimising the risk of introducing transmissible spongiform encephalopathy prions and other infectious agents through veterinary biologics</div>
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<a fg_scanned="1" href="https://bovineprp.blogspot.com/2019/09/veterinary-biologics-guideline-332e.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bovineprp.blogspot.com/2019/09/veterinary-biologics-guideline-332e.html</a></div>
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FRIDAY, OCTOBER 25, 2019 </div>
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Experts testify United States is underprepared for bioterrorism threats Transmissible Spongiform Encephalopathy TSE Prion disease</div>
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<a fg_scanned="1" href="https://usdameatexport.blogspot.com/2019/10/experts-testify-united-states-is.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://usdameatexport.blogspot.com/2019/10/experts-testify-united-states-is.html</a></div>
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WEDNESDAY, AUGUST 7, 2019 </div>
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The Nation Faces Long Standing Challenges Related to Defending Against Biological Threats</div>
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<a fg_scanned="1" href="http://animalhealthreportpriontse.blogspot.com/2019/08/the-nation-faces-long-standing.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://animalhealthreportpriontse.blogspot.com/2019/08/the-nation-faces-long-standing.html</a></div>
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>>> Acts of terrorism against U.S. agriculture are highly possible, but not highly likely, according to Stephen Goldsmith, a veterinarian with the Biological Countermeasures Unit of the Federal Bureau of Investigation. <<<</div>
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now that is an oxymoron of a statement if I ever heard one.</div>
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That kind of mentality is what brought the twin towers down. you sit back on one’s laurels, and people can die. see ;</div>
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USDA, APHIS, FSIS, HHS, ET AL, on animal disease preparedness grade score = F+.</div>
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With Bovine Spongiform Encephalopathy BSE TSE prion disease aka mad cow disease, one mad cow caused total chaos, and to this day, the USA is not, and has never been prepared.</div>
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Docket No: 02-088-1 Agricultural Bioterrorism Protection Act of 2002; Possession, Use, and Transfer of Biological Agents and Toxins</div>
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Subject: Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002;</div>
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Date: Mon, 27 Jan 2003 15:54:57 –0600</div>
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From: Terry S. Singeltary Sr.</div>
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To: regulations@aphis.usda.gov Docket No: 02-088-1</div>
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Title: Agricultural Bioterrorism Protection Act of 2002; Possession, Use, and Transfer of Biological Agents and Toxins</div>
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<a href="http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=2002_register&docid=fr13de02-15.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname=2002_register&docid=fr13de02-15.pdf</a></div>
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i would like to kindly submit to this docket and warn of the potential for biological 'suitcase bombs' from civilian air-traffic populations from known BSE/FMD and other exotic animal disease pathogens coming into the USA. please be warned;</div>
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Date: Thu, 21 Mar 2002 08:42:56 –0800</div>
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Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform Encephalopathy</div>
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snip...see full text;</div>
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WEDNESDAY, AUGUST 7, 2019 </div>
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The Nation Faces Long Standing Challenges Related to Defending Against Biological Threats</div>
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TUESDAY, OCTOBER 20, 2015 </div>
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FBI: Agroterrorism not likely, but very possible, Dr. Stephen Goldsmith FBI Laboratory Division, here's your sign </div>
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CC-Dr. Steve Goldsmith, FBI Laboratory Division </div>
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Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Docket Type Rulemaking Document APHIS-2007-0033-0001 Document Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Public Submission APHIS-2007-0033-0002.1 Public Submission Title Attachment to Singeltary comment</div>
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# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0)</div>
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Docket Management</div>
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Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC-254 [TSS SUBMISSION]</div>
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<a fg_scanned="1" href="http://www.aphis.usda.gov/vs/ceah/cei/bse_greece0701.htm" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.aphis.usda.gov/vs/ceah/cei/bse_greece0701.htm</a></div>
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MONDAY, OCTOBER 21, 2019 </div>
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Departmental Freedom of Information Act Regulations FOIA Dumbing Down of America Under the Trump Regime</div>
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THURSDAY, SEPTEMBER 26, 2019 </div>
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USDA Scientific Integrity Policy Departmental Regulation 1074-001 Breached</div>
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TUESDAY, JULY 23, 2019 </div>
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APHIS USDA Administrator Announces Several Senior Leadership Changes As Trump Prepares Apparently To Fire 100's of Scientists That Don't Agree With Him, what about mad cow type disease tse prion?</div>
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<a fg_scanned="1" href="https://usdameatexport.blogspot.com/2019/07/aphis-usda-administrator-announces.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://usdameatexport.blogspot.com/2019/07/aphis-usda-administrator-announces.html</a></div>
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TUESDAY, MARCH 26, 2019 </div>
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Joint Statement from President Donald J. Trump USA and President Jair Bolsonaro Brazil FOREIGN POLICY BSE TSE Prion aka mad cow disease</div>
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<a fg_scanned="1" href="https://bseusa.blogspot.com/2019/03/joint-statement-from-president-donald-j.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://bseusa.blogspot.com/2019/03/joint-statement-from-president-donald-j.html</a></div>
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SATURDAY, JUNE 01, 2019 </div>
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Brazil reports another cases of mad cow disease atypical BSE TSE Prion</div>
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PLEASE BE ADVISED THERE IS NO SCIENTIFIC PROOF THAT ANY ATYPICAL BSE TSE PRION IS OF A SPONTANEOUS OLD AGE DISEASE, NOT CAUSED BY FEED, THIS IS FALSE AND UNPROVEN, IN FACT, ATYPICAL BSE OF THE L AND H TYPE ARE TRANSMISSIBLE BY ORAL ROUTE. THIS STATEMENT THAT ATYPICAL BSE IS A SPONTANEOUS EVENT CAUSED BY OLD AGE, CAUSED BY NOTHING, IS ABSOLUTELY A LIE, AND THE GOVERNMENT OF BRAZIL, AND OTHER GOVERNMENTS THAT PRODUCE SUCH STATEMENTS, KNOWS THIS IS AN UNPROVEN STATEMENT...TERRY SINGELTARY SR.</div>
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<a fg_scanned="1" href="https://bse-atypical.blogspot.com/2019/06/brazil-reports-another-cases-of-mad-cow.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://bse-atypical.blogspot.com/2019/06/brazil-reports-another-cases-of-mad-cow.html</a></div>
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MONDAY, FEBRUARY 25, 2019</div>
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***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</div>
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<span style="line-height: 1.22em;">MONDAY, JANUARY 09, 2017 </span></div>
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<span style="line-height: 1.22em;">Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle </span></div>
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<span style="line-height: 1.22em;">CDC Volume 23, Number 2—February 2017 </span></div>
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<span style="line-height: 1.22em;">*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.</span></div>
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<span style="line-height: 1.22em;">*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.</span></div>
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<a fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/23/2/16-1416_article" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://wwwnc.cdc.gov/eid/article/23/2/16-1416_article</a></div>
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<span style="font-family: arial, helvetica;">WEDNESDAY, APRIL 24, 2019 </span></div>
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<span style="font-family: arial, helvetica;">USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019 </span></div>
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<a fg_scanned="1" href="https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">USDA finds BSE infection in Florida cow 08/28/18 6:43 PM</span></span></div>
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<a fg_scanned="1" href="http://animalhealthreportpriontse.blogspot.com/2018/08/usda-finds-bse-infection-in-florida-cow.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://animalhealthreportpriontse..blogspot.com/2018/08/usda-finds-bse-infection-in-florida-cow.html</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT</span></span></div>
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<a fg_scanned="1" href="http://bse-atypical.blogspot.com/2018/08/usda-announces-atypical-bovine.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bse-atypical.blogspot.com/2018/08/usda-announces-atypical-bovine.html</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">WEDNESDAY, AUGUST 29, 2018 </span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 13.3333px; line-height: 1.22em;">Transmissible Spongiform Encephalopathy TSE Prion Atypical BSE Confirmed Florida Update USA August 28, 2018</span></span></div>
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<a fg_scanned="1" href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/08/transmissible-spongiform-encephalopathy.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/08/transmissible-spongiform-encephalopathy.html</a></div>
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<span style="font-size: 10pt;">P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge </span></div>
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Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States. </div>
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reading up on this study from Prion 2018 Conference, very important findings ;</div>
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***> This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. </div>
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***> These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.</div>
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PRION 2018 CONFERENCE ABSTRACT</div>
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<a fg_scanned="1" href="https://prion2018.org/" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2018.org/</a></div>
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P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States. </div>
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In 2006, a case of H-type bovine spongiform encephalopathy (BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K). </div>
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The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease. </div>
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Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route. </div>
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The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure. </div>
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Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with either H-type BSE from the 2004 US Htype BSE case (n=3) or from the 2006 US H-type case associated with the E211K polymorphism (n=4) using 10% w/v brain homogenates. </div>
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Cattle were observed daily throughout the course of the experiment for the development of clinical signs. </div>
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At approximately 50 months post-inoculation, one steer (EK211 inoculated with E211K associated H-BSE) developed clinical signs including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and was euthanized. </div>
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Enzyme immunoassay confirmed that abundant misfolded protein was present in the brainstem, and immunohistochemistry demonstrated PrPSc throughout the brain. </div>
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Western blot analysis of brain tissue from the clinically affected steer was consistent with the E211K H-type BSE inoculum. </div>
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With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease. This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. </div>
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These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains. </div>
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PRION 2018 CONFERENCE ABSTRACT</div>
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<span style="font-size: 13.3333px;">WEDNESDAY, AUGUST 15, 2018 </span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">***> The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge</span></span></div>
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<a fg_scanned="1" href="http://bovineprp.blogspot.com/2018/08/the-agent-of-h-type-bovine-spongiform.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2018/08/the-agent-of-h-type-bovine-spongiform.html</a></div>
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<span style="line-height: 1.22em;">***> P.108: Successful oral challenge of adult cattle with classical BSE</span></div>
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<span style="line-height: 1.22em;">Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada</span></div>
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<span style="line-height: 1.22em;">Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only. </span></div>
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<span style="line-height: 1.22em;">***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. </span></div>
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<span style="line-height: 1.22em;">We are further examining explanations for the unusual disease presentation in the third challenged animal.</span></div>
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<a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files..wordpress.com/2015/05/prion2015abstracts.pdf</a></div>
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<span style="line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.</span></div>
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<span style="line-height: 1.22em;">P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification</span></div>
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<span style="line-height: 1.22em;">Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama</span></div>
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<span style="line-height: 1.22em;">National Institute of Animal Health; Tsukuba, Japan</span></div>
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<span style="line-height: 1.22em;">To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).</span></div>
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<span style="line-height: 1.22em;">Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.</span></div>
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<span style="line-height: 1.22em;">Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.</span></div>
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<span style="line-height: 1.22em;">P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion</span></div>
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<span style="line-height: 1.22em;">***P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion</span></div>
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<span style="line-height: 1.22em;">Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food Inspection Agency; Lethbridge, AB Canada</span></div>
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<span style="line-height: 1.22em;">Keywords: Atypical BSE, oral transmission, RT-QuIC</span></div>
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<span style="line-height: 1.22em;">The detection of bovine spongiform encephalopathy (BSE) has had a significant negative impact on the cattle industry worldwide. In response, governments took actions to prevent transmission and additional threats to animal health and food safety. While these measures seem to be effective for controlling classical BSE, the more recently discovered atypical BSE has presented a new challenge. To generate data for risk assessment and control measures, we have challenged cattle orally with atypical BSE to determine transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon presentation of clinical symptoms, animals were euthanized and tested for characteristic histopathological changes as well as PrPSc deposition.</span></div>
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<span style="line-height: 1.22em;">The H-type challenged animal displayed vacuolation exclusively in rostral brain areas but the L-type challenged animal showed no evidence thereof. To our surprise, neither of the animals euthanized, which were displaying clinical signs indicative of BSE, showed conclusive mis-folded prion accumulation in the brain or gut using standard molecular or immunohistochemical assays. To confirm presence or absence of prion infectivity, we employed an optimized real-time quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain Laboratory, Hamilton, USA.</span></div>
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<span style="line-height: 1.22em;">Detection of PrPSc was unsuccessful for brain samples tests from the orally inoculated L type animal using the RT-QuIC. It is possible that these negative results were related to the tissue sampling locations or that type specific optimization is needed to detect PrPSc in this animal. We were however able to consistently detect the presence of mis-folded prions in the brain of the H-type inoculated animal. Considering the negative and inconclusive results with other PrPSc detection methods, positive results using the optimized RT-QuIC suggests the method is extremely sensitive for H-type BSE detection. This may be evidence of the first successful oral transmission of H type atypical BSE in cattle and additional investigation of samples from these animals are ongoing.</span></div>
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<span style="line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline.com/doi/pdf/10.4161/pri.29370" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.29370</a></span></div>
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<span style="line-height: 1.22em;"><a fg_scanned="1" href="http://transmissiblespongiformencephalopathy.blogspot.com/2014/06/prion-2014-typical-and-atypical-bse-and.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2014/06/prion-2014-typical-and-atypical-bse-and.html</a></span></div>
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<span style="line-height: 1.22em;"><a fg_scanned="1" href="http://bse-atypical.blogspot.com/2016/05/a-comparison-of-classical-and-h-type.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bse-atypical.blogspot.com/2016/05/a-comparison-of-classical-and-h-type.html</a></span></div>
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<span style="line-height: 1.22em;"><a fg_scanned="1" href="http://bse-atypical.blogspot.com/2017/01/oral-transmission-of-l-type-bovine.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://bse-atypical.blogspot.com/2017/01/oral-transmission-of-l-type-bovine.html</a></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a fg_scanned="1" href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a> </span></div>
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ZOONOSIS OF SCRAPIE TSE PRION</div>
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O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">============== </span></div>
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***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a fg_scanned="1" href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="font-size: 12px;">***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***</span></span><span style="font-size: 12px;"> </span></div>
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SATURDAY, JUNE 23, 2018</div>
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***> Diagnosis of Methionine/Valine Variant Creutzfeldt-Jakob Disease by Protein Misfolding Cyclic Amplification </div>
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Volume 24, Number 7—July 2018 Dispatch</div>
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<span face="Arial, Helvetica, sans-serif" style="color: #222222; font-size: 12px;">4. The link between BSE and vCJD </span></div>
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<span face="Arial, Helvetica, sans-serif" style="color: #222222; font-size: 12px;">4.29 The evidence discussed above that vCJD is caused by BSE seems overwhelming. Uncertainties exist about the cause of CJD in farmers, their wives and in several abattoir workers. It seems that farmers at least might be at higher risk than others in the general population. 1 Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrPSc found in vCJD. It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people...end...BSE INQUIRY</span></div>
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<span face="Roboto, sans-serif" style="color: #222222; font-size: 12px;">> However, to date, no CWD infections have been reported in people. </span></div>
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sporadic, spontaneous CJD, 85%+ of all human TSE, just not just happen. never in scientific literature has this been proven.</div>
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if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;</div>
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sporadic = 54,983 hits <a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic</a></div>
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spontaneous = 325,650 hits <a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous</a></div>
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key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </div>
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ALL iatrogenic CJD is, is sporadic CJD, until the iatrogenic event is discovered, traced back, proven, documented in the academic domain, and finally the public domain, which very seldom happens due to lack of trace back efforts, thus, all iatrogeic events stay as sporadic cjd.</div>
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THERE should be a mandatory trace out of these patients, and all patients should know, and if they choose not to, so be it, but the victim, patient, and Doctors of all involved must be made aware, and the hospital, this information should be put in some sort of confidential registry (WHERE INSURANCE COMPANIES CANNOT GAIN ACCESS OF SAID PATIENT/VICTIM), where hospitals and doctors can assess and be made aware of iatrogenic TSE Prion event, so that further iatrogenic transmission can hopefully be avoided. IF not, it's all pointless imo. ...terry</div>
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CJD TSE Prion Blood Products, iatrogenic transmission, Confucius is confused again, WHAT IF?</div>
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''In the 2016 guidance, we recommended that prospective blood donors should be indefinitely deferred if they report having a blood relative with CJD. However, almost all cases reported are sCJD, not a genetic form of CJD. Blood relatives of individuals with sCJD are not at increased risk of developing the disease. The rare genetic forms of CJD (e.g., fCJD, GSS, FFI) share pathophysiological features with sCJD, and the transmission risk by blood components remains theoretical. Consequently, we recommend that establishments may stop asking prospective donors about having blood relatives with CJD.''<div>
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<a fg_scanned="1" href="http://%20https//www.regulations.gov/docket?D=FDA-2012-D-0307" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http:// https://www.regulations.gov/docket?D=FDA-2012-D-0307</a></div>
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FRIDAY, JANUARY 31, 2020 </div>
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CJD TSE Prion Blood Products, iatrogenic transmission, Confucius is confused again, WHAT IF? Docket Number: FDA-2012-D-0307</div>
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<a fg_scanned="1" href="https://creutzfeldt-jakob-disease.blogspot.com/2020/01/cjd-tse-prion-blood-products-iatrogenic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2020/01/cjd-tse-prion-blood-products-iatrogenic.html</a></div>
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Confucius is confused again?</div>
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''The rare genetic forms of CJD (e.g., fCJD, GSS, FFI) share pathophysiological features with sCJD, and the transmission risk by blood components remains theoretical. Consequently, we recommend that establishments may stop asking prospective donors about having blood relatives with CJD.''</div>
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YET, vpspr, sporadic FFI, sporadic GSS, or the pending cases that can't be identified, are all now listed as sporadic CJD.</div>
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WHAT IF, sGSS, sFFI, are of an iatrogenic event from iatrogenic donor being from GSS or FFI?</div>
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what if vpspr is another strain of a different sporadic CJD, or familial? see;</div>
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7Includes 21 (21 from 2019) cases with type determination pending in which the diagnosis of vCJD has been excluded. </div>
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8The sporadic cases include 3831 cases of sporadic Creutzfeldt-Jakob disease (sCJD), 67 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 35 cases of sporadic Fatal Insomnia (sFI). </div>
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9Total does not include 264 Familial cases diagnosed by blood test only.</div>
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<a fg_scanned="1" href="https://case.edu/medicine/pathology/divisions/national-prion-disease-pathology-surveillance-center/resources-professionals/tables-cases-examined" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://case.edu/medicine/pathology/divisions/national-prion-disease-pathology-surveillance-center/resources-professionals/tables-cases-examined</a></div>
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under new proposed guidelines ''<span style="font-size: 10pt;">we recommend that establishments may stop asking prospective donors about having blood relatives with CJD'' (of which i strongly oppose due to the fact sporadic cjd is not a single entity or a spontaneous event, never which have been proven), but under these guidelines, you will miss the vpspr, sgss, and sffi, because they are under sporadic cjd terminology, would you not?</span></div>
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The occurrence of the disease in a patient who had contact with cases of familial C.J.D., but was not genetically related, has been described in Chile (Galvez et al., 1980) and in France (Brown et al., 1979b). In Chile the patient was related by marriage, but with no consanguinity, and had social contact with subsequently affected family members for 13 years before developing the disease. The contact case in France also married into a family in which C.J.D. was prevalent and had close contact with an affected member. In neither instance did the spouse of the non-familial case have the disease. The case described in this report was similarly related to affected family members and social contact had occurred for 20 years prior to developing C.J.D. If contact transmission had occurred, the minimum transmission period would be 11 years. Contact between sporadic cases has not been described and it is remarkable that possible contact transmissions have all been with familial cases. No method of transmission by casual social contact has been suggested.</div>
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***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent.</div>
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snip...see full text here;</div>
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<a href="http://web.archive.org/web/20050425210551/http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20050425210551/http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf</a></div>
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<a fg_scanned="1" href="http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html</a></div>
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<span style="font-family: serif; font-size: 15.9991px;">FRIDAY, JANUARY 10, 2014</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">Greetings Friends, Neighbors, and Colleagues,</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">Confucius is confused again.</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">I was just sitting and thinking about why there is no genetic link to some of these TSE prion sGSS, sFFi, and it’s really been working on my brain, and then it hit me today.</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">what if, vpspr, sgss, sffi, TSE prion disease, was a by-product from iatrogenic gss, ffi, familial type prion disease ???</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">it could explain the cases of no genetic link to the gss, ffi, familial type prion disease, to the family.</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">sporadic and familial is a red herring, in my opinion, and underestimation is spot on, due to the crude prehistoric diagnostic procedures and criteria and definition of a prion disease.</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">I say again, what if, iatrogenic, what if, with all these neurological disorders, with a common denominator that is increasingly showing up in the picture, called the prion.</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">I urge all scientist to come together here, with this as the utmost of importance about all these neurological disease that are increasingly showing up as a prion mechanism, to put on the front burners, the IATROGENIC aspect and the potential of transmission there from, with diseases/disease??? in question.</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">by definition, could they be a Transmissible Spongiform Encephalopathy TSE prion type disease, and if so, what are the iatrogenic chances of transmission?</span></div>
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<span style="font-family: serif; font-size: 15.9991px;">this is very important, and should be at the forefront of research, and if proven, could be a monumental breakthrough in science and battle against the spreading of these disease/diseases.</span></div>
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<a fg_scanned="1" href="http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: small;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2014/01/vpspr-sgss-sffi-tse-iatrogenic-by.html</a> </div>
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<span style="font-family: Times New Roman, stixgeneral, serif;"><span style="font-size: 15.9991px;">sporadic CJD, along with new TSE prion disease in humans, of which the young are dying, of which long duration of illness from onset of symptoms to death have been documented, only to have a new name added to the pot of prion disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a familial type disease could be sporadic with no genetic link to any family member? when the USA is the only documented Country in the world to have documented two different cases of atypical H-type BSE, with one case being called atypical H-G BSE with the G meaning Genetic, with new science now showing that indeed atypical H-type BSE is very possible transmitted to cattle via oral transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada, USA, and the UK, with the same old excuse, better surveillance. You can only use that excuse for so many years, for so many decades, until one must conclude that CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a blip or a reason of better surveillance, it is a mathematical rise in numbers. More and more we are seeing more humans exposed in various circumstance in the Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same time in North America, more and more humans are becoming exposed to the TSE prion disease via consumption of the TSE prion via deer and elk, cattle, sheep and goats, and for those that are exposed via or consumption, go on to further expose many others via the iatrogenic modes of transmission of the TSE prion disease i.e. friendly fire. I pondered this mode of transmission via the victims of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone sub-clinical with sFFI or sGSS ? what if?</span></span></div>
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<a fg_scanned="1" href="http://vpspr.blogspot.com/2014/11/transmission-characteristics-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://vpspr.blogspot.com/2014/11/transmission-characteristics-of.html</a></div>
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<span style="font-size: x-small;">Furthermore, GSS A117V infected vole brains were able to induce the same disease phenotype in recipient voles within 3–4 months after challenge, proving that a prion agent propagated in the brains of infected animals. These findings imply that brains of GSS patients harbor infectious prions with transmissibility features similar to those found in other human and animal TSEs.</span></div>
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<span style="font-size: x-small;"><a fg_scanned="1" href="https://www.nature.com/articles/srep20443" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/srep20443</a></span></div>
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<span style="font-family: Georgia; font-size: 13px;">*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery *** </span><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><span style="font-family: Georgia; font-size: 13px;">Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. </span><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><span style="font-family: Georgia; font-size: 13px;">Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. </span><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" /><a fg_scanned="1" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract</a><span style="font-family: Georgia; font-size: 13px;"> </span></div>
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*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</div>
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*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </div>
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<a fg_scanned="1" href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a> </div>
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<a fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </span></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</span></span></div>
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***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" />***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" />*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action?root=86610" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; line-height: 1.22em;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=86610</a></div>
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<span style="font-family: arial, helvetica; font-size: 10pt;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply</span></div>
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FDA's FAILED MAD COW FEED POLICY, IN LIVING COLOR!</div>
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FDA Reports on VFD Compliance</div>
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Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary.</div>
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America BSE 589.2001 FEED REGULATIONS, BSE SURVEILLANCE, BSE TESTING, and CJD TSE Prion</div>
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so far, we have been lucky. to date, with the science at hand, no cwd transmitted to cattle, that has been documented, TO DATE, WITH THE SCIENCE AT HAND, it's not to say it has not already happened, just like with zoonosis of cwd i.e. molecular transmission studies have </span><span style="font-size: 10pt;">shown that cwd transmission to humans would look like sporadic cjd, NOT nvCJD or what they call now vCJD. the other thing is virulence and or horizontal transmission. this is very concerning with the recent fact of what seems to be a large outbreak of a new tse prion disease in camels in Africa. there is much concern now with hay, straw, grains, and such, with the cwd tse prion endemic countries USA, Canada. what is of greatest concern is the different strains of cwd, and the virulence there from? this thing (cwd) keeps mutating to different strains, and to different species, the bigger the chance of one of these strains that WILL TRANSMIT TO CATTLE OR HUMANS, and that it is documented (i believe both has already occured imo with scienct to date). with that said, a few things to ponder, and i am still very concerned with, the animal feed. we now know from transmission studies that cwd and scrapie will transmit to pigs by oral routes. the atypical bse strains will transmit by oral routes. i don't mean to keep kicking a mad cow, just look at the science; </span><span style="font-size: 13.3333px;"></span><div style="font-size: 13.3333px;">
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***> cattle, pigs, sheep, cwd, tse, prion, oh my! </div>
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***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div>
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Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.<span style="font-size: 10pt;"> </span></div>
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<span style="font-size: 10pt;"><a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a></span><span style="font-size: 10pt;"> </span></div>
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<span style="font-size: 10pt;"><a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html</a></span><span style="font-size: 10pt;"> </span></div>
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<span style="font-size: 10pt;">cwd scrapie pigs oral routes </span></div>
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<span style="font-size: 10pt;">***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </span></div>
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<span style="font-size: 10pt;">>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </span></div>
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<span style="font-size: 10pt;">***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </span></div>
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<span style="font-size: 10pt;">***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </span></div>
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<a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div>
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<a fg_scanned="1" href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div>
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<a fg_scanned="1" href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Friday, December 14, 2012</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Animals considered at high risk for CWD include:</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div>
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<a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">TUESDAY, APRIL 18, 2017 </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</span></div>
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<a fg_scanned="1" href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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***> Wednesday, January 23, 2019 </div>
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***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***</div>
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<a fg_scanned="1" href="https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html</a></div>
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Friday, September 27, 2019</div>
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Prion disease and recommended procedures for flexible endoscope reprocessing – a review of policies worldwide and proposal for a simplified approach Singeltary, GUT journal and Bramble et al </div>
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<a fg_scanned="1" href="https://prionprp.blogspot.com/2019/09/prion-disease-and-recommended.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prionprp.blogspot.com/2019/09/prion-disease-and-recommended.html</a></div>
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<span style="font-family: arial, helvetica;">***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***</span></div>
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<span style="font-size: 13.3333px;">***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<*** </span></div>
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<span style="font-size: 13.3333px;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***</span></div>
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<span style="font-size: 13.3333px;">***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<*** </span></div>
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<span style="font-family: arial, helvetica;">***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***</span></div>
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<span style="font-family: arial, helvetica;"><a fg_scanned="1" href="https://familialcjdtseprion.blogspot.com/2019/02/cwd-gss-tse-prion-spinal-cord-confucius.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://familialcjdtseprion.blogspot.com/2019/02/cwd-gss-tse-prion-spinal-cord-confucius.html</a></span></div>
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THURSDAY, DECEMBER 12, 2019 </div>
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Heidenhain Variant Creutzfeldt Jakob Disease hvCJD, sporadic spontaneous CJD and the TSE Prion December 14, 2019</div>
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<a fg_scanned="1" href="https://creutzfeldt-jakob-disease.blogspot.com/2019/12/heidenhain-variant-creutzfeldt-jakob.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2019/12/heidenhain-variant-creutzfeldt-jakob.html</a></div>
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TUESDAY, FEBRUARY 25, 2020 </div>
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***> Novel Strain of the Chronic Wasting Disease Agent Isolated From Experimentally Inoculated Elk With LL132 Prion Protein</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/02/novel-strain-of-chronic-wasting-disease.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/02/novel-strain-of-chronic-wasting-disease.html</a></div>
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MONDAY, DECEMBER 16, 2019 </div>
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Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update</div>
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***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***</div>
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What if?</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/12/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/12/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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> However, to date, no CWD infections have been reported in people.</div>
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key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry</div>
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*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</div>
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*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***</div>
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<a fg_scanned="1" href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a></div>
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<a fg_scanned="1" href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true</a></div>
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<a fg_scanned="1" href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a></div>
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Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis</div>
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We hypothesize that:</div>
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(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;</div>
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(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;</div>
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(3) Reliable essays can be established to detect CWD infection in humans; and</div>
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(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.</div>
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<a fg_scanned="1" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></div>
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ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE</div>
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<span style="color: #222222; font-size: 16px;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </span></div>
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<span style="color: #222222; font-size: 16px;">University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </span></div>
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<span style="color: #222222; font-size: 16px;">This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </span></div>
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<span style="color: #222222; font-size: 16px;">Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </span></div>
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<span style="color: #222222; font-size: 16px;">At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </span></div>
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PRION 2018 CONFERENCE</div>
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Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice</div>
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Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).</div>
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To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.</div>
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After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.</div>
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Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.</div>
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The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<br clear="none" />Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.</div>
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The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..</div>
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***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***</div>
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<a fg_scanned="1" href="https://prion2018.org/" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://prion2018.org/</a></div>
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READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;</div>
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P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States</div>
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Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..</div>
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SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD<br clear="none" />states.</div>
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AND ANOTHER STUDY;</div>
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P172 Peripheral Neuropathy in Patients with Prion Disease</div>
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Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..</div>
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IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,</div>
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AND</div>
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included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),</div>
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AND</div>
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THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.</div>
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snip…</div>
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see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry</div>
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<a href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a></div>
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<a fg_scanned="1" href="https://prion2018.org/" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://prion2018.org/</a></div>
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PRION 2019 ABSTRACTS </div>
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1. Interspecies transmission of the chronic wasting disease agent</div>
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Justin Greenlee</div>
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Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service</div>
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ABSTRACT</div>
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The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.</div>
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53. Evaluation of the inter-species transmission potential of different CWD isolates</div>
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Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa</div>
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aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile</div>
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ABSTRACT</div>
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Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.</div>
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56. Understanding chronic wasting disease spread potential for at-risk species</div>
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Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman</div>
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Department of Biological Sciences, University of Alberta, Edmonton AB, Canada</div>
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CONTACT Catherine I. Cullingham <a href="mailto:cathy.cullingham@ualberta.ca" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:cathy.cullingham@ualberta.ca">cathy.cullingham@ualberta.ca</a></div>
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Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.</div>
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KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates</div>
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Thursday, May 23, 2019 </div>
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Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts</div>
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<a fg_scanned="1" href="https://prionconference.blogspot.com/2019/05/prion-2019-emerging-concepts-cwd-bse.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionconference.blogspot.com/2019/05/prion-2019-emerging-concepts-cwd-bse.html</a></div>
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see full Prion 2019 Conference Abstracts</div>
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<span style="color: #0096ef;"><a fg_scanned="1" href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a></span></div>
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THURSDAY, OCTOBER 04, 2018</div>
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Cervid to human prion transmission 5R01NS088604-04 Update</div>
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<a fg_scanned="1" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></div>
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<a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html</a></div>
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snip…full text;</div>
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SATURDAY, FEBRUARY 09, 2019</div>
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Experts: Yes, chronic wasting disease in deer is a public health issue — for people</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html</a></div>
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SATURDAY, FEBRUARY 23, 2019 </div>
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Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/02/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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TUESDAY, NOVEMBER 04, 2014 </div>
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Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011</div>
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Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "</div>
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<a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2014/11/six-year-follow-up-of-point-source.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/11/six-year-follow-up-of-point-source.html</a> </div>
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Transmission Studies</div>
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Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS</div>
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resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</div>
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snip.... </div>
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<a href="https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20090506002237/http://www..bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ </div>
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Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</div>
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In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species. </div>
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<a fg_scanned="1" href="http://jvi.asm.org/content/83/18/9608.full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://jvi.asm.org/content/83/18/9608.full</a> </div>
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Prions in Skeletal Muscles of Deer with Chronic Wasting Disease </div>
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Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure. </div>
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<a fg_scanned="1" href="http://science.sciencemag.org/content/311/5764/1117..long" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://science.sciencemag.org/content/311/5764/1117..long</a> </div>
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*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.</div>
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see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”</div>
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From: TSS (<a class="yiv9821099117linkified" fg_scanned="1" href="http://216-119-163-189.ipset45.wt.net/" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">216-119-163-189.ipset45.wt.net</a>)</div>
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Subject: CWD aka MAD DEER/ELK TO HUMANS ???</div>
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Date: September 30, 2002 at 7:06 am PST</div>
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From: "Belay, Ermias"</div>
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To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</div>
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Sent: Monday, September 30, 2002 9:22 AM</div>
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Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div>
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Dear Sir/Madam,</div>
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In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</div>
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Ermias Belay, M.D. Centers for Disease Control and Prevention</div>
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-----Original Message-----</div>
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From: Sent: Sunday, September 29, 2002 10:15 AM</div>
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To: <a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:rr26k@nih.gov">rr26k@nih.gov</a>; <a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:rrace@niaid.nih.gov">rrace@niaid.nih.gov</a>; <a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank" ymailto="mailto:ebb8@CDC.GOV">ebb8@CDC.GOV</a></div>
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Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</div>
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Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS</div>
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Thursday, April 03, 2008</div>
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A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</div>
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snip...</div>
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*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</div>
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snip... full text ; </div>
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<a fg_scanned="1" href="http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html</a> </div>
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> However, to date, no CWD infections have been reported in people. </div>
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sporadic, spontaneous CJD, 85%+ of all human TSE, just not just happen. never in scientific literature has this been proven.</div>
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if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;</div>
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sporadic = 54,983 hits <a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic</a></div>
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spontaneous = 325,650 hits <a fg_scanned="1" href="https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous</a></div>
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key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </div>
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*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</div>
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*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </div>
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<a fg_scanned="1" href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a> </div>
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FRIDAY, JULY 26, 2019 </div>
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Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2019/07/chronic-wasting-disease-in-cervids.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/07/chronic-wasting-disease-in-cervids.html</a></div>
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TUESDAY, JANUARY 21, 2020 </div>
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***> 2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/01/2004-european-commission-chronic.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/01/2004-european-commission-chronic.html</a></div>
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SUNDAY, APRIL 12, 2020 </div>
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PENNSYLVANIA REVISED CWD RESPONSE PLAN DRAFT AVAILABLE FOR REVIEW</div>
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<a fg_scanned="1" href="https://chronic-wasting-disease.blogspot.com/2020/04/pennsylvania-revised-cwd-response-plan.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2020/04/pennsylvania-revised-cwd-response-plan.html</a></div>
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Suspect symptoms</div>
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What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?</div>
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28 Mar 01 Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.</div>
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Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.</div>
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"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb...</div>
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2001</div>
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Suspect symptoms</div>
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What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?</div>
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28 Mar 01</div>
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Like lambs to the slaughter</div>
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31 March 2001</div>
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by Debora MacKenzie Magazine issue 2284.</div>
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FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.</div>
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Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.</div>
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Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.</div>
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"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.</div>
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snip...</div>
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There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.</div>
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Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.</div>
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<a fg_scanned="1" href="http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.newscientist.com/article/mg16922840.300-like-lambs-to-the-slaughter.html</a> </div>
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26 March 2003 </div>
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Terry S. Singeltary, retired (medically) CJD WATCH </div>
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I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? </div>
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<a fg_scanned="1" href="http://www.neurology.org/content/60/2/176/reply#neurology_el_535" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.neurology.org/content/60/2/176/reply#neurology_el_535</a></div>
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The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI </div>
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Tracking spongiform encephalopathies in North America </div>
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Original </div>
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“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ... </div>
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Volume 3, Number 8 01 August 2003 </div>
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Newsdesk </div>
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Tracking spongiform encephalopathies in North America </div>
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My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost </div>
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my mom to hvCJD (Heidenhain variant CJD) and have been searching for </div>
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answers ever since. What I have found is that we have not been told the </div>
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truth. CWD in deer and elk is a small portion of a much bigger problem. </div>
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rapidly progressive dementia compatible with spontaneous </div>
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Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of </div>
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documents on transmissible spongiform encephalopathies (TSE) and </div>
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realised that if Britons could get variant CJD from bovine spongiform </div>
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encephalopathy (BSE), Americans might get a similar disorder from </div>
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chronic wasting disease (CWD) the relative of mad cow disease seen among </div>
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deer and elk in the USA. Although his feverish search did not lead him </div>
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people, it did uncover a largely disappointing situation. </div>
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Singeltary was greatly demoralised at the few attempts to monitor the </div>
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occurrence of CJD and CWD in the USA. Only a few states have made CJD </div>
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reportable. Human and animal TSEs should be reportable nationwide and </div>
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internationally, he complained in a letter to the Journal of the </div>
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American Medical Association (JAMA 2003; 285: 733). I hope that the CDC </div>
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<br /></div>
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does not continue to expect us to still believe that the 85% plus of all </div>
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<br /></div>
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CJD cases which are sporadic are all spontaneous, without route or source. </div>
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Until recently, CWD was thought to be confined to the wild in a small </div>
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<br /></div>
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region in Colorado. But since early 2002, it has been reported in other </div>
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areas, including Wisconsin, South Dakota, and the Canadian province of </div>
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<br /></div>
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Saskatchewan. Indeed, the occurrence of CWD in states that were not </div>
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endemic previously increased concern about a widespread outbreak and </div>
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possible transmission to people and cattle. </div>
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To date, experimental studies have proven that the CWD agent can be </div>
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transmitted to cattle by intracerebral inoculation and that it can cross </div>
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the mucous membranes of the digestive tract to initiate infection in </div>
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lymphoid tissue before invasion of the central nervous system. Yet the </div>
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plausibility of CWD spreading to people has remained elusive. </div>
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Part of the problem seems to stem from the US surveillance system. CJD </div>
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is only reported in those areas known to be endemic foci of CWD. </div>
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Moreover, US authorities have been criticised for not having performed </div>
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enough prionic tests in farm deer and elk. </div>
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Although in November last year the US Food and Drug Administration </div>
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issued a directive to state public-health and agriculture officials </div>
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prohibiting material from CWD-positive animals from being used as an </div>
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ingredient in feed for any animal species, epidemiological control and </div>
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research in the USA has been quite different from the situation in the </div>
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UK and Europe regarding BSE. </div>
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Getting data on TSEs in the USA from the government is like pulling </div>
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<br /></div>
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teeth, Singeltary argues. You get it when they want you to have it, </div>
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and only what they want you to have. </div>
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Norman Foster, director of the Cognitive Disorders Clinic at the </div>
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<br /></div>
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University of Michigan (Ann Arbor, MI, USA), says that current </div>
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surveillance of prion disease in people in the USA is inadequate to </div>
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detect whether CWD is occurring in human beings; adding that, the </div>
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cases that we know about are reassuring, because they do not suggest the </div>
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appearance of a new variant of CJD in the USA or atypical features in </div>
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<br /></div>
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patients that might be exposed to CWD. However, until we establish a </div>
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system that identifies and analyses a high proportion of suspected prion </div>
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disease cases we will not know for sure . The USA should develop a </div>
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<br /></div>
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system modelled on that established in the UK, he points out. </div>
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Ali Samii, a neurologist at Seattle VA Medical Center who recently </div>
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<br /></div>
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reported the cases of three hunters two of whom were friends who died </div>
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<br /></div>
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from pathologically confirmed CJD, says that at present there are </div>
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insufficient data to claim transmission of CWD into humans; adding that </div>
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[only] by asking [the questions of venison consumption and deer/elk </div>
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hunting] in every case can we collect suspect cases and look into the </div>
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plausibility of transmission further. Samii argues that by making both </div>
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doctors and hunters more aware of the possibility of prions spreading </div>
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<br /></div>
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through eating venison, doctors treating hunters with dementia can </div>
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<br /></div>
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consider a possible prion disease, and doctors treating CJD patients </div>
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<br /></div>
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will know to ask whether they ate venison. </div>
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CDC spokesman Ermias Belay says that the CDC will not be investigating </div>
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<br /></div>
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the [Samii] cases because there is no evidence that the men ate </div>
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<br /></div>
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CWD-infected meat. He notes that although the likelihood of CWD </div>
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<br /></div>
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jumping the species barrier to infect humans cannot be ruled out 100% </div>
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<br /></div>
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and that [we] cannot be 100% sure that CWD does not exist in humans& </div>
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<br /></div>
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the data seeking evidence of CWD transmission to humans have been very </div>
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<br /></div>
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limited. </div>
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<a fg_scanned="1" href="http://infection.thelancet.com/journal/journal.isa" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://infection.thelancet.com/journal/journal.isa</a> </div>
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BRITISH MEDICAL JOURNAL </div>
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<br /></div>
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SOMETHING TO CHEW ON </div>
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<br /></div>
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BMJ </div>
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<br /></div>
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Terry S Singeltary, NA medically retired Send response to journal: Re: Re: vCJD in the USA * BSE in U.S. </div>
<div>
<br /></div>
<div>
In reading the recent article in the BMJ about the potential BSE tests being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize me, that the U.S. has been concealing vCJD. There have been people dying from CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for some time. It just seems that when there is one found, they seem to change the clarical classification of the disease, to fit their agenda. I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt Jakob disease. Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so bad at times, it would take 3 of us to hold her down, while she screamed "God, what's wrong with me, why can't I stop this." 1st of symptoms to death, 10 weeks, she went blind in the first few weeks. But, then they told me that this was just another strain of sporadic CJD. They can call it what ever they want, but I know what I saw, and what she went through. Sporadic, simply means, they do not know. My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following; vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD. The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch? </div>
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<br /></div>
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CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997. So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie. Cats becoming infected with a TSE. Have you ever read the ingredients on the labels of cat and dog food? But, they do not put these tissues from these animals in pharmaceuticals, cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and the many more products that come from bovine, ovine, or porcine tissues and organs. So, as I said, this CWD would be a small piece of a very big puzzle. But, it is here, and it most likely has killed. You see, greed is what caused this catastrophe, rendering and feeding practices. But, once Pandora's box was opened, the potential routes of infection became endless. </div>
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No BSE in the U.S.A.? I would not be so sure of that considering that since 1990; </div>
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Since 1990 the U.S. has raised 1,250,880,700 cattle; </div>
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Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of Oct. 4, 1999; </div>
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There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until Aug. 4, 1997 went to the renders for feed; </div>
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Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of Aug. 1999; </div>
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Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains. </div>
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<br /></div>
<div>
I believe all these TSE's are going to be related, and originally caused by the same greedy Industries, and they will be many. Not just the Renders, but you now see, that they are re-using medical devices that were meant for disposal. Some medical institutions do not follow proper auto- claving procedures (even Olympus has put out a medical warning on their endescopes about CJD, and the fact you cannot properly clean these instruments from TSE's), and this is just one product. Another route of infection. </div>
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<br /></div>
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Regardless what the Federal Government in the U.S. says. It's here, I have seen it, and the longer they keep sweeping it under the rug and denying the fact that we have a serious problem, one that could surpass aids (not now, but in the years to come, due to the incubation period), they will be responsible for the continued spreading of this deadly disease. </div>
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<br /></div>
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It's their move, it's CHECK, but once CHECKMATE has been called, how many thousands or millions, will be at risk or infected or even dead. You can't play around with these TSE's. I cannot stress that enough. They are only looking at body bags, and the fact the count is so low. But, then you have to look at the fact it is not a reportable disease in most states, mis-diagnosis, no autopsies performed. The fact that their one-in-a- million theory is a crude survey done about 5 years ago, that's a joke, under the above circumstances. A bad joke indeed........ </div>
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<br /></div>
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The truth will come, but how many more have to die such a hideous death. It's the Government's call, and they need to make a serious move, soon. This problem, potential epidemic, is not going away, by itself. </div>
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<br /></div>
<div>
Terry S. Singeltary Sr., Bacliff, Texas 77518 USA flounder@wt.net </div>
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<br /></div>
<div>
<a fg_scanned="1" href="http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2</a></div>
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BMJ </div>
<div>
<br /></div>
<div>
2 January 2000 </div>
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<br /></div>
<div>
Terry S Singeltary retired Send response to journal: Re: U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well... </div>
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<br /></div>
<div>
In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it. </div>
<div>
<br /></div>
<div>
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all; </div>
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"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level." </div>
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<br /></div>
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Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages. </div>
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Something else I find odd, page 16; </div>
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"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries." </div>
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<br /></div>
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A few more factors to consider, page 15; </div>
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"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom." </div>
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<br /></div>
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"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply." </div>
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"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom." </div>
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<br /></div>
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Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e. </div>
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<br /></div>
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To be continued... </div>
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<br /></div>
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2 January 2000 </div>
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<br /></div>
<div>
British Medical Journal </div>
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<br /></div>
<div>
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well </div>
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<br /></div>
<div>
<a fg_scanned="1" href="http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well</a></div>
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<div>
15 November 1999 </div>
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<br /></div>
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British Medical Journal </div>
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<div>
vCJD in the USA * BSE in U.S. </div>
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<br /></div>
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<a fg_scanned="1" href="http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us</a> </div>
</div>
<div>
<br /></div>
<div>
Diagnosis and Reporting of Creutzfeldt-Jakob Disease </div>
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<br /></div>
<div>
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease </div>
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<br /></div>
<div>
To the Editor: </div>
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<br /></div>
<div>
In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally. </div>
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<br /></div>
<div>
Terry S. Singeltary, Sr Bacliff, Tex </div>
<div>
<br /></div>
<div>
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. </div>
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<a fg_scanned="1" href="http://jama.jamanetwork.com/article.aspx?articleid=1031186" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://jama.jamanetwork.com/article.aspx?articleid=1031186</a></div>
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To the Editor: </div>
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<br /></div>
<div>
At the time of my mother's death, various diagnoses were advanced such as "rapid progressive Alzheimer disease," psychosis, and dementia. Had I not persisted and personally sought and arranged a brain autopsy, her death certificate would have read cardiac failure and not CJD. </div>
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<br /></div>
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Through CJD Voice1 I have corresponded with hundreds of grief-stricken families who are so devastated by this horrific disease that brain autopsy is the furthest thing from their minds. In my experience, very few physicians suggest it to the family. After the death and when families reflect that they never were sure what killed their loved one it is too late to find the true cause of death. In the years since my mother died I think that the increasing awareness of the nature of CJD has only resulted in fewer pathologists being willing to perform an autopsy in a suspected case of CJD. </div>
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<br /></div>
<div>
People with CJD may die with incorrect diagnoses of dementia, psychosis, Alzheimer disease, and myriad other neurological diseases. The true cause of death will only be known if brain autopsies are suggested to the families. Too often the physician's comment is, "Well, it could be CJD but that is so rare it isn't likely." </div>
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<br /></div>
<div>
Until CJD is required to be reported to state health departments, as other diseases are, there will be no accurate count of CJD deaths in the United States and thus no way to know if the number of deaths is decreasing, stable, or increasing as it has recently in the United Kingdom. </div>
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<br /></div>
<div>
Dorothy E. Kraemer Stillwater, Okla </div>
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<br /></div>
<div>
In Reply: </div>
<div>
<br /></div>
<div>
Mr Singeltary and Ms Kraemer express an underlying concern that our recently reported mortality surveillance estimate of about 1 CJD case per million population per year in the United States since 1985 may greatly underestimate the true incidence of this disease. Based on evidence from epidemiologic investigations both within and outside the United States, we believe that these national estimates are reasonably accurate. </div>
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<br /></div>
<div>
Even during the 1990s in the United Kingdom, where much attention and public health resources have been devoted to prion disease surveillance, the reported incidence of classic CJD is similar to that reported in the United States. </div>
<div>
<br /></div>
<div>
In addition, in 1996, active US surveillance for CJD and new variant (nv) CJD in 5 sites detected no evidence of the occurrence of nvCJD and showed that 86% of the CJD cases in these sites were identifiable through routinely collected mortality data. </div>
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<br /></div>
<div>
Our report provides additional evidence against the occurrence of nvCJD in the United States based on national mortality data analyses and enhanced surveillance. It specifically mentions a new center for improved pathology surveillance. We hope that the described enhancements along with the observations of Singeltary and Kraemer will encourage medical care providers to suggest brain autopsies for more suspected CJD cases to facilitate the identification of potentially misdiagnosed CJD cases and to help monitor the possible occurrence of nvCJD. </div>
<div>
<br /></div>
<div>
Creutzfeldt-Jakob disease is not on the list of nationally notifiable diseases. In those states where surveillance personnel indicate that making this disease officially notifiable would meaningfully facilitate collection of data that are needed to monitor the incidence of CJD and nvCJD, including the obtaining of brain autopsy results, we encourage such a change. However, adding CJD to the notifiable diseases surveillance system may lead to potentially wasteful, duplicative reporting because the vast majority of the diagnosed cases would also be reported through the mortality surveillance system. </div>
<div>
<br /></div>
<div>
Furthermore, making CJD a notifiable disease may not necessarily help identify undiagnosed CJD cases. The unique characteristics of CJD make mortality data a useful surrogate for ongoing surveillance. Unlike many other neurologic diseases, CJD is invariably fatal and in most cases rapidly progressive and distinguishable clinically from other neurologic diseases. </div>
<div>
<br /></div>
<div>
Because CJD is least accurately diagnosed early in the course of the illness, notifiable disease surveillance of CJD could be less accurate than mortality surveillance of CJD. In addition, because death as a condition is more completely and consistently reported, mortality surveillance has the advantage of being ongoing and readily available. </div>
<div>
<br /></div>
<div>
The absence of CJD and nvCJD from the list of nationally notifiable diseases should not be interpreted to mean that they are not important to public health; this list does not include all such diseases. We encourage medical caregivers to report to or consult with appropriate public health authorities about any diagnosed case of a transmissible disease for which a special public health response may be needed, including nvCJD, and any patient in whom iatrogenic transmission of CJD may be suspected. </div>
<div>
<br /></div>
<div>
Robert V. Gibbons, MD, MPH Robert C. Holman, MS Ermias D. Belay, MD Lawrence B. Schonberger, MD, MPH Division of Viral and Rickettsial Diseases National Center for Infectious Diseases Centers for Disease Control and Prevention Atlanta, Ga <span style="font-size: 10pt;"> </span></div>
<div>
<br /></div>
<div>
Singeltary, Sr et al. JAMA </div>
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<a fg_scanned="1" href="http://jama.jamanetwork.com/article.aspx?articleid=1031186" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://jama.jamanetwork.com/article.aspx?articleid=1031186</a></div>
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Alzheimer's, TSE, Prion disease ???</div>
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<div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;">
<span style="background-color: rgba(255, 255, 255, 0);">>>> The only tenable public line will be that "more research is required’’ <<< </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);"><br clear="none" style="line-height: 1.22em;" /></span></div>
<div style="font-family: Arial, Helvetica, sans-serif; font-size: 12px; line-height: 1.22em;">
<span style="background-color: rgba(255, 255, 255, 0);">>>> possibility on a transmissible prion remains open<<< </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);"><br clear="none" style="line-height: 1.22em;" /></span></div>
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<span style="background-color: rgba(255, 255, 255, 0);"><span style="line-height: 1.22em;">O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ? </span></span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015) </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">snip...see full Singeltary Nature comment here; </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Alzheimer's disease</span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease... </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy</span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d</a></span></span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0111492" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0111492</a></span></span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full</a></span></span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">*** Singeltary comment PLoS *** </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">Posted by flounder on 05 Nov 2014 at 21:27 GMT </span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a fg_scanned="1" href="http://www.plosone.org/annotation/listThread.action?root=82860" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=82860</a></span></span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">IN CONFIDENCE</span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">5 NOVEMBER 1992</span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES</span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">There are also results to be made available shortly </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">(1) concerning a farmer with CJD who had BSE animals, </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">(2) on the possible transmissibility of Alzheimer’s and </span></div>
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<span style="background-color: rgba(255, 255, 255, 0);">(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]</span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a href="https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf</a></span></span></div>
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<span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a href="https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf</a></span></span></div>
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<span face="Helvetica, Arial, sans-serif" style="color: #1d2129;"><span style="font-size: 14px; white-space: pre-wrap;">MONDAY, JANUARY 20, 2020 </span></span></div>
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<span face="Helvetica, Arial, sans-serif" style="color: #1d2129;"><span style="font-size: 14px; white-space: pre-wrap;">sporadic CJD one in a million, FAKE NEWS PEOPLE! </span></span></div>
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<span face="Helvetica, Arial, sans-serif" style="color: #1d2129;"><span style="font-size: 14px; white-space: pre-wrap;">this myth has been incorrect for decades, and had been stated as such by a few, but again, the media is too lazy to do it's job and print the facts. human tse prion, including 85%+ of all human tse i.e. sporadic cjd, is now one in 5,000! </span></span></div>
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MONDAY, AUGUST 26, 2019</div>
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Creutzfeldt Jakob Disease CJD, TSE, Prion, Surveillance Update August 2019</div>
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SUNDAY, MARCH 10, 2019 </div>
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National Prion Disease Pathology Surveillance Center Cases Examined¹ Updated Feb 1, 2019 Variably protease-sensitive prionopathy VPSPr</div>
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National Variability in Prion Disease–Related Safety Policies for Neurologic Procedures</div>
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Wednesday, September 11, 2019 </div>
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Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion</div>
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<span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 12px; line-height: 1.22em;">Disinfection of Multi-Use Ocular Equipment for Ophthalmological Procedures: A Review of Clinical Effectiveness, Cost-Effectiveness, and Guidelines</span></span></div>
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MONDAY, AUGUST 26, 2019</div>
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Creutzfeldt Jakob Disease CJD, TSE, Prion, Surveillance Update August 2019</div>
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SUNDAY, MARCH 10, 2019 </div>
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National Prion Disease Pathology Surveillance Center Cases Examined¹ Updated Feb 1, 2019 Variably protease-sensitive prionopathy VPSPr</div>
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<a fg_scanned="1" href="https://prionunitusaupdate.blogspot.com/2019/03/national-prion-disease-pathology.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://prionunitusaupdate.blogspot.com/2019/03/national-prion-disease-pathology.html</a></div>
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<span style="font-family: arial, helvetica;">***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***</span></div>
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<span style="font-size: 13.3333px;">***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<*** </span></div>
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<span style="font-size: 13.3333px;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***</span></div>
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<span style="font-size: 13.3333px;">***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<*** </span></div>
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<span style="font-family: arial, helvetica;">***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***</span></div>
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<span style="font-family: arial, helvetica;"><a fg_scanned="1" href="https://familialcjdtseprion.blogspot.com/2019/02/cwd-gss-tse-prion-spinal-cord-confucius.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://familialcjdtseprion.blogspot.com/2019/02/cwd-gss-tse-prion-spinal-cord-confucius.html</a></span></div>
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THURSDAY, JANUARY 30, 2020 </div>
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Docket Number: FDA-2012-D-0307 Recommendations to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and Blood Components; Draft Guidance for Industry Draft Guidance for Industry Singeltary Submission</div>
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<a fg_scanned="1" href="https://creutzfeldt-jakob-disease.blogspot.com/2020/01/docket-number-fda-2012-d-0307.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2020/01/docket-number-fda-2012-d-0307.html</a></div>
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FRIDAY, JANUARY 31, 2020</div>
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CJD TSE Prion Blood Products, iatrogenic transmission, Confucius is confused again, WHAT IF? Docket Number: FDA-2012-D-0307</div>
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<a fg_scanned="1" href="https://creutzfeldt-jakob-disease.blogspot.com/2020/01/cjd-tse-prion-blood-products-iatrogenic.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2020/01/cjd-tse-prion-blood-products-iatrogenic.html</a></div>
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Updated April 3, 2020</div>
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Year Total Referrals² Prion Disease Sporadic Familial Iatrogenic vCJD</div>
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1999 & earlier 381 230 200 27 3 0</div>
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2000 145 102 90 12 0 0</div>
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2001 209 118 110 8 0 0</div>
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2002 241 144 124 18 2 0</div>
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2003 259 160 137 21 2 0</div>
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2004 316 181 164 16 0 1³</div>
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2005 327 178 156 21 1 0</div>
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2006 365 179 159 17 1 2⁴</div>
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2007 374 210 191 19 0 0</div>
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2008 384 221 205 16 0 0</div>
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2009 397 231 210 20 1 0</div>
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2010 401 246 218 28 0 0</div>
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2011 392 238 214 24 0 0</div>
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2012 413 244 221 23 0 0</div>
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2013 416 258 223 34 1 0</div>
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2014 355 208 185 21 1 1⁵</div>
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2015 401 263 243 20 0 0</div>
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2016 396 277 248 29 0 0</div>
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2017 375 266 247 19 0 0</div>
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2018 309 223 204 18 1 0</div>
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2019 416 270 240 21 0 0</div>
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2020 84 56 21 2 0 0</div>
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TOTAL 73566 45037 40108 4349 13 4</div>
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1Listed based on the year of death or, if not available, on the year of referral; </div>
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2Cases with suspected prion disease for which brain tissue was submitted; </div>
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3Disease acquired in the United Kingdom; </div>
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4Disease acquired in the United Kingdom in one case and in Saudi Arabia in the other; </div>
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5Disease possibly acquired in a Middle Eastern or Eastern European country; </div>
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6Includes 14 cases in which the diagnosis is pending, and 19 inconclusive cases; </div>
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7Includes 42 (9 from 2019, 33 from 2020) cases with type determination pending in which the diagnosis of vCJD has been excluded. </div>
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8The sporadic cases include 3906 cases of sporadic Creutzfeldt-Jakob disease (sCJD), 69 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 35 cases of sporadic Fatal Insomnia (sFI). </div>
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9Total does not include 272 Familial cases diagnosed by blood test only.</div>
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<span style="line-height: 1.22em;">Monday, February 3, 2020 </span></div>
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<span style="line-height: 1.22em;">Informing Patient Contacts About Iatrogenic Creutzfeldt Jakob Disease</span></div>
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<a fg_scanned="1" href="https://itseprion.blogspot.com/2020/02/informing-patient-contacts-about.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://itseprion.blogspot.com/2020/02/informing-patient-contacts-about.html</a></div>
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to be continued...</div>
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TSS</div>
Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-5783466110981773845.post-56018940281786734482019-05-23T16:35:00.001-07:002019-05-23T16:35:31.637-07:00Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts<span style="font-family: arial; font-size: 13.3333px;">Prion 2019 Emerging Concepts</span><br />
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Prion 2019 Congress Full Schedule</div>
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SCHEDULE: TUESDAY, MAY 21</div>
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8:30 - 12:05 WORKSHOP 1: Animal Prion Disease-Interspecies Transmission</div>
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WORKSHOP ORGANIZERS: Debbie McKenzie, Judd Aiken, Olivier Andreoletti</div>
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Moved from Salon 4 to Salon 8</div>
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8:30 - 8:35 Welcome</div>
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8:35 - 9:05 Interspecies transmission of the chronic wasting disease agent</div>
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Justin Greenlee, USDA, ARS, National Animal Disease Center, Ames, Iowa, USA</div>
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9:05 - 9:20 Evaluation of interspecies transmission potential of different CWD isolates</div>
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Rodrigo Morales, University of Texas Health Science Center, San Antonio, Texas, USA</div>
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9:20 - 9:35 CWD transmissibility to humans: Investigation using humanized mouse models and sCJD tissues</div>
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Qingzhong Kong, Case Western Reserve University, Cleveland, Ohio, USA</div>
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9:35 - 9:50 Chronic wasting disease transmission studies to non-human primates & transgenic mice</div>
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Brent Race, Rocky Mountain Labs, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA</div>
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9:50 - 10:05 Alteration of prion strain emergence by non-host factors</div>
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Sara Holec, Creighton University, Omaha, Nebraska, USA</div>
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10:05 - 10:20 HOSPITALITY BREAK Salon 8</div>
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10:20 - 10:35 Establishment of PrPCWD extraction and detection in farm soil</div>
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Hyun Joo Sohn, Animal and Plant Quarantine Agency, South Korea</div>
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10:35 - 10:50 Detection of CWD prion seeding activity in feces demonstrates both consistent shedding and potential for environmental monitoring</div>
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Joanne Tennant, Colorado State University, Fort Collins, Colorado, USA</div>
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10:50 - 11:05 Longitudinal Studies of CWD Infection After Low-Dose Exposure</div>
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Ed Hoover, Colorado State University, Fort Collins, Colorado, USA</div>
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11:05 - 11:20 Detection of hematogenous prions in longitudinal CWD studies</div>
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Amy Nalls, Prion Research Centre, Colorado State University, Fort Collins, Colorado, USA</div>
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11:20 - 11:35 Identification of novel CWD strains</div>
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Debbie McKenzie, University of Alberta, Edmonton, Canada</div>
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11:35 - 11:50 Mixtures of prion substrains in mice bioassay of natural scrapie cases</div>
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Rosa Bolea, University of Zaragoza, Centre for TSE and Emerging Animal Diseases, Zaragoza, Spain</div>
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11:50 - 12:05 Structural analyses of chronic wasting disease using electron microscopy and molecular dynamics simulations</div>
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Sara Amidian, University of Alberta, Edmonton, Canada</div>
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12:05 - 12:20 PrPSc aggregation state dictates biochemical properties of prions and disease pathogenesis</div>
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Chris Chang, CPRU, University of Calgary, Calgary, Canada</div>
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12:20 - 1:00 BUFFET LUNCH Salon 8</div>
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SCHEDULE: TUESDAY, MAY 21 Workshops have been moved from Salon 4 to Salon 8</div>
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PRION 2019</div>
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@PRION2019 #PRION2019</div>
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1:00 - 5:00 WORKSHOP 2: Biomarkers and Diagnostics for Protein Folding Diseases</div>
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WORKSHOP ORGANIZERS: Inga Zerr, Kurt Giles, Sonia Vallabh</div>
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1:00 - 1:30 Seed amplification assays for diagnosis, etiological biomarker measurement, and strain discrimination in protein folding diseases</div>
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Byron Caughey, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA</div>
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1:30 - 1:50 Ultrasensitive detection and seeding selectivity of tau aggregates of Alzheimer disease and chronic traumatic encephalopathy</div>
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Alison Kraus, Rocky Mountain Laboratories, National Institutes of Health, Hamilton, Montana, USA</div>
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1:50 - 2:10 Diagnosis and biomarkers of Parkinson’s and Dementia with Lewy bodies: rapid and ultra-sensitive quantitation of disease-associated α-synuclein by αSyn RT-QuIC</div>
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Christina Orru, Rocky Mountain Laboratories, National Institutes of Health, Hamilton, Montana, USA</div>
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2:10 - 2:30 Skin biomarkers as diagnostic tests across neurodegenerative diseases</div>
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Wen-Quan Zou, Case Western Reserve University, Cleveland, Ohio, USA</div>
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2:30 - 2:50 Neurofilament light chain (NfL) as a possible biomarker for drug efficacy in mouse models of neurodegenerative diseases</div>
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Masakazu Hirouchi, University of California, San Franscisco, California, USA</div>
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2:50 - 3:10 HOSPITALITY BREAK Salon 8</div>
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3:10 - 3:30 Diagnostic accuracy of cerebrospinal fluid RT-QuIC in cases of suspected prion disease and the potential utility of using RT-QuIC for public health surveillance</div>
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Brian Appleby, Case Western Reserve University, Cleveland, Ohio, USA</div>
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3:30 - 3:50 Domain-specific quantification of PrP in cerebrospinal fluid by targeted mass spectrometry</div>
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Eric Minikel, Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA</div>
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3:50 - 4:10 Conversion kinetics of sporadic CJD prions using multiple substrates and RT-QuIC-based detection and discrimination</div>
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Stephanie Booth, Public Health Agency of Canada, Ottawa, Canada</div>
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4:10 - 4:30 High efficiency detection of all prion subtypes of sporadic Creutzfeldt Jakob disease by PMCA</div>
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Sandra Prizkow, The University of Texas Health Science Center at Houston, Houston, Texas, USA</div>
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4:30 - 4:50 Utility of RT-QuIC in predicting case status of potential Creutzfeldt-Jakob Disease (CJD) cases</div>
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Natalie Marzec, Colorado Department of Public Health and Environment, Denver, Colorado, USA</div>
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5:30 - 6:30 PRION STRAIN PHENOMENA 2019 – two perspectives; a presentation to assess the progress of prion strain concepts</div>
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CHAIR: Jason Bartz</div>
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John Collinge, University College London, London, England Surachai Supattapone, Dartmouth College, New Hampshire, USA</div>
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Salon 9</div>
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6:30 - 8:00 WELCOME RECEPTION Hall D Foyer</div>
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<a href="https://docs.wixstatic.com/ugd/961217_2ed64d8ab2f540139015ed2c3b298758.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://docs.wixstatic.com/ugd/961217_2ed64d8ab2f540139015ed2c3b298758.pdf</a></div>
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SCHEDULE: WEDNESDAY, MAY 22</div>
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7:30 - 8:15 BREAKFAST Foyer, Hall D</div>
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8:15 - 8:30 WELCOME</div>
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David Westaway, Hermann Schaetzl, Kevin Keough</div>
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Co-Chairs, PRION 2019 Congress</div>
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Hall D</div>
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8:30 - 10:10 STRUCTURAL BIOLOGY OF MAMMALIAN PRIONS</div>
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CHAIRS: D. Riesner & G. Legname</div>
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Hall D</div>
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8:30 - 9:10 Structural insights into the mechanism of mammalian prion propagation</div>
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Witold K. Surewicz, Case Western Reserve University, Cleveland, USA</div>
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9:10 - 9:30 Full atomistic model of PrPSc structure and conversion</div>
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<br /></div>
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G. Spagnolli, CIBIO, University of Trento, Trento, Italy</div>
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<br /></div>
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9:30 - 9:50 A shared β-solenoid structure for all PrPSc strains tested</div>
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<br /></div>
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H. Wille, CPPFD, University of Alberta, Edmonton, Canada</div>
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<br /></div>
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9:50 - 10:10 Large-scale production of recombinant prions with high specific infectivity</div>
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D. Walsh, Dartmouth College, Hanover, New Hampshire, USA</div>
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10:10 - 10:30 REFRESHMENT BREAK/POSTER PRESENTATIONS Foyer, Hall D</div>
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<br /></div>
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10:30 - 12:10 HUMAN DISEASE 1</div>
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CHAIRS: A. Rozemuller & B. Appleby</div>
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Hall D</div>
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<br /></div>
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10:30 - 11:10 Seed-induced Aβ deposition impairs adult neurogenesis in mouse models of Alzheimer’s disease</div>
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<br /></div>
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Melanie Meyer-Luehmann, Universitats Klinikum-Freiburg, Freiburg, Germany</div>
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11:10 - 11:30 Critical impact of cofactors on transmissibility of human prions</div>
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J. Safar, Case Western Reserve University, Cleveland, Ohio, USA</div>
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<br /></div>
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11:30 - 11:50 Investigating the clinical correlation between sCJD and other neurodegenerative pathologies</div>
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<br /></div>
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J. Lumsden, National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland</div>
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<br /></div>
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11:50 - 12:10 sCJD Prions Distribute throughout the Eye</div>
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<br /></div>
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C. Orru, Rocky Mountain Labs, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA</div>
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12:10 - 12:55 LUNCH Foyer, Hall D</div>
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SCHEDULE: WEDNESDAY, MAY 22</div>
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PRION 2019</div>
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@PRION2019 #PRION2019</div>
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12:55 - 2:35 ANIMAL DISEASE 1</div>
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<br /></div>
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CHAIRS: G. Telling & M. Zabel</div>
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Hall D</div>
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<br /></div>
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12:55 - 1:35 Modifying prion spread through the CNS</div>
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<br /></div>
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Christina Sigurdson, University of California, San Diego, USA</div>
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<br /></div>
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1:35 - 1:55 Cervid Prnp polymorphism at codon 116 generates new and distinct CWD strains</div>
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<br /></div>
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S. Hannaoui, CPRU, University of Calgary, Calgary, Canada</div>
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<br /></div>
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1:55 - 2:15 Binding prions to soils impact PrPCWD recovery but not infectivity</div>
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<br /></div>
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A. Kuznetsova, CPPFD, University of Alberta, Edmonton, Canada</div>
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<br /></div>
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2:15 - 2:35 Diversity of chronic wasting disease prion strains</div>
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<br /></div>
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C. Duque Velásquez, CPPFD, University of Alberta, Edmonton, Canada</div>
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<br /></div>
<div>
2:35 - 2:55 REFRESHMENT BREAK/POSTER PRESENTATIONS Foyer, Hall D</div>
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<br /></div>
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2:55 - 4:35 CELL BIOLOGY 1</div>
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<br /></div>
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CHAIRS: C. Lasmezas & M. Horiuchi</div>
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<br /></div>
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Hall D</div>
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<br /></div>
<div>
2:55 - 3:35 Drivers of neurotoxicity in prion diseases</div>
<div>
<br /></div>
<div>
Adriano Aguzzi, University Hospital Zurich, Zurich, Switzerland</div>
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<br /></div>
<div>
3:35 - 3:55 Pathological consequences of ROCK-PDK1 kinases overactivation in prion diseases</div>
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<br /></div>
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B. Schneider, Université Paris Descartes - Inserm, Paris, France</div>
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<br /></div>
<div>
3:55 - 4:15 Human cerebral organoids propagate sporadic CJD prions</div>
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<br /></div>
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C. Haigh, National Institute of Alergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA</div>
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<br /></div>
<div>
4:15 - 4:35 How the PrPC C-terminal domain regulates its toxic N-terminal domain</div>
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<br /></div>
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G. Millhauser, University of California, Santa Cruz, USA</div>
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4:40 - 5:55 PRION 2019 DEBATE: PrPC function in the brain</div>
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<br /></div>
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CHAIR: James Hope</div>
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PARTICIPANTS: A. Aguzzi, C. Haigh, G. Millhauser, G. Schmitt-Ulms</div>
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Hall D</div>
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6:00 - 8:00 POSTER PRESENTATION AND RECEPTION</div>
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*Cash Bar</div>
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Hall D</div>
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SCHEDULE: WEDNESDAY, MAY 22</div>
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PRION 2019</div>
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7:30 - 8:15 BREAKFAST Foyer</div>
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8:15 - 8:25 INTRODUCTORY SESSION Hall D</div>
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8:25 - 10:05 OTHER PRIONS</div>
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<br /></div>
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CHAIRS: H. True & J. Ma</div>
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<br /></div>
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Hall D</div>
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<br /></div>
<div>
8:25 - 9:05 Targeting proteopathic seeds in Alzheimer’s disease</div>
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<br /></div>
<div>
Mathias Jucker, University Tübingen, Tübingen, Germany</div>
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<br /></div>
<div>
9:05 - 9:25 Seeding Aβ accelerates AD-like pathology without cognitive impairment</div>
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S. G. Lacoursiere, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge, Canada</div>
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<div>
9:25 - 9:45 Alpha-synuclein strains initiate distinct transmissable synucleinopathies</div>
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J. Watts, Tanz Centre, University of Toronto, Toronto, Canada</div>
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9:45 - 10:05 Multiple sclerosis brain transmits pathology to humanized transgenic mice</div>
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S. Tsutsui, HBI, Cumming School of Medicine, University of Calgary, Calgary, Canada</div>
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10:05 - 10:25 REFRESHMENT BREAK/POSTER PRESENTATIONS Foyer, Hall D</div>
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10:25 - 12:05 ANIMAL DISEASE 2</div>
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CHAIRS: C. Mathiason & M. Beekes</div>
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Hall D</div>
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10:25 - 11:05 Prion accumulation in the Bone Marrow: the origin of Prionemia?</div>
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Olivier Andreoletti, École Nationale Vétérinaire de Toulouse, Toulouse, France</div>
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11:05 - 11:25 BSE discrimination and geographical variation of goat scrapie</div>
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R. Nonno, Istituto Superiore di Sanità, Rome, Italy</div>
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11:25 - 11:45 Prion tropism for the spleen: role of PrPC expression levels </div>
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V. Béringue, VIM, INRA, Université Paris-Saclay, Jouy-en-Josas, France</div>
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11:45 - 12:05 Rapid bioassay of mammalian prions in Drosophila</div>
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R. Bujdoso, Cambridge University, Cambridge, United Kingdom</div>
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11:25 - 12:05 CJD INTERNATIONAL SUPPORT ALLIANCE AND ADVISORS ECC Boardroom, Hall D Foyer</div>
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<br /></div>
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12:05 - 1:55 LUNCH AND POSTER PRESENTATIONS Foyer, Hall D</div>
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TRAINEE/SENIOR RESEARCHER ROUNDTABLES Salon 2</div>
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SCHEDULE: THURSDAY, MAY 23</div>
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PRION 2019</div>
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@PRION2019 #PRION2019</div>
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1:55 - 3:55 THERAPEUTIC APPROACHES</div>
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CHAIRS: S. Priola & K. Doh-ura</div>
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Hall D</div>
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1:55 - 2:55 Arguments for Alzheimer’s and Parkinson’s Diseases Being Caused by Prions</div>
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Stanley B. Prusiner, Institute for Neurodegenerative Diseases, University of California, San Francisco, USA</div>
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2:55 - 3:15 Antisense oligonucleotides for the prevention of genetic prion disease</div>
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<br /></div>
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S. Vallabh, Broad Institute of Harvard and MIT, Massachusetts, USA</div>
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3:15 - 3:35 Substrate-specific manipulation of the ADAM10-mediated shedding of PrPC</div>
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L. Linsenmeier, Institute of Neuropathology, UKE Hamburg, Germany</div>
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3:35 - 3:55 Evaluating plasma tau and NfL as biomarkers for prion disease</div>
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A. Thompson, MRC Prion Unit, University College London, London, United Kingdom</div>
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3:55 - 4:15 REFRESHMENT BREAK/POSTER PRESENTATIONS Foyer, Hall D</div>
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4:15 - 4:45 INTERNATIONAL CJD SUPPORT ALLIANCE Hall D</div>
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4:45 - 6:05 GENETICS</div>
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CHAIR: R. Wickner</div>
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Hall D</div>
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4:45 - 5:25 Genetic risk factors for sporadic CJD: replication, expression, function</div>
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Simon Mead, University College London, London, United Kingdom</div>
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5:25 - 5:45 Familial Parkinson’s point mutation abolishes multiple system atrophy prion replication</div>
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A. Woerman, University of California, San Franscisco, California, USA</div>
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5:45 - 6:05 Potential insights into avoiding amyloidosis from the functional amyloid PMEL</div>
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T. Allison, CPPFD, University of Alberta, Edmonton, Canada</div>
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7:00 - 10:00 ART GALLERY OF ALBERTA RECEPTION Art Gallery of Alberta</div>
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SCHEDULE: THURSDAY, MAY 23</div>
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PRION 2019</div>
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7:30 - 8:15 BREAKFAST Foyer</div>
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8:15 - 8:25 INTRODUCTORY SESSION Hall D</div>
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8:25 - 10:05 FOLDING AND REPLICATION OF PATHOGENIC PROTEINS</div>
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CHAIRS: B. Sykes & C. Soto</div>
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Hall D</div>
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8:25 - 9:05 A Solid-state Conceptualization of Information Transfer from Gene to Message to Protein</div>
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Steve McKnight, University of Texas Southwestern, Dallas, Texas, USA</div>
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<br /></div>
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9:05 - 9:25 Purification of small, non-fibrillar and infectious prions from GSS disease</div>
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I. Vanni, Istituto Superiore di Sanità, Rome, Italy</div>
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9:25 - 9:45 Seeding ability of olfactory mucosa samples from patients with synucleinopathies</div>
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F. Moda, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milano, Italy</div>
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9:45 - 10:05 Generation of bona fide prions by large-scale PMCA</div>
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F. Wang, University of Texas Health, Houston, Texas, USA</div>
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10:05 - 10:25 REFRESHMENT BREAK/POSTER PRESENTATIONS Foyer, Hall D</div>
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10:25 - 12:05 HUMAN DISEASE 2</div>
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CHAIRS: P. Parchi & W.-Q. Zou</div>
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Hall D</div>
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10:25 - 11:05 Beyond Neurofibrillary Tangles in Tauopathy</div>
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Karen Ashe, University of Minnesota, Mineapolis, Minnesota, USA</div>
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11:05 - 11:25 microRNAs profiling identifies a novel signature associated with sCJD progression</div>
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<br /></div>
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E. Vire, Institute of Prion Diseases, University College London, United Kingdom</div>
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11:25 - 11:45 Anti-PrPC autoantibodies in PRNP mutation carriers</div>
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K. Frontzek, University of Zurich, Zurich, Switzerland</div>
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11:45 - 12:05 Diverse Tau signatures in an inbred model mimic heterogeneity in a primary Tauopathy</div>
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D. Westaway, CPPFD, University of Alberta, Edmonton, Canada</div>
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12:05 - 1:50 LUNCH AND POSTER VIEWING Hall D</div>
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TRAINEE/SENIOR RESEARCHER ROUNDTABLES Salon 2</div>
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SCHEDULE: FRIDAY, MAY 24</div>
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PRION 2019</div>
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@PRION2019 #PRION2019</div>
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12:50 - 1:50 NEUROPRION ASSOCIATION GENERAL MEETING</div>
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NeuroPrion members</div>
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Hall D</div>
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1:50 - 3:30 CELL BIOLOGY 2</div>
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CHAIRS: V. Lawson & J. Braun</div>
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Hall D</div>
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1:50 - 2:30 Cellular prion infection: from traffic jams to new drug targets</div>
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Sabine Gilch, University of Calgary, Calgary, Canada</div>
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2:30 - 2:50 Propagation of human sCJD prions in organotypic slice culture</div>
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V. Sim, CPPFD, University of Alberta, Edmonton, Canada</div>
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2:50 - 3:10 Hsp110 modifies prion infection in vitro and in vivo</div>
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C. Marrero-Winkens, CPRU, University of Calgary, Calgary, Canada</div>
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3:10 - 3:30 The FXR1 Protein Is A Functional Amyloid Of Mammalian Brain</div>
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A. Sergeeva, St. Petersburg State University, Department of Genetics and Biotechnology, St. Petersburg, Russia</div>
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3:30 - 3:50 REFRESHMENT BREAK/POSTER PRESENTATIONS Foyer, Hall D</div>
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3:50 - 4:50 LATE BREAKING NEWS Hall D</div>
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3:50 - 4:02 CWD in a 16-year-old moose in Sweden</div>
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Maria Nöremark, National Veterinary Institute, Uppsala, Sweden</div>
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4:02 - 4:14 Generation of chemically optimized molecules suppressing PrP toxicity</div>
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Emiliano Biasini, University of Trento, Trento, Italy</div>
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4:14 - 4:26 A first glimpse of infectious recombinant PrPSc using solid state NMR</div>
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Jesús Requena, University of Santiago de Compostela, Spain</div>
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4:26 - 4:38 Nascent β-structure in the hydrophobic region of a GSS PrP allele</div>
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Z.-L. Fu, University of Alberta, Edmonton, Canada</div>
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4:38 - 4:50 Covalently-linked PrP fragments in two major GSS variants</div>
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Laura Cracco, Case Western Reserve University, Cleveland, USA</div>
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4:50 - 5:20 AWARDS, PRION 2020 ANNOUNCEMENT AND CLOSING REMARKS Hall D</div>
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SCHEDULE: FRIDAY, MAY 24</div>
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CO-CHAIRS: D. Westaway and H. Schaetzl</div>
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<div>
<a href="https://docs.wixstatic.com/ugd/961217_134c8115df634dafa348102328614e0b.pdf" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://docs.wixstatic.com/ugd/961217_134c8115df634dafa348102328614e0b.pdf</a></div>
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<a href="https://www.prion2019.ca/" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.prion2019.ca/</a></div>
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SEE FULL ABSTRACT SUBMISSION AND MANY THANKS TO CANADA PRION 2019 FOR THE OPEN ACCESS TO PRION 2019 !!!</div>
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here are a few of the abstracts on CHRONIC WASTING DISEASE CWD TSE PRION...terry</div>
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PRION 2019 ABSTRACTS </div>
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1. Interspecies transmission of the chronic wasting disease agent</div>
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Justin Greenlee</div>
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Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service</div>
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ABSTRACT</div>
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The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.</div>
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53. Evaluation of the inter-species transmission potential of different CWD isolates</div>
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Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa</div>
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aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile</div>
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ABSTRACT</div>
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Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.</div>
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56. Understanding chronic wasting disease spread potential for at-risk species</div>
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Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman</div>
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Department of Biological Sciences, University of Alberta, Edmonton AB, Canada</div>
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CONTACT Catherine I. Cullingham cathy.cullingham@ualberta.ca</div>
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ABSTRACT</div>
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Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.</div>
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KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates</div>
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60. Caribou Prnp polymorphism distribution in Canada and its impact on CWD pathogenesis</div>
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Maria I. Arifina, Samia Hannaouia, Yuan-Hung Huanga, Gordon Mitchellb, Antanas Staskeviciusb, Lech Kaczmarczykc,d, Walker Jacksonc,d and Sabine Gilcha</div>
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aDepartment of Ecosystem and Public Health, University of Calgary; bNational and OIE Reference Laboratory for Scrapie and CWD, Ottawa Laboratory Fallowfield, Canadian Food Inspection Agency; cWallenberg Center for Molecular Medicine, Department of Clinical and Experimental Medicine, Linköping University; dGerman Center for Neurodegenerative Disease (DZNE), Bonn</div>
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CONTACT Maria I. Arifin maria.arifin@ucalgary.ca</div>
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ABSTRACT</div>
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Wild reindeer in Norway were recently diagnosed with chronic wasting disease (CWD) [1]. Prions from CWD-infected deer were also transmissible to other reindeer in experimental settings [2,3]. Although CWD has not yet been reported in wild reindeer (caribou) in Canada, these studies show that they are at risk of infection. The wild-type reindeer, homozygous for serine at prion protein (PrP) residue 138 (138SS), developed clinical disease upon oral inoculation. Animals carrying at least one asparagine allele (138SN, 138NN) accumulated prions only in the periphery. However, both genotypes were susceptible to intracerebral prion inoculation [2,3]. Fallow deer are wild-type 138NN and are resistant to peripheral but not intracerebral prion infection [4]. Thus, we hypothesize that the138N allele, present in caribou herds in Alberta [5], alters CWD pathogenesis by limiting prion transport from the periphery to the CNS. Our aim is to elucidate the mechanisms involved in this process.</div>
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We extracted DNA from ±800 caribou, sequenced the Prnp open reading frame and determined the 138N allele prevalence in Canadian caribou populations. Results show that the 138N allele was highly prevalent in the Chinchaga woodland caribou population in BC (64%). It was also higher in barren-ground (37%) than in other woodland caribou populations (26%). To analyse how the 138N allele affects CWD pathogenesis, we generated knock-in (KI) mice where the mouse PrP is replaced by wild-type 138SS or 138NN cervid PrP. The KIs were obtained by injecting CRISPR/Cas9-edited C57BL6 embryonic stem cells (Bruce4) into wild-type blastocysts, generating chimeras, and breeding progeny to homozygosity in a C57BL6 background. PrP expression was determined using western blotting and qPCR. Correct PrP post-translational modifications were confirmed by PNGase-F and Endo-H digestion. We will inoculate our KIs with CWD-positive material from the corresponding reindeer genotypes [1,2]. The CWD-infected reindeer material was characterized by real-time quaking-induced conversion (RT-QuIC) and its transmissibility to transgenic mice overexpressing elk PrP (TgElk). Attack rate in the TgElks were almost 100%, except for those inoculated with 138SN lymph node material. Western blotting confirmed the presence of proteinase-K resistant PrP in all terminally ill mice. Our goal is to analyse the susceptibility of KIs carrying the 138N allele to intracerebral and peripheral prion infection. We will also assess the efficiency of prion transport from the periphery to the CNS in intraperitoneally inoculated KIs. Prion strain propagation within a host is highly dependent on its PrP genotype. This study will provide insight into how the 138N PrP specifically influences CWD propagation in caribou.</div>
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KEYWORDS: Chronic wasting disease; polymorphism; caribou; reindeer; cervid; transgenic mice; knock-in mice</div>
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71. Challenging assumptions: an empirical analysis of hunter response to chronic wasting disease in Alberta</div>
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John K. Pattison-Williamsa, Lusi Xiea, Vic (W.L.) Adamowicza, Margo Pybusb and Anne Hubbsb</div>
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aDepartment of Resource Economics and Environmental Sociology, University of Alberta, Edmonton, Alberta, Canada; bAlberta Environment and Parks, Edmonton, Alberta, Canada</div>
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CONTACT John K. Pattison-Williams johnp@ualberta.ca</div>
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ABSTRACT</div>
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Background: Chronic Wasting Disease (CWD) has fundamentally impacted wildlife management in North America. An integral partner in CWD management strategies is the hunting community, whose membership contributes in surveillance, harvest, and policy development. A conventional assumption has been that hunters will avoid or reduce hunting in areas where CWD is identified as high prevalence due to potential human health risks [1], requiring policy incentives to promote continued or increased hunting in these areas. However, this assumption has recently been challenged [2].</div>
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Methods: Using mule deer hunter draw information and CWD surveillance data from the Alberta Ministry of Environment and Parks (AEP), we empirically explore the response of mule deer hunters to CWD using license application trends in wildlife management units (WMUs) where CWD has been positively detected. Using a fixed effects (FE) approach, we model the relationship between total resident draw applications and covariates of CWD head counts, quotas, draw success rates between 2005 and 2016 in 39 WMUs.</div>
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Results: Our model indicates that mule deer hunters in Alberta are continuing to hunt in WMUs with high CWD prevalence and no significant relationship exists between CWD count and draw applications. These results suggest that (i) hunter decisions regarding license applications are not significantly affected by CWD presence or prevalence, or (ii) hunters perceive CWD in a WMU as a factor that does not detract from, and may be attractive for hunting opportunities.</div>
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Conclusions: Our results have important policy implications for CWD management. First, it challenges the assumption that hunters are avoiding CWD zones. Second, it suggests that alternative hunter-based strategies – such as expanded hunting seasons, increased tags or replacement tags – may be more effective and less costly than previously thought to manage the disease. One caveat is that our analysis is based on analyses of aggregate demand for hunting licenses at the WMU level, rather than individual hunter demands over time.</div>
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KEYWORDS: Chronic wasting disease; recreational hunting; cervids; alberta; mule deer; wildlife management</div>
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75. Mortality surveillance of individuals potentially exposed to chronic wasting disease</div>
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Ryan A. Maddoxa, Rachel F. Klosb, Suzanne N. Gibbons-Burgenerb, Bobbi L. Bryanta, Joseph Y. Abramsa, Brian S. Applebyc, Lawrence B. Schonbergera and Ermias D. Belaya</div>
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aNational Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA, USA; bWisconsin Department of Health Services, Division of Public Health, Madison, WI, USA; cNational Prion Disease Pathology Surveillance Center (NPDPSC), Case Western Reserve University, Cleveland, OH, USA</div>
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CONTACT Ryan A. Maddox rmaddox@cdc.gov</div>
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ABSTRACT</div>
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Introduction: Chronic wasting disease (CWD) is a prion disease of cervids. It is unknown whether CWD prions can infect people; if so, transmission would most likely occur through consumption of meat from infected animals. Since 2003, Wisconsin Department of Health Services, Division of Public Health (WDHS) personnel have maintained a database consisting of information collected from hunters who reported eating, or an intention to eat, venison from cervids positive for CWD. This data source makes it possible to evaluate causes of mortality in individuals potentially exposed to CWD.</div>
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Methods: The WDHS database contains the name, date of birth, when available, year of CWD-positive deer harvest, and city and state of residence for each potentially exposed individual. The database also includes information on how the deer was processed (self-processed or by a commercial operator) and when applicable, names of others with whom the venison was shared. Duplicate entries (i.e. those who consumed venison from CWD-positive deer in multiple hunt years) are determined by first name, last name, and date of birth. All names in the database are cross-checked with the National Prion Disease Pathology Surveillance Center (NPDPSC) neuropathology database. Vital status of individuals with date of birth available will be tracked through the identification of possible matches in the National Death Index (NDI) and the evaluation of corresponding cause of death codes.</div>
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Results: The database consists of 1561 records for hunt years 2003–2017. Of these, 613 records had accompanying date of birth; 14 entries were removed as duplicates, 1 of whom had consumed venison from a CWD-positive deer during three different hunt years, leaving 599 unique individuals for pending submission to NDI. Of these individuals, 265 of 399 (66%) who ate venison from a CWD-positive deer and provided processing information reported self-processing. No matches were found among persons in the database cross-checked with NPDPSC data.</div>
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Conclusion: Because of the robust data link between person and CWD-positive animal, reviewing the cause of mortality in potentially exposed persons is possible; those individuals who self-processed and consumed the meat are likely the best source of information about the potential for zoonotic transmission. The expected long incubation period, should transmission to humans occur, necessitates many years of vital status tracking.</div>
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76. Prion disease incidence, United States, 2003–2016 </div>
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Ryan A. Maddoxa, Marissa K. Persona, Janis E. Blevinsb, Joseph Y. Abramsa, Bobbi L. Bryanta, Brian S. Applebyb, Lawrence B. Schonbergera and Ermias D. Belaya</div>
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aNational Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA, USA; bNational Prion Disease Pathology Surveillance Center (NPDPSC), Case Western Reserve University, Cleveland, OH, USA</div>
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CONTACT Ryan A. Maddox rmaddox@cdc.gov</div>
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ABSTRACT</div>
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Introduction: Mortality data and the results of neuropathological and genetic testing are used to estimate the incidence of prion diseases in the United States.</div>
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Methods: Prion disease decedents were identified from restricted-use U.S. national multiple cause-of-death data, via a data use agreement with the National Center for Health Statistics, and from the National Prion Disease Pathology Surveillance Center (NPDPSC) database for 2003–2016. NPDPSC decedents with neuropathological or genetic test results positive for prion disease for whom no likely match was found in the multiple cause-of-death data were added as cases for incidence calculations; those with negative neuropathology results but with cause-of-death data indicating prion disease were removed. Age-adjusted average annual incidence rates for the combined data were calculated using the year 2000 as the standard population.</div>
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Results: A total of 5737 decedents were identified as having prion disease during 2003–2016 for an age-adjusted average annual incidence of 1.2 per million populations. The age-adjusted annual incidence ranged from 1.0 per million in 2004 and 2006 to 1.4 per million in 2013; there was an increasing trend in age-adjusted incidence over the entire period (p <0.0001) but no significant increase during the second half (2010–2016, p = 0.08). The age-adjusted incidence between males and females (1.3 and 1.1 per million, respectively) differed significantly (p <0.0001). Twelve cases during 2003–2016 were <30 years of age for an age-specific incidence of 6.9 per billion; only two of these very young cases were sporadic, with the rest being familial (7), variant (2), or iatrogenic (1). The age-specific average annual incidence among those <55 and ≥55 during the time period was 0.2 and 4.7 per million, respectively; incidence among those ≥65 was 5.9 per million.</div>
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Conclusion: The incidence of prion diseases, which are invariably fatal, can be estimated through analysis of mortality data supplemented with the results of neuropathological and genetic testing. Incidence in the United States over the last 7 years appears to be relatively stable. Cases <30 years of age continue to be very rare and usually indicate an exogenous source of infection or the presence of a genetic mutation.</div>
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77. Assessing chronic wasting disease strain differences in free-ranging cervids across the United States </div>
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Kaitlyn M. Wagnera, Caitlin Ott-Connb, Kelly Strakab, Bob Dittmarc, Jasmine Battend, Robyn Piercea, Mercedes Hennessya, Elizabeth Gordona, Brett Israela, Jenn Ballarde and Mark D Zabela</div>
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aPrion Research Center at Colorado State University; bMichigan Department of Natural Resources; cTexas Parks and Wildlife Department; dMissouri Department of Conservation, 5. Arkansas Game and Fish Commission</div>
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CONTACT Kaitlyn M. Wagner miedkait@rams.colostate.edu</div>
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ABSTRACT</div>
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Background/Introduction: Chronic wasting disease (CWD) is an invariably fatal prion disease affecting captive and free-ranging cervids, including white-tailed deer, mule deer, moose, elk, and reindeer. Since the initial description of the disease in the 1960’s, CWD has spread to 23 states, 3 Canadian Provinces, South Korea, Norway and, most recently, Finland. While some outbreaks of CWD were caused by transport of infected animals from endemic regions, the origin of CWD in other epizootics is unclear and has not been characterized. Previous studies have shown that there are two distinct strains of CWD. However, the continuous spread and the unclear origin of several outbreaks warrant continued surveillance and further characterization of strain diversity.</div>
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Materials and Methods: To address these knowledge gaps, we used biochemical tests to assess strain differences between CWD outbreaks in Michigan, Texas, Missouri, and Colorado, USA. Brain or lymph node samples were homogenized and digested in 50 µg/mL proteinase K (PK). These samples were then run on a Western blot to assess glycoform ratio and electrophoretic mobility. Texas samples were digested in 100 µg/mL PK. To assess conformational stability, brain or lymph node homogenates were incubated in increasing concentrations of guanidine hydrochloride from 0 M to 4 M in 0.5 M increments. Samples were then precipitated in methanol overnight, washed and PK digested in 50 µg/mL PK before slot blotting.</div>
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Results: Our results have found significant differences in glycoform ratio between CWD from Michigan and Colorado, but no differences were observed in conformational stability assays. Interestingly, when testing our CWD isolates from Texas to analyse electrophoretic mobility and glycoform ratio, we found that these samples did not exhibit the characteristic band shift when treated with PK, but PK resistant material remained. Additionally, results from our conformational stability assay demonstrate a unique profile of these Texas isolates. Testing of samples from Missouri is currently underway.</div>
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Conclusions: Thus far, our data indicate that there are strain differences between CWD circulating in Michigan and CWD in Colorado and provide important insight into CWD strain differences between two non-contiguous outbreaks. We have also identified a unique strain of CWD in Texas with biochemical strain properties not seen in any of our other CWD isolates. These results highlight the importance of continued surveillance to better understand this devastating disease. These results have important implications for CWD emergence, evolution and our understanding of prion strain heterogeneity on the landscape.</div>
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105. Differential binding of prions to vegetation </div>
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Elizabeth Triscotta, Alsu Kuznetsovab, Debbie McKenziea and Judd Aikenc</div>
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aCentre for Prions and Protein Folding Diseases, Department of Biological Sciences, University of Alberta; bDepartment of Renewable Resources, University of Alberta; cCentre for Prions and Protein Folding Diseases, Department of Agriculture Food and Nutritional Sciences, University of Alberta</div>
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CONTACT Elizabeth Triscott etriscot@ualberta.ca</div>
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ABSTRACT</div>
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Chronic wasting disease (CWD), a prion disease of cervids, is present in North America and Europe. It affects a variety of captive and free ranging animals, including mule deer, white tailed deer, reindeer, moose, and elk. Preclinical and clinical animals shed infectivity in a number of bodily fluids, including saliva, faeces, and nasal secretions. These prions are resistant to degradation and can contaminate the environment for many years. Factors such as the surface composition of materials and the mineralogy of soils can affect where infectivity accumulates in the environment. Given, however, that in most environments prions will initially contact vegetation, understanding the factors that affect the interaction between prion infectivity and vegetation is of utmost importance. We developed an assay in which infectious brain homogenate is applied to vegetation samples, which are then rinsed. The proteins are precipitated from the rinse water and the amount of PrP that rinses off each vegetation sample was compared. Given that surface composition affects prion adherence, we first compared lichen, which is coated with polysaccharides, and grass, which is covered with a waxy cuticle. Our data indicate that less prions rinse off lichen than grass. Furthermore, the binding of CWD prions to a variety of plants shows that the prion-vegetation interaction is affected by properties of the plant, e.g. microarchitecture and precise chemical composition. Freezing and drying of the plants alters this interaction. These data give us insight in how infectivity moves through the environment and has ramifications for the plausibility of environmental CWD transmission. Understanding where prions accumulate will help in developing methods for environmental monitoring and decontamination.</div>
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113. Diagnosis of CWD in a herd of farmed red deer </div>
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Ines Walther, Antanas Staskevicius, Andrei Soutyrine and Gordon Mitchell</div>
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National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, ON, Canada</div>
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CONTACT Gordon Mitchell gordon.mitchell2@canada.ca</div>
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ABSTRACT</div>
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Chronic wasting disease (CWD) continues to adversely impact wild and farmed cervids of North America, affecting primarily white-tailed deer (Odocoileus virginianus), mule deer (Odocoileus hemionus), and elk (Cervus canadensis). Red deer (Cervus elaphus) are closely related to elk, and occasional cases of CWD have been reported in farmed red deer in the United States and the Republic of Korea, and in a wild red deer in Norway. CWD was recently detected in farmed red deer for the first time in Canada, in a region geographically distinct from all previous cases of CWD. Understanding the diagnostic features and pathogenesis of CWD in red deer is essential to developing effective disease detection and control strategies in this species. The index case of this herd, a clinically healthy 15-month old male red deer, was initially detected during routine slaughter surveillance testing by ELISA. Confirmatory testing by immunohistochemistry (IHC) demonstrated modest aggregates of pathological prion protein (PrPCWD) in restricted regions of the obex of the medulla and retropharyngeal lymph nodes. Western blot of the obex homogenate revealed a banding pattern consistent with that of other Canadian CWD cases, and distinct from what has been observed in red deer experimentally infected with bovine spongiform encephalopathy. Subsequent disease control measures in this herd resulted in the testing of over 1700 red deer and an additional 10 cases of CWD were identified in females ranging in age from 18 to 28 months. All cases were positive in the obex by ELISA, IHC, and Western blot, although the extent of PrPCWD deposition detected by IHC was somewhat variable. A higher degree of variability in PrPCWD accumulation was found in lymphoid tissues, with PrPCWD not detectable by IHC in the tonsils of several cases. Sequencing of the prion protein gene from all positive cases and a subset of negative cases identified variability at several codons (98, 168, and 226) although the extent to which these polymorphisms may influence susceptibility to infection is not yet evident. Natural transmission of CWD occurs relatively efficiently amongst cervids, facilitating the geographical dissemination of disease to previously naive populations. Determining the unique characteristics of CWD in different cervid species is needed to inform the refinement of disease management approaches.</div>
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115. Diversity of chronic wasting disease prion strains </div>
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Camilo Duque Velásqueza, Elizabeth Triscotta, Chiye Kima, Jacques Van der Merwea, Samia Hannaouib, Trent Bollingerc, Christina Carlsond, Sylvie Benestade, Sabine Gilchb, Judd Aikenf and Debbie McKenziea</div>
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aDepartment of Biological Sciences, Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Canada; bDepartment of Ecosystem and Public Health, Calgary Prion Research Unit, University of Calgary, Calgary, Canada; cDepartment of Veterinary Pathology, Canadian Wildlife Health Cooperative, University of Saskatchewan, Saskatoon, Canada; dU.S. Geological Survey-National Wildlife Health Center, Madison, WI, USA; eNorwegian Veterinary Institute, Oslo and Trondheim, Norway; fDepartment of Agricultural, Food and Nutritional Sciences, Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Canada</div>
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ABSTRACT</div>
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Chronic Wasting Disease (CWD) prions affect a variety of cervid species. The expansion of the CWD geographic range and the increasing prevalence makes CWD a concern for wildlife, livestock, and human health. Prion pathogenesis results from the template-directed misfolding of cellular prion proteins (PrPC) into conformational species (e.g. PrPCWD) associated with distinct strains. We propose that cervid cellular prion protein (PrPC) polymorphisms have resulted in prion conformational diversification and speciation (i.e. by adaptive radiation) resulting in emergence of novel CWD strains. New prion strain conformers emerge following transmission between cervids expressing different PrPC amino acid polymorphisms [1-4]. Emergent CWD strains can have novel transmission properties that enable them to infect host species previously considered resistant, suggesting an increase in zoonotic risk as strain-conformers diversify and evolve [2, 3]. We are comparing field CWD isolates of different cervid species from various regions of North America and Norway and have identified differences in biochemical properties of PrPCWD, in vitro and ex vivo propagation and transmission into transgenic mice expressing deer and elk PrP (tgDeer – 96G, tgDeer – 96S, and tgElk-E226) as well as C57Bl6 mice and hamsters. Variations in PrP-res type and protease sensitivity were observed following treatment with proteinase K. Comparison of the PMCA seeding activity using deer and elk PrPC as substrates revealed differences between elk CWD isolates. ElK21 cells also responded differently to various cervid prions. Transmission was efficient for all isolates in tg33 and tgElk mice; however, only a few isolates were able to propagate in host expressing S96 deer PrPC, which has been shown to impose a strong transmission barrier, providing a means of differential selection of CWD strains [2]. Transmission differences were observed following interspecies transmission. While some white-tailed deer and mule deer isolates failed to transmit into hamsters, other isolates transmitted with a low attack rate but considerable sub-clinical infection. These isolates had a migration pattern similar to the hamster-passaged Wisc-1 strain. Two other isolates, transmitted more efficiently into hamsters and produced two different PrP-res migration profiles compared to Wisc-1-like PrP-res. Transmission of Norwegian moose and reindeer CWD isolates is ongoing; preliminary results will be presented. Our data indicate the existence of at least five different CWD strains based on transmission properties.</div>
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117. Bank vole bioassay for detection of prion infection in CWD-challenged cynomolgus macaques </div>
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Karla A. Schwenkea, Joo-Hee Waelzleina, Hermann M. Schatzlb, c, Walter Schulz-Schaeffere, Christiane Stahl-Hennigf, Stefanie Czubc, d and Michael Beekesa</div>
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aRobert Koch Institute, Prion and Prionoid Research Unit, ZBS 6, Berlin, Germany; bUniversity of Calgary, Calgary Prion Research Unit, Calgary, Canada; cUniversity of Calgary, Faculty of Veterinary Medicine, Calgary, Canada; dCanadian Food Inspection Agency (CFIA), Lethbridge, Canada; eUniversity of Homburg/Saar, Homburg, Germany; f German Primate Center, Goettingen, Germany</div>
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CONTACT Karla A. Schwenke SchwenkeK@rki.de WaelzleinJ@rki.de</div>
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ABSTRACT</div>
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Although Chronic Wasting Disease (CWD) was detected in cervids in the late 1960s, the risk of CWD transmission from cervids to humans is still puzzling. The zoonotic potential which might emanate from CWD was studied by several research groups using a multitude of in vitro and in vivo approaches. These studies provided evidence for a significant transmission barrier for CWD between cervids and humans, but do not allow the definite exclusion of such inter-species transmission. Old- world monkeys such as macaques are currently considered the most reliable animal model for testing the zoonotic potential of CWD prions. Using oral and parenteral transmission routes, our research consortium challenged cynomolgus monkeys with characterized CWD material starting 10 years ago. To test the presence or absence of prion infection in these macaques, we injected bank voles intracerebrally with homogenized brain, spinal cord and spleen tissue from monkeys sacrificed 5–7years after CWD inoculation. Bank voles have been shown to be a universal acceptor for prions derived from various species and were found to be particularly susceptible to infection with CWD prions. Therefore, in our study bank vole bioassays provide a method of choice for the detection of prion infection in the CWD-challenged cynomolgus monkeys. Potential prion disease of macaques will be detected by assessment of prion-specific clinical signs in bank voles. The clinical assessment includes weight monitoring and routine observation of the animals according to a clinical score sheet. Further, CNS and spleen tissue will be examined post mortem for PrPres by Western blot analysis. In case of ambiguous results, we plan to perform second passage inoculations in bank voles. Taken together, these studies are expected to contribute to a definite evaluation of the zoonotic risk of CWD.</div>
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120. Detection of CWD prion seeding activity in faeces demonstrates both consistent shedding and potential for environmental monitoring </div>
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Joanne M. Tennanta, Manci Lia, Davin M. Hendersona, Nicholas J. Haleyb, Candace K. Mathiasona and Edward A. Hoovera</div>
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aPrion Research Center, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA; bDepartment of Microbiology and Pathology, Midwestern State University, Glendale, AZ, USA</div>
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CONTACT Joanne M. Tennant Joanne.tennant@rams.colostate.edu</div>
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ABSTRACT</div>
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Background: Chronic wasting disease (CWD) is spreading in susceptible cervid populations in North America, Korea, and Europe. Environmental contamination and exposure to prions is considered to be a significant factor in horizontal CWD transmission. Currently disease surveillance is limited by the necessary presence and testability of infected animals. Previous studies have shown that excreta from CWD infected deer and elk contains prion seeding activity. The detection of CWD through excreta, specifically faeces, could be beneficial in passive monitoring of CWD prevalence in endemic and emerging habitats.</div>
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Methods: Longitudinal collections of faeces from low-dose CWD inoculated deer were evaluated by real-time quaking induced conversion (RT-QuIC). To emulate common environmental weathering conditions, CWD-positive faecal samples were dried and exposed to UV light and prion seeding activity was evaluated by RT-QuIC before and after treatment. In addition, faeces from premises known to contain either CWD positive or negative cervids were collected and tested in RT-QuIC for prion seeding activity in a blinded experiment.</div>
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Results: CWD prion seeding activity was detected by RT-QuIC in faeces of five out of six low-dose CWD inoculated 96GG deer. The RT-QuIC detectable prion shedding in these deer corresponded with detection of PrPCWD by IHC in rectoanal mucosa-associated lymphoid tissue (RAMALT) biopsy and prion shedding was detected during both the pre-symptomatic and symptomatic stages of disease. Prion seeding activity was little affected by drying and exposure to ultraviolet light as both rectal collected and dried faeces showed prion seeding activity. Faeces collected from the pens containing CWD positive vs. negative deer correlated with presence vs. absence prion seeding activity, respectively.</div>
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Conclusion: These studies demonstrate that low-dose inoculated deer shed prion seeding activity in faeces through much of their disease course. Further, the prion seeding activity in faeces was still detectable after exposure to UV light and desiccation. These findings suggest that environmental monitoring of CWD via landscape faecal deposits may be possible as a means for monitoring CWD in populations of free-ranging deer and elk.</div>
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124. Longitudinal studies of CWD after low-dose oral exposure in white-tailed deer </div>
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<div>
Clare E. Hoover*, Nathaniel D. Denkers, Kristen A. Davenport, Davin M. Henderson, Amy V. Nalls, Erin McNulty, Joanne Tennant, Sarah Cooper, Manci Li, Lauren Bracchi, Candace K. Mathiason and Edward A. Hoover</div>
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<br /></div>
<div>
Prion Research Center, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA</div>
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<div>
CONTACT Edward A. Hoover edward.hoover@colostate.edu</div>
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*Present address: AstraZeneca, Waltham, NJ</div>
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ABSTRACT</div>
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<div>
Background: The facile transmission of chronic wasting disease (CWD) in North America, Asia and Europe continues despite exposure to very low concentrations of prions shed by infected cervids in secreta and excreta. Explanations for this enigma could be that excreted prions may have enhanced infectivity and/or that the infectious prion dose is just quite low. Historical studies exploring CWD pathogenesis in deer have used exposures to CWD-positive brain homogenates containing from 0.5 to 10 g of brain – doses much higher than those measured in excreta, and thereby likely to ever occur in nature. We thereby sought to more closely emulate natural exposure context in our current experimental studies.</div>
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Methods: To explore how the origin or infectious dose of CWD prions may influence disease transmission or pathogenesis, we orally exposed cohorts of n = 4/group white-tailed deer to low doses of CWD presented as either CWD-positive brain homogenate (containing either 1 mg or 300 ng of brain) or to an amount of pooled saliva from CWD+ donors and containing prion seeding activity (by RT-QuIC) equivalent to 300 ng of CWD+ brain [1]. Inoculated deer were then longitudinally monitored for: (a) onset of prion infection in biopsied tonsil and recto-anal lymphoid tissues by RT-QuIC and immunohistochemistry; (b) prion shedding in saliva and faeces (by RT-QuIC); (c) onset of clinical signs (weekly observation and scoring); and (d) time to clinical disease.</div>
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Results: We first detected CWD infection by RT-QuIC seeding activity in tonsil biopsies at 6 or 9 months post exposure, in all inoculation cohorts. Prion shedding in saliva was detected (by RT-QuIC or PMCA-RT-QuIC [2]) concurrent with the first positive tonsil biopsy. Detection of prion seeding activity in faeces was less common overall and its onset observed after positivity in recto-anal lymphoid tissue biopsies. In comparison to historical studies, in which >1,000-fold higher inoculation doses were used, the time to first detection on infection (by tonsil biopsy) was prolonged by ~6 months. However, among the low-dose inoculation cohorts in this study, neither the attack rate, prion shedding profile, nor long-term disease course differed significantly, including the deer exposed to prions of saliva vs. brain origin.</div>
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Conclusions: These studies demonstrate that (a) much lower doses of CWD prions that have been used historically for point source exposure studies are sufficient to induce prion infection, shedding, and disease; and (b) although time to first detectable positivity is lengthened, the qualitative aspects of disease pathogenesis thereafter are indistinguishable by inoculum source or exposure magnitude.</div>
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Our future studies will aim at establishing the minimum oral infectious dose for CWD in deer and on exploring exposure cofactors.</div>
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Supported by NIH R01-NS-061902, P01-AI-077774, F30-ODO-118,143, T32-OD0-10,437</div>
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<div>
128. Strain profiles of CJD in venison consumers and non-consumers from Alberta and Saskatchewan </div>
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<br /></div>
<div>
Jennifer Myskiwa,b, Lise Lamourieuxa, Michael Coulthartc, Valerie Simd and Stephanie Bootha,b</div>
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<br /></div>
<div>
aZoonotic Diseases and Special Pathogens, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg; bDepartment of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg; cCanadian CJD Surveillance System, Public Health Agency of Canada, Ottawa; dDivision of Neurology, Department of Medicine Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton</div>
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<br /></div>
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CONTACT Jennifer Myskiw Myskiwj@myumanitoba.ca</div>
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ABSTRACT</div>
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<div>
Chronic wasting disease (CWD) is a fatal neurodegenerative disease that is spreading rapidly through wild cervid populations in Alberta and Saskatchewan. The epidemic of CWD in Canada not only has implications for tourism and hunting but it is also a concern over possible zoonotic transmission to humans who eat venison from infected deer. When bovine spongiform encephalopathy (BSE) reached epidemic proportions, variant CJD was identified as an acquired form of BSE due to the unique biochemical fingerprint of the pathologic prion protein (PrP). While the Canadian CJD Surveillance System (CJDSS) is staying vigilant to identify CWD human cases, it is impossible to know what the phenotype of human CWD prions would present with or whether they would be distinct from sporadic CJD cases. Additionally, there is currently no convenient laboratory model to study these differences experimentally. For these reasons we are undertaking a systematic analysis of the molecular diversity of CJD cases in patients who resided in Alberta and Saskatchewan at their time of death. We are comparing CJD profiles of venison consumers and non-consumers using a variety of clinical imaging, pathological and biochemical markers. Firstly, MRIs have been reviewed and neuropathology of over 40 patients for whom CJD was confirmed as the cause of death analysed. In this way we are able to select clinically affected areas for further biochemical analysis of prion protein. We will present data including our analysis to date of levels of protease sensitive and resistant prion protein, temperature and detergent denaturation profiles, and glycoform typing. By combining these methodologies, we intend to extend the baseline CJD typing that is already completed by the CJDSS. Importantly we aim to increase our understanding of the human prion strains that affect the Canadian population. By doing so, we will establish a baseline for the identification of any future atypical CJD cases. For example, those that could arise as a result of exposure to CWD.</div>
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130. Evaluation of the sensitivity of different RT-QuIC substrates in detecting and characterizing CWD prions in brains of Norwegian cervids </div>
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Edoardo Bistaffaa, Tram Thu Vuongb, Linh Tranb, Federico Angelo Cazzanigaa, Giulia Salzanoc, Giuseppe Legnamec, Giorgio Giacconea, Sylvie Benestadb and Fabio Modaa</div>
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<div>
aDivision of Neurology 5 and Neuropathology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milano, Italy; bNorwegian Veterinary Institute, Oslo, Norway; cLaboratory of Prion Biology, Department of Neuroscience, Scuola Internazionale Superiore di Studi Avanzati (SISSA), Trieste, Italy</div>
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CONTACT Tram Thu Vuong tram.thu.vuong@vetinst.no</div>
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ABSTRACT</div>
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<div>
Chronic wasting disease (CWD) is a highly contagious prion pathology affecting captive and free-ranging cervid populations. From its first description 50 years ago, CWD has been detected in United States, Canada, South Korea and, most recently, in Norway. At present, we do not know if these diseases are caused by the same prion strain or whether they spontaneously arose in different countries. CWD spreading among cervids is one of the most important issue for public health due to the ability of this agent to infect a large number of animals and the possible transmission to other animal species, including humans and ovine. Indeed, possible transmission of CWD to ovine that share, in some countries, the same geographic areas of CWD infected animals cannot be excluded. For this reason, it is of fundamental importance to develop a strategy allowing identification of CWD infected samples and verify their ability to propagate within the same or different species. To this aim, we are optimizing RT-QuIC assay coupled with specific biochemical analysis for evaluating whether different CWD samples could produce final reactions products with peculiar differences useful for CWD strain’s identification. RT-QuIC were performed using different substrates of reaction (truncated PrP protein from hamster, reindeer and deer species) for evaluating their sensitivity and specificity in detecting CWD in brains of Norwegian moose, red deer and reindeer. Moreover, through biochemical assessments (PK digestion, guanidine hydrochloride evaluation and use of antibodies against different PrP epitopes), we evaluated whether and to what extent final RT-QuIC products were able to acquire distinct biochemical features according to the strain of CWD. Preliminaryresults showed that deer PrP detected CWD in all species with higher efficiency compared to hamster and reindeer. Notably, truncated deer-PrP was able to rapidly detect positive samples (within 3 h from the beginning of the reaction) compared to the other substrates. Although with less sensitivity, reindeer-PrP identified red deer, reindeer and moose CWD, with this latter being characterized by lower resistance to PK digestion and different PrP banding profile (at Western blot) compared to the others. Therefore, RT-QuIC can be exploited for detecting CWD infected species with high sensitivity and specificity, while biochemical data seem to indicate the possibility of identifying the species of CWD origin. If confirmed, such information will be of fundamental importance for planning actions to contain the spread of the infection (especially to other species, like ovines) in CWD affected regions.</div>
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KEYWORDS: Prion; CWD; RT-QuIC</div>
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142. Effects of Elk-PrPC expression levels on CWD strain properties </div>
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Camilo Duque Velásqueza, Alicia Oteroa, Chiye Kima, Elizabeth Triscotta, Jeffrey Narayana, Jacques Van der Merweb, Judd Aikenc and Debbie McKenziea</div>
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<br /></div>
<div>
aDepartment of Biological Sciences, Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Canada; bDepartment of Medicine, Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB, Canada; cDepartment of Agricultural, Food and Nutritional Sciences, Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB, Canada</div>
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CONTACT Alicia Otero oterogar@ualberta.ca</div>
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ABSTRACT</div>
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<br /></div>
<div>
Chronic Wasting Disease (CWD) is a contagious prion disease affecting various species of free-ranging and/or captive cervids on three continents. Species-specific prion protein (PrPC) polymorphisms influence prion conversion into PrPCWD. PrPC amino acid variation can also regulate disease susceptibility to particular prion strains and has been implicated in the diversification of prion strain conformers [1, 2, 3]. Elk and deer PrPC differ at residue E226Q and this amino acid difference has been implicated in the selection of CWD1 and CWD2 prion strains [4]. As PrPC expression has been suggested to affect prion strain evolution [5], we hypothesized that elk PrPC levels affect CWD strain generation. To test this hypothesis, transgenic (tg) FVB mice over-expressing elk PrPC [6] were crossed with prnp knock-out FVB mice to generate tg-elk with different PrPC expression levels. Both tg-elk+/+ and tg-elk± were exposed to white-tailed deer CWD strains (Wisc-1 and H95+) [2, 3]. The H95+ strain was a mixture generated on passage of Wisc-1 in deer heterozygous for H95G96 and Q95S96 [2]. Tg-elk+/+ mice succumbed to Wisc-1 with a mean incubation period of 116 ± 7 days post infection (dpi) compared to 164 ± 11 dpi for the H95+ strain mixture. Consistent with the reduced PrPC expression, the same deer prion strains resulted in longer incubation periods (157 ± 21 dpi and >180 dpi, respectively) when passaged in tg-elk± mice. After first passage, transmission of Wisc-1 and H95+ in tg-elk+/+ mice resulted in a single neuropathological profile that differed from the profile produced by passage of elk prions (described as the CWD2 strain [1]). Our results show that, upon first passage, the E226Q polymorphism did not affect the strain properties of deer prions and indicates a single strain (Wisc-1) was selected by the tg-elk+/+ mice. The comparative analysis of neuropathological profiles between high and low expression tg-elk on first and second passage will be presented.</div>
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156. Screening and characterization of unusual sCJD cases in a CWD endemic state in the USA </div>
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<br /></div>
<div>
Yihui Liua, Manuel Camachoa, Wenquan Zoua,b,c, Qingzhong Konga,b,c</div>
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<br /></div>
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aDepartment of Pathology, Case Western Reserve University (CWRU), Cleveland, USA; bDepartment of Neurology, CWRU, Cleveland, OH, USA; cNational Center for Regenerative Medicine, CWRU, Cleveland, USA</div>
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CONTACT Qingzhong Kong qxk2@case.edu</div>
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ABSTRACT</div>
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<br /></div>
<div>
Background: Chronic wasting disease (CWD) has spread to 26 states in the USA and three provinces in Canada, and it has been detected recently in Norway and Finland. Potential CWD zoonosis is a serious public health concern. It is unclear whether CWD transmission to humans has already occurred. We aim to start to address this question by examining all available sCJD cases from a CWD endemic state in the USA.</div>
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<div>
Methods: Frozen brain tissues from all available sCJD cases archived in the National Prion Disease Pathology Surveillance Center from a US state that has been significantly impacted by CWD were sampled at five brain regions. These brain samples were subjected to detailed biochemical analysis to look for unusual patterns, characteristics, and/or distribution of PrPSc in comparison with sCJD samples from states that have not detected CWD. Unusual cases are further scrutinized for their clinical presentations, histopathological features, and history of cervid hunting and venison consumption.</div>
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Results and Conclusions: We have found some unusual sCJD cases in this CWD endemic state. We will report our preliminary findings on their features. Currently there is no convincing evidence to support a direct link to CWD for any of these unusual sCJD cases.</div>
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<div>
Disclaimer: The findings and conclusions in this report are those of the authors and do not necessarily represent the position of the National Prion Disease Pathology Surveillance Center.</div>
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175. Environmental pathways of CWD prions </div>
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<br /></div>
<div>
Alsu Kuznetsovaa, Debbie McKenzieb and Judd M. Aikena</div>
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aAgricultural Life and Environmental Sciences Faculty, University of Alberta, Edmonton, Canada; bFaculty of Science, University of Alberta, Edmonton, Canada</div>
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CONTACT Alsu Kuznetsov alsu@ualberta.ca</div>
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ABSTRACT</div>
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<br /></div>
<div>
Soil can serve as a reservoir and route for horizontal transmission of chronic wasting disease (CWD) by interaction with the infectious prion protein (PrPCWD) shed by infected animals. Prion fate in environment is determined by structure of ecosystems including soil and vegetation types. In boreal ecosystems, lichen and shrubs cover sandy textured, quartz-illite soils with surface plant litter horizon. In prairie ecosystems, grassy meadows grow on humus-enriched, loamy or clay montmorillonite soils. Once shed onto the soil surface, prion persistence in the environment primarily depends on the binding and transportation capacity of soils. Factors responsible for prion migration are soil properties such as mineralogical composition, texture, soil organic matter content and pH. We investigated PrPCWD migration in soil profiles by comparing their passage through pure soil minerals and diverse soils using lab-scale soil columns. PrP-res was detected by western blot or protein misfolding cyclic amplification in leachates of columns containing quartz, surface plant litter – soil organic horizon (LFH) of boreal Luvisolic and Brunisolic soils, illite, or the mineral horizons of Luvisol and Brunisol. Infectivity in leachates from quartz, illite and Luvisolic columns was confirmed by bioassay. Analysis of the solid phase of the columns confirmed the migration of PrPCWD to lower layers in the illite, while the PrPCWD in the montmorillonite column remained close to the column surface. While mineralogical composition of soils determines movement of prions, other constituents, such as soil organic matter, microbial population, composition of soil solutions, might affect prion infectivity. To investigate the impact of humic acids (a major component of soil organic material), we incubated CWD agent with humic acids for various lengths of time. Analysis by western blot and bioassay demonstrated that humic acids can reduce PrPres and infectivity over time. Thus, in soils of temperate regions, including the Chernozems of Northern America and Cambisols of Europe, prions would remain at the soil surface due to strong binding to montmorillonite, while in boreal and tundra regions soils (Luvisols, Podzols, and Brunisols), most of the prions would be transported through the plant litter LFH, and partially through the upper soil mineral horizon into lower horizons. Although these soils also have lower levels of humic acids, a soil organic matter compound that has the capacity to reduce CWD infectivity levels, soils of the boreal and tundra regions are less favourable to the horizontal transmission of CWD as these soils make PrPCWD less bioavailable.</div>
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199. Chronic wasting disease transmission studies to non-human primates and transgenic mice </div>
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<br /></div>
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Brent Race, Katie Williams, Christina D. Orrù, Andrew G. Hughson, Lori Lubke and Bruce Chesebro</div>
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National Institute of Allergy and Infectious Diseases, Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, Hamilton, MT, USA</div>
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CONTACT Brent Race raceb@niaid.nih.gov</div>
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ABSTRACT</div>
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Introduction: Chronic wasting disease (CWD) is the only prion disease affecting free-ranging animals, reported in North America, South Korea and Norway. Unlike in most other prion disease CWD agents are shed in blood, urine and feces which most likely contribute to the horizontal transmission between cervid species. The developments of amplification-based seeding assays have been instrumental in the detection of low levels of prions in clinical samples. Using real-time quaking-induced conversion (RT-QUIC), we established an ultrasensitive detection method for PrPCWD in the urine from CWD-infected sequentially sampled transgenic mice overexpressing elk prion protein (TgElk mice). In addtion, RT-QUIC was performed in the kidney and brain of theses mice model to trace abnormal prion. Materials and Methods: 44 brain and kidney, urine samples from sequentially collected from CWD-infected TgElk mice (TgElk CWD) were stored at -80℃. In brain and kidney, 10% (w/v) homogenate was prepared in 0.9% sterilized saline. In urine 100uL of each sample was mixed with 10uL 2.8% sodium phosphotungustic acid (NaPTA) and incubated for 1hr at 37℃ with shaking at 1,350 rpm. Samples were centrifuged for 30min at 16,100g. The pellet was resuspended in 10uL of 0.1% SDS/PBS for 30min at 55℃. RT-QUIC reactions were set up in 96-well clear bottom optic plates and consisted of 98uL RT-QUIC buffer [final concentrations of 1XPBS, 1mM EDTA, 10uM Thioflavin, 300mM NaCl buffer and 0.1mg/ml recombinant Syrian hamster recombinant protein (23-231) and 2uL of sample. The RT-QUIC assay was performed on a FLUOstar Omega fluorescence plate reader that was preheated to 42℃ for 60hr with 90sec shaking at 700rpm followed by 1min incubation. Results: Five randomly selected mice were sequentially culled on every 15 days from 30dpi to 120dpi during CWD infected TgElk mice reached terminal stage. Rough hair coats among clinical signs were showed from 90 dpi. PrPCWD in the brain in TgElk CWD was detectable persistently from early stages (30dpi), and in the kidney PrPCWD was also detectable in clinical and terminal stages (90 dpi and 120dpi). PrPCWD in the urine in TgElk CWD reached the highest levels at 120dpi. NaPTA/RT-QUIC was applied to measure PrPCWD in urine samples collected on every 15 days from 30dpi to 120dpi when CWD infected TgElk mice reached terminal stage. PrPCWD in the urine in TgElk CWD reached the highest levels at 90dpi. PrPCWD was also detectable in late and terminal stages (120dpi). Conclusions: We demonstrate that CWD prions can be detected by RT-QUIC or NaPTA/RT-QUIC in the brain, kidney and urine of TgElk mice at the early and terminal stages of disease. Based on these data, we suggest that PrPCWD is excreted into only urine until 90 dpi and then slowly accumulated in kidney. Our results can be used in designing future study of CWD pathogenesis in TgElk mice.</div>
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KEYWORDS: Cynomolgus macaques; squirrel monkeys; non-human primate; transgenic mice; CWD; RT-QuIC; prion; cross-species transmission; barrier; chronic wasting disease</div>
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214. Identification of novel CWD strains </div>
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<div>
Debbie McKenziea, Camilo Duque Velasqueza, Allen Herbsta, Elizabeth Triscotta, Jacques van der Merwea, Samia Hannaouib, Leonardo Corteza, Sara Amidiana, Valerie Sima, Holger Willea, Hermann Schaetzlb, Sabine Gilchb and Judd Aikena</div>
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aCentre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB, Canada; bCalgary Prion Centre, University of Calgary, Calgary, AB, Canada</div>
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<br /></div>
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CONTACT Debbie McKenzie Debbie.mckenzie@ualberta.ca</div>
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ABSTRACT</div>
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<div>
Chronic wasting disease is a set of prion diseases infecting captive and wild cervids. As different CWD agents are transmitted between different cervid species and between the same species having different Prnp polymorphisms, novel CWD strains can be generated. These new strains can exhibit different biochemical properties as well as different conformers. Identification of novel CWD strains is critically important as the different strains may vary in their host ranges, increasing the potential for transmission to economically important species as well as zoonotic transmission.</div>
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<div>
A rate limiting step in the characterization of CWD strains is the identification of deer samples that potentially contain novel strains. Much of the strain generation likely occurs during early passage between different Prnp genotypes (of the same or different species). Traditionally these differences have been identified following passages into rodent models (strains of lab mice, transgenic mice expressing different Prnp sequences and/or hamsters). Incubation periods can be long and the number of potential isolates is high making transmission experiments a slow, tedious, and expensive process. To streamline the process, we have identified a panel of in vitro analyses to help target samples for further characterization. For some isolates, potential new strains have been identified by western blot analysis, others by cervid cell assay, changes in the Prnp sequence, folding and/or aggregation differences as well as ability to seed reactions in RT-QuIC. Isolates of interest are then further characterized by transmission in a variety of different tg mouse lines, wild-type mice, hamsters, and voles. Using these criteria, five potential CWD strains have been identified.</div>
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223. Scrapie in white-tailed deer: a strain of the CWD agent that efficiently transmits to sheep? </div>
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Justin J. Greenleea, Robyn D. Kokemullera, S. Jo Moorea and Heather West Greenleeb</div>
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aVirus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, IA, USA; bDepartment of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, USA</div>
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CONTACT Justin J. Greenlee Justin.Greenlee@ars.usda.gov</div>
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ABSTRACT</div>
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<div>
Scrapie is a transmissible spongiform encephalopathy of sheep and goats that is associated with widespread accumulation of abnormal prion protein (PrPSc) in the central nervous and lymphoid tissues. Chronic wasting disease (CWD) is the natural prion disease of cervid species, and the tissue distribution of PrPSc in affected cervids is similar to scrapie in sheep. There are several lines of evidence that suggest that multiple strains of CWD exist, which may affect the agent’s potential to transmit to hosts of the same or different species. We inoculated white-tailed deer with the scrapie agent from ARQ/ARQ sheep, which resulted in 100% attack rates by either the intracranial or oronasal route of inoculation. When examining tissues from the brainstems or lymphoid tissues by traditional diagnostic methods such as immunohistochemistry or western blots, it is difficult to differentiate tissues from deer infected with scrapie from those infected with CWD. However, there are several important differences between tissues from scrapie-infected white-tailed deer (WTD scrapie) and those infected with CWD (WTD CWD). First, there are different patterns of PrPSc deposition in the brains of infected deer: brain tissues from deer with WTD scrapie had predominantly particulate and stellate immunoreactivity whereas those from deer with WTD-CWD had large aggregates and plaque-like deposits. Secondly, the incubation periods of WTD scrapie isolates are longer than CWD isolates in mice expressing cervid prion protein. Most notably, the transmission potential of these two isolates back to sheep is distinctly different. Attempts to transmit various CWD isolates to sheep by the oral or oronasal routes have been unsuccessful despite observation periods of up to 7 years. However, WTD scrapie efficiently transmitted back to sheep by the oronasal route. Upon transmission back to sheep, the WTD scrapie isolate exhibited different phenotypic properties when compared to the sheep receiving the original sheep scrapie inoculum including different genotype susceptibilities, distinct PrPSc deposition patterns, and much more rapid incubation periods in transgenic mice expressing the ovine prion protein. The scrapie agent readily transmits between sheep and deer after oronasal exposure. This could confound the identification of CWD strains in deer and the eradication of scrapie from sheep.</div>
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234. The European Union Summary Report On Surveillance For The Presence Of Transmissible Spongiform Encephalopathies (TSE): The Situation In 2017 </div>
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Angel Ortiz Pelaeza, Valentina Rizzia, Giuseppe Rub, Francesco Ingravalleb and Yves Van der Stedea</div>
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aUnit on Biological Hazards and Contaminants, Department of Risk Assessment & Scientific Assistance, European Food Safety Authority (EFSA); bBiostatistics, Epidemiology and Risk Analysis (BEAR) Unit. Istituto Zooprofilattico Sperimentale di Piemonte, Liguria e Valle d ’Aosta, Torino (Italia)</div>
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CONTACT Angel Ortiz Pelaez angel.ortizpelaez@efsa.europa.eu</div>
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ABSTRACT</div>
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<div>
The European Food Safety Authority publishes a yearly summary of the surveillance activities on transmissible spongiform encephalopathies (TSE) in bovine animals, sheep, goats, cervids, and other species, in the European Union (EU), and in Iceland, Norway and Switzerland. Target groups include: animals clinically suspected of being infected by TSE; animals culled under TSE eradication measures; animals with clinical signs at ante-mortem; emergency slaughtered; fallen stock/not slaughtered for human consumption and healthy slaughtered animals for human consumption, for cervids also hunted and road or predator-injured or killed.</div>
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<div>
For the first time since bovine spongiform encephalopathy (BSE) had been reported, no cases of classical BSE were reported world-wide in 2017 [1]. Six atypical BSE cases were reported by Spain (1 H /2 L), France (1 H/1 L) and Ireland (1 L), out of the 1,312,714 cattle tested by 28 EU Member States (MS) and 18,526 tested by three non-MS.</div>
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<div>
In total 431,815 small ruminants were tested in 2017 in the EU. Compared with 2016, there was a 36.2% increase in the number of cases of classical scrapie (CS) in sheep (933), mostly reported by Greece, Spain, Italy and Romania, although over 75% of the cases were sourced in infected flocks. Atypical scrapie (AS) was confirmed in 94 animals. In goats, a decrease of 10% in the number of cases of classical scrapie (567) were reported, 84% in Cyprus. Atypical scrapie was confirmed in nine animals.</div>
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Ten-year trend analysis showed a statistically significant decrease in the sheep proportion of CS cases per 10,000 tested animals and an increase in goats. For AS, 10-year data did not detect any statistically significant trend in both species.</div>
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After the discovery of chronic wasting disease (CWD) in Norway in 2016, TSE testing in cervids increased in the EU: 10 MS tested 3,585 cervids (75% in Romania, 98.5% from wildlife), all negative. Norway tested 25,736 deer in 2017, leading to the detection of the first case of CWD in a red deer, nine cases in wild reindeer and one in a wild moose. Following EFSA recommendations, the European Commission introduced a 3-year mandatory surveillance programme for six member states starting on 1 January 2018.</div>
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By the time of submitting this abstract, CS/AS cases were not yet available, but one new classical BSE case was confirmed in Scotland (2018), one L-type BSE case in Poland (2019) and one case of CWD in a wild moose in Finland in March 2018.</div>
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KEYWORDS: BSE; scrapie; CWD; EU; surveillance</div>
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244. The use of recreational hunters in Chronic Wasting Disease (CWD) management: behaviour and incentives </div>
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Lusi Xiea, Vic Adamowicza and Patrick Lloyd-Smithb</div>
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aUniversity of Alberta; bUniversity of Saskatchewan</div>
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CONTACT Lusi Xie lxie@ualberta.ca</div>
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ABSTRACT</div>
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Background:While many jurisdictions in North America have implemented some management programmes to address Chronic Wasting Disease (CWD), the disease continues to spread. Although epidemiological models have proposed depopulating infected animals to reduce disease prevalence and spread by increasing hunter harvest (e.g. Potapov et al. 2016) [1], these models do not evaluate the incentives required to increase hunter harvest or the impacts of wildlife disease and management programmes on recreational activity and value. A better understanding of human behavioural responses will help effectively incorporate recreational hunters in wildlife disease control. The objective of this study is to examine the use of incentives to recreational hunters for CWD management by studying hunting trip decisions in response to CWD and its management. We develop an empirical model, with a focus on spatial and temporal substitution patterns of recreational activities, as well as economic benefits of a new recreation season.</div>
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Materials and Methods:The data used in this study are from an online survey of recreational hunters in Alberta and Canada. Five thousand hunters were sampled and a response rate of approximately 20% resulted in a usable sample of 707. Hunters were asked to recall hunting trips in 2017 and stated intended visitation with proposed extended hunting seasons for CWD management. We develop a discrete-continuous empirical model that captures hunting trip decisions on sites, periods and frequencies. Explanatory variables included in the model are CWD prevalence levels, policy dummy variables, individuals’ socio-demographic variables as well as travel and time costs. With the estimated parameters, spatial and temporal substitution patterns are captured, measures of the potential harvest of affected deer populations, and economic benefits, are calculated.</div>
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Results and Conclusions:We find a negative but insignificant coefficient of CWD which indicates that individuals do not avoid hunting in CWD-infected areas. Individuals are likely to take around six additional trips on average during the extended seasons – this is more than half of the average trips (around 10) they actually took in 2017. We find that individuals are likely to substitute from hunting in areas with lower CWD risks to hunting in the most CWD-infected areas in both seasons. Individuals are better off from an extended season for CWD management. Our findings indicates that it is possible to direct hunting trips for CWD control by extending hunting seasons in CWD-infected areas without additional monetary or non-monetary incentives.</div>
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KEYWORDS: Chronic wasting disease; recreation demand</div>
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252. RT-QuIC as an antemortem diagnostic tool to detect chronic wasting disease in deer skin </div>
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Natália C. Ferreiraa, Jorge M. Charcob, Michael A. Metricka, Christina D. Orrua, Andrew G. Hughsona, Joaquín Castillaa, Michael W. Millerc and Byron Caugheya</div>
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aLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, USA; 2 CIC bioGUNE, Derio (Bizkaia), Spain; 3Colorado Division of Parks and Wildlife, Wildlife Health Program, Fort Collins, Colorado, USA</div>
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CONTACT Natália C. Ferreira natalia.docarmoferreiradearaujo@nih.gov</div>
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Chronic wasting disease (CWD) is a fatal prion disease which affects cervids. This disease has an asymptomatic incubation time of 2–4 years, and during this period they can shed prions through saliva, feces, urine and placental tissue, contaminating the environment. Indeed, CWD highly contagious between cervids and shedding from live, infected animals likely contributes to its rapid spread. So far, CWD has been reported at least in 24 states in the US, as well as Canada, South Korea and Norway. To date, there is no evidence of CWD transmission to humans. However, in infected areas, deer population can drop as much as ~25 percent. Currently, there are two tests approved to diagnose CWD: immunohistochemistry and ELISA. However, these tests are applied postmortem and tissue types approved are the medial retropharyngeal lymph nodes and a specific region of brainstem (obex). Here we describe our efforts to adapt the real time quaking-induced conversion (RT-QuIC) as a diagnostic tool to detect PrPCWD in deer ear skin. Our initial analysis of a blinded panel of 50 samples yielded 82% sensitivity and 75% specificity. We are working to improve the conditions and performance of this assay, given that it might be useful for antemortem CWD diagnostics and surveillance.</div>
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123. Detection of prion seeds throughout the eyes of sporadic Creutzfeldt-Jakob disease patients</div>
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Christina Orrua, Katrin Soldaub, Christian Cordanoc, Jorge Llibre-Guerrad, Ari J. Greene, Henry Sanchezc, Bradley R. Grovemana, Steven D. Edlandf,g, Jiri G. Safarh,i, Jonathan H. Linb, Byron Caugheya, Michael D. Geschwindc and Christina J. Sigurdsonb,j</div>
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aLaboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Hamilton, MT, USA; bDepartment of Pathology, University of California, San Diego, La Jolla, CA USA; cDepartment of Neurology, Memory and Aging Center, University of California, San Francisco (UCSF), San Francisco, CA, USA; dCognitive and Behavioral Research Unit, National Institute of Neurology, Havana, Cuba; eDepartment of Neurology, Multiple Sclerosis Center, University of California, San Francisco (UCSF), San Francisco, CA, USA; fDepartments of Family Medicine & Public Health and gNeurosciences, University of California, San Diego, La Jolla, CA USA; hDepartments of Pathology and iNeurology, Case Western Reserve University, Cleveland, OH, USA; jDepartment of Pathology, Immunology, and Microbiology, University of California, Davis, Davis, CA, USA</div>
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CONTACT Christina Orru christina.orru@nih.gov</div>
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Orrù and Soldau, mBIO 2018 9:e02095–18. https://doi.org/10.1128/ mBio.02095-18</div>
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Cases of iatrogenic Creutzfeldt-Jakob disease (CJD) have been reported from corneal transplants, yet the levels of prions in the eye remain unknown. Approximately, 40% of sporadic CJD patients develop visual symptoms and often seek ophthalmological consultation. This study probed the occurrence, level, and distribution of prions in the eyes of patients with sCJD, the most common prion disease in humans. We used the highly sensitive real time quaking-induced conversion (RT-QuIC) assay to measure post-mortem levels of prion seeding activity in cornea, lens, ocular fluid, retina, choroid, sclera, optic nerve, and extraocular muscle. This is the largest series of sCJD patient eyes studied by any assay to date. We detected prion seeding activity in 100% of sCJD eyes representing three common sCJD subtypes with a four log-fold range of seeding activity observed across individuals. The retina consistently showed the highest prion seeding activity. Within the retina, prion deposits were also detected by immunohistochemistry in the outer plexiform layer, and in some eyes the inner plexiform layer. With increased distance from the brain prion seed levels by RT-QuIC declined in eye tissues. Collectively, these results reveal that sCJD patients accumulate prions throughout the eyes, indicating the potential diagnostic utility as well as the possible biohazard.</div>
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<a href="https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197</a></div>
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<span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Chronic Wasting Disease CWD TSE Prion</span></div>
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<span style="background-color: #fcfce5;"><span style="color: #141414; font-family: Georgia, serif;"><span style="font-size: 14.6667px;">Cervid to human prion transmission </span></span></span></div>
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<span style="background-color: #fcfce5;"><span style="color: #141414; font-family: Georgia, serif;"><span style="font-size: 14.6667px;">Kong, Qingzhong Case Western Reserve University, Cleveland, OH, United States</span></span></span></div>
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<span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">We hypothesize that: </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(3) Reliable essays can be established to detect CWD infection in humans; and </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches. </span></div>
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<a href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></div>
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<br clear="none" style="background-color: #fcfce5;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE</span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">here is the latest;</span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">PRION 2018 CONFERENCE </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge). </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <*** </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv7303854509externalLink" href="https://prion2018.org/" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px;" target="_blank">https://prion2018.org/</a><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">states. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">AND ANOTHER STUDY; </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">P172 Peripheral Neuropathy in Patients with Prion Disease </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017, </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">AND </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%), </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">AND </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">THAT The Majority of cases were male (60%), AND half of them had exposure to wild game. </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">snip...</span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv7303854509externalLink" href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px;" target="_blank">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;"> </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv7303854509externalLink" href="https://prion2018.org/" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px;" target="_blank">https://prion2018.org/</a></div>
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Sunday, February 25, 2018 </div>
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PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW </div>
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<a href="http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html</a><br clear="none" style="background-color: #fcfce5;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">THURSDAY, OCTOBER 04, 2018 </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;">Cervid to human prion transmission 5R01NS088604-04 Update </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv7303854509externalLink" href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a><span style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;"> </span><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><a class="yiv7303854509externalLink" href="http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html" rel="noopener noreferrer" shape="rect" style="background-color: #fcfce5; border-radius: 5px; color: #0429e4; cursor: pointer; font-family: Georgia, serif; font-size: 14.6667px; margin: 0px -3px; padding: 0px 3px;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html</a><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" /><br clear="none" style="background-color: #fcfce5; color: #141414; font-family: Georgia, serif; font-size: 14.6667px;" />snip...full text;<div style="font-family: arial, helvetica;">
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SATURDAY, FEBRUARY 09, 2019 <div style="font-family: arial, helvetica;">
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Experts: Yes, chronic wasting disease in deer is a public health issue — for people</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/experts-yes-chronic-wasting-disease-in.html</a></div>
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<span style="font-family: arial, helvetica;">*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. </span></div>
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<a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf</a></div>
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you can see more evidence here ;</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html</a></div>
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Wednesday, May 24, 2017 </div>
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PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1</div>
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<a href="http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html</a></div>
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<span style="font-family: arial, helvetica; font-size: x-small;">PRION2017 DECIPHERING NEURODEGENERATIVE DISORDERS 23 – 26 May 2017 Edinburgh </span></div>
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<a href="http://prionprp.blogspot.com/2016/12/prion2017-deciphering-neurodegenerative.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">http://prionprp.blogspot.com/2016/12/prion2017-deciphering-neurodegenerative.html</a></div>
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WEDNESDAY, SEPTEMBER 08, 2010</div>
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CWD PRION CONGRESS SEPTEMBER 8-11 2010</div>
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PRION 2010</div>
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International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html</a></div>
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<span style="font-family: arial, helvetica;">Transmission Studies</span></div>
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<span style="font-family: arial, helvetica;">Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS</span></div>
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<span style="font-family: arial, helvetica;">resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.</span></div>
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<span style="font-family: arial, helvetica;">snip.... </span></div>
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<span style="font-family: arial, helvetica;"><a href="https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></span></div>
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Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ </div>
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<span style="font-family: arial, helvetica;">Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations</span></div>
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<span style="font-family: arial, helvetica;">In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species. </span></div>
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<span style="font-family: arial, helvetica;"><a href="http://jvi.asm.org/content/83/18/9608.full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://jvi.asm.org/content/83/18/9608.full</a> </span></div>
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<span style="font-family: arial, helvetica;">Prions in Skeletal Muscles of Deer with Chronic Wasting Disease </span></div>
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<span style="font-family: arial, helvetica;">Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure. </span></div>
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<span style="font-family: arial, helvetica;"><a href="http://science.sciencemag.org/content/311/5764/1117..long" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://science.sciencemag.org/content/311/5764/1117..long</a> </span></div>
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<span style="font-family: arial, helvetica;">*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.</span></div>
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<span style="font-family: arial, helvetica;">see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”</span></div>
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<span style="font-family: arial, helvetica;">From: TSS (<a class="yiv7303854509linkified" href="http://216-119-163-189.ipset45.wt.net/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">216-119-163-189.ipset45.wt.net</a>)</span></div>
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<span style="font-family: arial, helvetica;">Subject: CWD aka MAD DEER/ELK TO HUMANS ???</span></div>
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<span style="font-family: arial, helvetica;">Date: September 30, 2002 at 7:06 am PST</span></div>
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<span style="font-family: arial, helvetica;">From: "Belay, Ermias"</span></div>
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<span style="font-family: arial, helvetica;">To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</span></div>
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<span style="font-family: arial, helvetica;">Sent: Monday, September 30, 2002 9:22 AM</span></div>
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<span style="font-family: arial, helvetica;">Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</span></div>
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<span style="font-family: arial, helvetica;">Dear Sir/Madam,</span></div>
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<span style="font-family: arial, helvetica;">In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</span></div>
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<span style="font-family: arial, helvetica;">Ermias Belay, M.D. Centers for Disease Control and Prevention</span></div>
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<span style="font-family: arial, helvetica;">-----Original Message-----</span></div>
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<span style="font-family: arial, helvetica;">From: Sent: Sunday, September 29, 2002 10:15 AM</span></div>
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<span style="font-family: arial, helvetica;">To: <a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:rr26k@nih.gov">rr26k@nih.gov</a>; <a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:rrace@niaid.nih.gov">rrace@niaid.nih.gov</a>; <a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:ebb8@CDC.GOV">ebb8@CDC.GOV</a></span></div>
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<span style="font-family: arial, helvetica;">Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</span></div>
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<span style="font-family: arial, helvetica;">Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS</span></div>
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<span style="font-family: arial, helvetica;">Thursday, April 03, 2008</span></div>
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<span style="font-family: arial, helvetica;">A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</span></div>
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<span style="font-family: arial, helvetica;">snip...</span></div>
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<span style="font-family: arial, helvetica;">*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</span></div>
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<span style="font-family: arial, helvetica;">snip... full text ; </span></div>
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<span style="font-family: arial, helvetica;"><a href="http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html</a> </span></div>
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<span style="font-family: arial, helvetica;">> However, to date, no CWD infections have been reported in people. </span></div>
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<span style="font-family: arial, helvetica;">key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </span></div>
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<span style="font-family: arial, helvetica;">*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***</span></div>
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<span style="font-family: arial, helvetica;">*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </span></div>
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<span style="font-family: arial, helvetica;"><a href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a> </span></div>
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<span style="font-family: arial, helvetica;"><a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true</a> </span></div>
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<span style="font-family: arial, helvetica;"><a href="https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article</a> </span></div>
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TEXAS CWD TSE PRION STRAIN UNLIKE ANYTHING EVER SEEN</div>
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<span style="font-size: 13.3333px;">“Wow,” he said. “Unlike anything we've seen before.”</span></div>
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<span style="font-size: 13.3333px;">The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.</span></div>
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<span style="font-family: arial;">One day in late February, in their laboratory in Fort Collins, Colorado, Wagner and Zabel compared the prions from the brains of CWD-infected deer in Texas with those of elk in Colorado. They want to know if the proteins were all mangled in the same way, or not. “If they are different, this would suggest that we have different strain properties, which is evidence as we're building our case that we might have multiple strains of CWD circulating in the U.S.,” says Wagner.</span></div>
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<span style="font-size: 13.3333px;">Step one is to see if they’re equally easy to destroy using a chemical called guanidine. The shape of a prion dictates everything, including the way it interacts with an animal’s cells and the ease with which chemicals can unfold it.</span></div>
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<span style="font-size: 13.3333px;">“Moment of truth,” said Wagner, as she and Zabel huddled around a computer, waiting for results to come through. When they did, Zabel was surprised.</span></div>
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<span style="font-size: 13.3333px;">“Wow,” he said. “Unlike anything we've seen before.”</span></div>
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<span style="font-size: 13.3333px;">The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.</span></div>
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<span style="font-size: 13.3333px;">Now, these are only the preliminary results from a few animals. Wagner and Zabel have a lot more experiments to do. But if future tests come to the same conclusion, it would support their hypothesis that there are multiple strains of chronic wasting disease out there, all with different origins. That, in turn, could mean that this disease will become even trickier to manage than it already is.</span></div>
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<span style="font-size: 13.3333px;">And, Zabel adds, there’s something else. “If it's still evolving, it may still evolve into a form that could potentially, eventually affect humans,” he says.</span></div>
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<span style="font-size: 13.3333px;">Zabel is not the only one worried about that possibility. </span></div>
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<span style="font-size: 13.3333px;"> OSTERHOLM, THE EPIDEMIOLOGIST from Minnesota, is also concerned. He directs the Center for Infectious Disease Research and Policy at the University of Minnesota, and is serving a one-year stint as a “Science Envoy for Health Security” with the U.S. State Department. In February, he told Minnesota lawmakers that when it comes to chronic wasting disease, we are playing with fire. “You are going to hear from people that this is not going to be a problem other than a game farm issue. You're going to hear from people that it's not going to transmit to people, and I hope they're right, but I wouldn't bet on it,” he said. “And if we lose this one and haven’t done all we can do, we will pay a price.”</span></div>
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<span style="font-size: 13.3333px;">If that wasn’t warning enough, he added: “Just remember what happened in England.”</span></div>
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<span style="font-size: x-small;">WEDNESDAY, MAY 15, 2019 </span></div>
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<span style="font-size: x-small;">TAHC CWD TSE Prion Summary Minutes of the 402nd Commission Meeting – 12/11/2018</span></div>
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<span style="font-family: Georgia; font-size: x-small; line-height: 1.22em;">FRIDAY, APRIL 05, 2019 </span></div>
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<span style="font-family: Georgia; font-size: x-small; line-height: 1.22em;">TPWD CWD Sampling Effort Leads to Proposed Containment Zone Expansion</span></div>
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<span style="font-family: Georgia; font-size: x-small; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/04/tpwd-cwd-sampling-effort-leads-to.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/tpwd-cwd-sampling-effort-leads-to.html</a></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">TAHC CWD TSE PRION AT 144 POSITIVE MINUTES OF THE 401st COMMISSION MEETING Texas Animal Health Commission August 7, 2018 </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/tahc-cwd-tse-prion-at-144-positive.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/tahc-cwd-tse-prion-at-144-positive.html</a> </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">TUESDAY, FEBRUARY 26, 2019 </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">TEXAS CWD TSE PRION CASES RISE TO 144 CASES WITH 1 WILD, 1 BREEDER, AND 1 BREEDER RELEASE </span></span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/02/texas-cwd-tse-prion-cases-rise-to-144.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/texas-cwd-tse-prion-cases-rise-to-144.html</a></div>
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<span style="font-size: 13.3333px;">SUNDAY, JUNE 10, 2018 </span></div>
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<span style="font-size: 13.3333px;">TEXAS SUMMARY MINUTES OF THE 400th COMMISSION MEETING CWD TSE PRION TAHC April 17, 2018</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/06/texas-summary-minutes-of-400th.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/06/texas-summary-minutes-of-400th.html</a></div>
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<span style="font-size: 13.3333px;">SATURDAY, DECEMBER 02, 2017</span></div>
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<span style="font-size: 13.3333px;">TEXAS TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/12/texas-tahc-cwd-tse-prion-trace-herds.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/12/texas-tahc-cwd-tse-prion-trace-herds.html</a></div>
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<span style="font-family: arial; font-size: 10pt;">TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?</span></div>
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<span style="font-family: arial; font-size: x-small;">OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?</span><div style="font-family: arial; font-size: small;">
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apparently, no ID though. tell me it ain't so please...<br clear="none" /><div>
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''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''</div>
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Wyoming CWD Dr. Mary Wood</div>
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''first step is admitting you have a problem''</div>
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''Wyoming was behind the curve''</div>
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wyoming has a problem...</div>
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<a href="https://www.youtube.com/watch?v=y1bsK4Igt1o&index=10&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/watch?v=y1bsK4Igt1o&index=10&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj</a></div>
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<span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;">the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease. </span><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"><br clear="none" /></span></div>
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<a href="https://www.youtube.com/watch?v=bItnEElzuKo&index=6&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;" target="_blank">https://www.youtube.com/watch?v=bItnEElzuKo&index=6&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj</a><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"> </span><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"><br clear="none" /></span></div>
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<span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;">Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark... </span><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"><br clear="none" /></span></div>
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<a href="https://www.youtube.com/watch?v=JAK_YBZh2tA&feature=youtu.be&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj&t=299" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;" target="_blank">https://www.youtube.com/watch?v=JAK_YBZh2tA&feature=youtu.be&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj&t=299</a><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"> </span><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"><br clear="none" /></span></div>
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<span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;">WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO </span><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"><br clear="none" /></span></div>
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<a href="https://www.youtube.com/watch?v=JAK_YBZh2tA&feature=youtu.be&t=602&fbclid=IwAR04yvki5GDJqjAeNOeP3QETcUOmWHRNRrGXzRUTnsxvcLUO50kSDsBzHTs" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;" target="_blank">https://www.youtube.com/watch?v=JAK_YBZh2tA&feature=youtu.be&t=602&fbclid=IwAR04yvki5GDJqjAeNOeP3QETcUOmWHRNRrGXzRUTnsxvcLUO50kSDsBzHTs</a><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"> </span><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"><br clear="none" /></span></div>
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<span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;">cwd update on Wisconsin from Tammy Ryan... </span><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"><br clear="none" /></span></div>
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<a href="https://www.youtube.com/watch?v=hvy2SMGQt6o&index=11&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;" target="_blank">https://www.youtube.com/watch?v=hvy2SMGQt6o&index=11&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj</a><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"> </span><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"><br clear="none" /></span></div>
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<span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;">Wyoming CWD Dr. Mary Wood ''first step is admitting you have a problem'' ''Wyoming was behind the curve'' wyoming has a problem... </span><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"><br clear="none" /></span></div>
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<a href="https://www.youtube.com/watch?v=y1bsK4Igt1o&index=10&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;" target="_blank">https://www.youtube.com/watch?v=y1bsK4Igt1o&index=10&list=PL7ZG8MkruQh3wI96XQ8_EymytO828rGxj</a><span style="color: #1c1e21; font-family: Helvetica, Arial, sans-serif; font-size: 13px; white-space: pre-wrap;"> </span></div>
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SATURDAY, JANUARY 19, 2019 </div>
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Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS </div>
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<span style="color: black;"><a href="https://chronic-wasting-disease.blogspot.com/2019/01/texas-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/01/texas-chronic-wasting-disease-cwd-tse.html</a></span></div>
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TEXAS SUMMARY MINUTES OF THE 400th COMMISSION MEETING CWD TSE PRION TAHC April 17, 2018</div>
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V. SHEEP AND GOATS</div>
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A. Scrapie: The first positive scrapie case in Texas since 2008 was identified in the Panhandle in April 2016 and the flock and premises remains under quarantine.</div>
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Chronic Wasting Disease – NOT Approved – denied waiver to allow twin moose calves to enter Texas from a non-CWD monitored herd. According to Texas Administrative Code Title 4, Part 2, Chapter 51.10 all CWD susceptible species must meet federal requirements for interstate movements. Additionally, observation of an animal does not provide sufficient evidence of disease freedom, especially when applied to CWD.</div>
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VI. CERVIDS</div>
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A. Chronic Wasting Disease (CWD) in white-tailed deer (WTD): There are 5 positive WTD breeding facilities in Texas. The total number of positive WTD and current status of each facility is listed below:</div>
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1 Depopulated in 2015 4</div>
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2 Depopulated in early 2016 5</div>
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3 Quarantined January 2016, managed on herd plan 28, 12 suspects, 2 elk</div>
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4 Quarantined March 2016, recently depopulated ~100 does and managed on a herd plan, 25</div>
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5 Quarantined May 2017, depopulated herd October 2017 2</div>
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In late FY 2017, USDA informed TAHC that some end of year CWD indemnity funds were designated to Texas for the current positive herds. USDA required complete depopulation of the newest facility (Facility #5) based on the smaller size. The herd was depopulated in October and one additional positive doe was disclosed. The remaining available funds were allocated to use on facility 4 to remove deer in high risk pens. Of the 100 deer depopulated in facility #4, 9 were positive and all 9 were in pens in the same section as the index pen. In addition, a hunter harvested buck at facility #4 was positive that was harvested in November 2017.</div>
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In facility #3, since January 2016, there are a total of 28 positives and 12 suspects (tonsil biopsy confirmed positive only at this time) WTD. Of those, 31 are from the breeder pens or grower pens (17 bucks and 14 does). In addition, there were 9 positives disclosed from hunter harvested samples from 4 different pastures (6 bucks, 3 does). And there were 2 positive elk cows disclosed from 117 samples in 1 pasture. Both cows were natural additions to the elk herd.</div>
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The free ranging summary for the 2017-2018 hunting season include 2 positive mule deer from Hudspeth County, 2 mule deer from Hartley County, and 1 WTD from Hartley County. The WTD was on the Containment Zone border and a slight adjustment to that zone will be addressed before the next hunting season.</div>
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Summary Minutes of the 400th Commission Meeting – 4/17/2018</div>
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Statewide exotic CWD susceptible species surveillance monitoring in ongoing. General surveillance includes any facility that is testing CWD susceptible species for their annual premise requirement. Hunter harvest samples include samples collected at check stations in one of the 3 zones (the Panhandle, West Texas, or Medina area). Samples collected on positive premises include testing to meet requirements for a positive premise herd plan.</div>
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CWD Susceptible Species Surveillance 2017-18</div>
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Exotic Species General Statewide Surveillance Positive PremiseContainment Zone* Hunter Harvest in Zones for ’17-18</div>
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Positive Negative Positive Negative Positive Negative</div>
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Red Deer 0 70 0 14 0 8</div>
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Elk 0 30 2 (cows) 115 0 19</div>
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Sika 26 0 1 0 4</div>
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Total 0 126 2 130 0 31 </div>
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<a href="http://www.tahc.texas.gov/agency/meetings/TAHCCommissionMeeting400Summary.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tahc.texas.gov/agency/meetings/TAHCCommissionMeeting400Summary.pdf</a> </div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 13.3333px;">TUESDAY, JANUARY 29, 2019 </span></span></div>
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<span style="font-family: arial, helvetica; font-size: 13.3333px;">TEXAS REPORTS 2 MORE CWD TSE PRION ALL WILD CERVID TOTAL TO DATE 141</span></div>
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<span style="font-family: arial, helvetica;"><a href="https://chronic-wasting-disease.blogspot.com/2019/01/texas-reports-2-more-cwd-tse-prion-all.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/01/texas-reports-2-more-cwd-tse-prion-all.html</a></span></div>
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<span style="font-size: x-small;">*** Hartley County Sheep with Scrapie, and CWD in Hartley county ??? </span></div>
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<span style="font-size: x-small;">*** Friday, April 22, 2016 </span></div>
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<span style="font-size: x-small;">*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer </span></div>
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<a href="http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html</a></div>
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<span style="font-size: x-small;">CWD TSE PRION PAYING TO PLAY PROGRAM $$$</span></div>
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<span style="font-size: x-small;">SUNDAY, MAY 14, 2017 </span></div>
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<span style="font-size: x-small;">85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/05/85th-legislative-session-2017-and-texas.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/05/85th-legislative-session-2017-and-texas.html</a></div>
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<span style="font-size: x-small;">Wednesday, May 04, 2016 </span></div>
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<span style="font-size: x-small;">TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission </span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2016/05/tpwd-proposes-repeal-of-6590-6594-and_4.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/05/tpwd-proposes-repeal-of-6590-6594-and_4.html</a></div>
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<span style="font-size: x-small;">TUESDAY, DECEMBER 16, 2014</span></div>
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<span style="font-size: x-small;">Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION </span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2014/12/texas-84th-legislature-2015-hr-no-2597.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/12/texas-84th-legislature-2015-hr-no-2597.html</a></div>
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<span style="font-size: x-small;">SUNDAY, DECEMBER 14, 2014</span></div>
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<span style="font-size: x-small;">TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2014/12/texas-84th-legislature-commencing-this.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/12/texas-84th-legislature-commencing-this.html</a></div>
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<span style="font-size: x-small;">TEXAS HISTORY OF CWD Singeltary telling TAHC, that CWD was waltzing into Texas from WSMR around Trans Pecos region, starting around 2001, 2002, and every year, there after, until New Mexico finally shamed TAHC et al to test where i had been telling them to test for a decade. 2012 cwd was detected first right there where i had been trying to tell TAHC for 10 years. </span></div>
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<span style="font-size: x-small;">***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History <***</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/08/texas-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/08/texas-chronic-wasting-disease-cwd-tse.html</a></div>
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<span style="font-size: x-small;">FRIDAY, MAY 10, 2019 </span></div>
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<span style="font-size: x-small;">Wisconsin Portage County Deer Farm Depopulated due to CWD TSE Prion 6 Cases Confirmed</span></div>
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<span style="font-size: x-small;"><a href="https://chronic-wasting-disease.blogspot.com/2019/05/wisconsin-portage-county-deer-farm.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/05/wisconsin-portage-county-deer-farm.html</a></span></div>
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<span style="font-family: Georgia; line-height: 1.22em;">THURSDAY, MAY 09, 2019 </span></div>
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<span style="font-family: Georgia; line-height: 1.22em;">Minnesota Seven deer test positive for CWD at Crow Wing County deer farm</span></div>
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<span style="font-family: Georgia; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/05/minnesota-seven-deer-test-positive-for.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/05/minnesota-seven-deer-test-positive-for.html</a></span></div>
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<span style="font-family: Georgia; font-size: x-small;">THURSDAY, MAY 23, 2019 </span></div>
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<span style="font-family: Georgia; font-size: x-small;">Michigan Osceola County deer farm/ranch owner arraigned on several violations</span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/05/michigan-osceola-county-deer-farmranch.html" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">https://chronic-wasting-disease.blogspot.com/2019/05/michigan-osceola-county-deer-farmranch.html</a></div>
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<span style="font-family: arial, helvetica;">THURSDAY, MAY 09, 2019 </span></div>
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<span style="font-family: arial, helvetica;">Michigan CWD TSE Prion increases to 120 Cases to Date</span></div>
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<span style="font-family: arial, helvetica;"><a href="https://chronic-wasting-disease.blogspot.com/2019/05/michigan-cwd-tse-prion-increases-to-120.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/05/michigan-cwd-tse-prion-increases-to-120.html</a></span></div>
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THURSDAY, MARCH 28, 2019 </div>
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Michigan CWD Identified in a Montcalm County Farmed Deer</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/03/michigan-cwd-identified-in-montcalm.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/michigan-cwd-identified-in-montcalm.html</a></div>
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<span style="font-size: x-small;">WEDNESDAY, APRIL 24, 2019 </span></div>
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<span style="font-size: x-small;">Oklahoma Farmed Elk Lincoln County has tested positive for chronic wasting disease CWD TSE Prion </span></div>
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<span style="font-size: x-small;">JOINT RELEASE FROM THE OKLAHOMA DEPARTMENT OF AGRICULTURE, FOOD & FORESTRY AND THE OKLAHOMA DEPARTMENT OF WILDLIFE CONSERVATION </span></div>
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<span style="font-size: x-small;">Chronic Wasting Disease Confirmed in One Farmed Oklahoma Elk </span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/oklahoma-farmed-elk-lincoln-county-has.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/oklahoma-farmed-elk-lincoln-county-has.html</a></div>
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<span style="font-size: x-small; line-height: 1.22em;">THURSDAY, MARCH 21, 2019 </span></div>
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<span style="font-size: x-small; line-height: 1.22em;">South Dakota Chronic wasting disease (CWD) has been identified in a captive elk in Clark County</span></div>
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<span style="font-size: x-small; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/south-dakota-chronic-wasting-disease.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/south-dakota-chronic-wasting-disease.html</a></span></div>
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<span style="font-size: x-small; line-height: 1.22em;">WEDNESDAY, MARCH 20, 2019 </span></div>
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<span style="font-size: x-small; line-height: 1.22em;">North Dakota Deer Found Near Williston Tests Positive for CWD</span></div>
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<span style="font-size: x-small; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/north-dakota-deer-found-near-williston.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/north-dakota-deer-found-near-williston.html</a></span></div>
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THURSDAY, APRIL 25, 2019 </div>
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Missouri MDC reports 41 new positive test results for CWD have been confirmed following its sampling</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/missouri-mdc-reports-41-new-positive.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/missouri-mdc-reports-41-new-positive.html</a></div>
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<span style="font-family: Georgia; font-size: x-small;">TUESDAY, APRIL 23, 2019 </span></div>
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<span style="font-family: Georgia; font-size: x-small;">Virginia DGIF CWD TSE Prion As April 2019 the Department has diagnosed 68 positive cases since 2009 </span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/virginia-dgif-cwd-tse-prion-as-april.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/virginia-dgif-cwd-tse-prion-as-april.html</a></div>
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<span style="font-family: Georgia; font-size: x-small; line-height: 1.22em;">THURSDAY, APRIL 11, 2019 </span></div>
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<span style="font-family: Georgia; font-size: x-small; line-height: 1.22em;">Montana Chronic Wasting Disease CWD TSE Prion 2018 Report 26 New Cases</span></div>
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<span style="font-family: Georgia; font-size: x-small; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/04/montana-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/montana-chronic-wasting-disease-cwd-tse.html</a></span></div>
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THURSDAY, FEBRUARY 21, 2019 </div>
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Tennessee officials concerned after 183 deer test positive for CWD TSE Prion</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/02/tennessee-officials-concerned-after-183.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-weight: bold;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/02/tennessee-officials-concerned-after-183.html</a></div>
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<span style="font-family: arial, helvetica;">FRIDAY, MAY 10, 2019 </span></div>
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<span style="font-family: arial, helvetica;">Alabama Officially Invites CWD TSE Prion Into Their State When Bait Bill Becomes Law</span></div>
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<span style="font-family: arial, helvetica;"><a href="https://chronic-wasting-disease.blogspot.com/2019/05/alabama-officially-invites-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/05/alabama-officially-invites-cwd-tse.html</a></span></div>
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<span style="font-family: Georgia; font-size: 13px;">WEDNESDAY, APRIL 03, 2019 </span></div>
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<span style="font-family: Georgia; line-height: 1.22em;">Estimating the amount of Chronic Wasting Disease infectivity passing through abattoirs and field slaughter</span></div>
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<span style="font-family: Georgia; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/04/estimating-amount-of-chronic-wasting.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/estimating-amount-of-chronic-wasting.html</a></span></div>
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<span style="font-family: Georgia;">WEDNESDAY, MARCH 13, 2019 </span></div>
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<span style="font-family: Georgia;">CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood</span></div>
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<span style="font-family: Georgia;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/cwd-tse-prion-maternal-mother-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/cwd-tse-prion-maternal-mother-to.html</a></span></div>
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<span style="font-family: Georgia; font-size: x-small;">THURSDAY, MARCH 14, 2019</span></div>
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<span style="font-family: Georgia; font-size: x-small;">USDA APHIS CDC Cervids: Chronic Wasting Disease Specifics Updated 2019</span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/03/usda-aphis-cdc-cervids-chronic-wasting.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/usda-aphis-cdc-cervids-chronic-wasting.html</a></div>
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<span style="font-family: Georgia; font-size: x-small;">SATURDAY, MARCH 16, 2019</span></div>
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<span style="font-family: Georgia; font-size: x-small;">Chronic Wasting Disease CWD TSE Prion United States of America Update March 16, 2019</span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/03/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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<span style="font-family: Georgia; font-size: x-small;">TUESDAY, MARCH 26, 2019</span></div>
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<span style="font-family: Georgia; font-size: x-small;">USDA ARS 2018 USAHA RESOLUTIONS Investigation of the Role of the Prion Protein Gene in CWD Resistance and Transmission of Disease</span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/03/usda-ars-2018-usaha-resolutions.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/usda-ars-2018-usaha-resolutions.html</a></div>
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<span style="font-family: arial; font-size: x-small;">TUESDAY, APRIL 30, 2019 </span><div style="font-family: arial; font-size: small;">
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<div style="font-family: arial; font-size: small;">
Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies 2018 Annual Report</div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/pathobiology-genetics-and-detection-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/pathobiology-genetics-and-detection-of.html</a></div>
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<span style="font-family: Georgia; font-size: x-small;">FRIDAY, MARCH 29, 2019</span></div>
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<span style="font-family: Georgia; font-size: x-small;">First Detection of Chronic Wasting Disease in a Wild Red Deer (Cervus elaphus) in Europe</span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/03/first-detection-of-chronic-wasting.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/first-detection-of-chronic-wasting.html</a></div>
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let's review some recent science on the environmental effects of the exposure of the cwd tse prion, it's not pretty...</div>
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P-147 Infection and detection of PrPCWD in soil from CWD infected farm in Korea</div>
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Hyun Joo Sohn, Kyung Je Park, In Soon Roh, Hyo Jin Kim, Hoo Chang Park, Byounghan Kim</div>
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Animal and Plant Quarantine Agency (QIA), Korea</div>
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Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. Chronic wasting disease (CWD) is the prion disease that is known spread horizontally. CWD has confirmed last in Republic of Korea in 2010 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and feces of TSE-infected animals. Using serial protein misfolding cyclic amplification (sPMCA), we developed a detection method for CWD PrPSc in soil from CWD affected farm in 2010. We found to detect PrPSc in soil from CWD infected farm, but not detect PrPSc in soil of wild cervid habitats and normal cervid farm in Korea. We also tried the bioassay on transgenic mice overexpressing elk prion protein (TgElk mice) to confirm infectivity of CWD-infected farm soil and washing solution of it. As the results, there was the presence of infectious prions in them. The attack rates were each 12.5% (1/8, soil) and 100% (6/6, soil washing solution). Our method appears to be a very useful technique for monitoring PrPSc levels in environmental conditions. </div>
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Prion 2016 Conference Poster Abstracts</div>
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<a href="https://www.tandfonline.com/doi/full/10.1080/19336896.2016.1162644?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2016.1162644?src=recsys</a></div>
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Prion 2016 Oral Abstracts</div>
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<a href="https://www.tandfonline.com/doi/full/10.1080/19336896.2016.1163103?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/full/10.1080/19336896.2016.1163103?src=recsys</a></div>
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Prion 2016 Prion Diseases in Animals</div>
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<a href="https://www.tandfonline.com/doi/abs/10.4161/pri.24864?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/abs/10.4161/pri.24864?src=recsys</a></div>
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Prion 2016 Prion Diseases in Humans</div>
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<a href="https://www.tandfonline.com/doi/abs/10.4161/pri.24865?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/abs/10.4161/pri.24865?src=recsys</a></div>
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see full text;</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/07/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/07/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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2018 - 2019</div>
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***> This is very likely to have parallels with control efforts for CWD in cervids.</div>
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Rapid recontamination of a farm building occurs after attempted prion removal</div>
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<a href="http://dx.doi.org/10.1136/vr.105054" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://dx.doi.org/10.1136/vr.105054</a></div>
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Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2</div>
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The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. </div>
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Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. </div>
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Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. </div>
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Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). </div>
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A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. </div>
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Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3. </div>
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The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.</div>
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snip...</div>
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As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.</div>
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This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.</div>
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Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.</div>
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Funding This study was funded by DEFRA within project SE1865. </div>
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Competing interests None declared. </div>
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<a href="https://veterinaryrecord.bmj.com/content/early/2019/01/02/vr.105054.long" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://veterinaryrecord.bmj.com/content/early/2019/01/02/vr.105054.long</a></div>
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Saturday, January 5, 2019 </div>
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Rapid recontamination of a farm building occurs after attempted prion removal </div>
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<a href="https://prionprp.blogspot.com/2019/01/rapid-recontamination-of-farm-building.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionprp.blogspot.com/2019/01/rapid-recontamination-of-farm-building.html</a></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">THURSDAY, FEBRUARY 28, 2019 </span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">BSE infectivity survives burial for five years with only limited spread</span></div>
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<a href="https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html</a></div>
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<span style="font-family: "New serif"; font-size: 16px;">***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018</span></div>
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<span style="font-size: 16px;">P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer </span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD. </span></span></div>
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<a href="https://prion2018.org/" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prion2018.org/</a></div>
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<span style="font-size: 16px; letter-spacing: 0px;">***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years</span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-size: 16px;">***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, </span><span style="font-size: 16px;">but outside entry could not always be absolutely excluded. </span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Correspondence</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Gudmundur Georgsson <a href="mailto:ggeorgs@hi.is" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:ggeorgs@hi.is">ggeorgs@hi.is</a></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">3 Bethesda, Maryland, USA</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Received 7 March 2006 Accepted 6 August 2006</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><a href="http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1540908280&id=id&accname=guest&checksum=ED0572E1E5B272C100A32212A3E3761A</a></span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"> </span></span></div>
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<span style="font-size: 16px;">TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION </span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261</a></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"> </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"> *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"> </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">SEE;</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Some unofficial information from a source on the inside looking out -</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Confidential!!!!</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">---end personal email---end...tss</span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<a href="http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html</a></div>
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Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).</div>
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<a href="http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf</a></div>
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Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document</div>
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<a href="https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf</a></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">=========================</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.</span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">========================</span></span></div>
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="https://prion2015.files.wordpress.com/2015/05/programguide1.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/programguide1.pdf</a></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="http://www.pnas.org/content/97/7/3418.full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.pnas.org/content/97/7/3418.full</a></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/</a></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Detection of protease-resistant cervid prion protein in water from a CWD-endemic area </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="https://www.ncbi...nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi...nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf</a></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract</a></div>
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals </span></span></div>
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html</a></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">PPo4-4: </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Survival and Limited Spread of TSE Infectivity after Burial </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html</a></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. </span></span></div>
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<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full</a></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
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<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">Wednesday, December 16, 2015 </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;">*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** </span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<span style="font-family: Times New Roman, serif;"><span style="font-size: 16px;"><br clear="none" /></span></span></div>
<div class="yiv1512629044aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="font-family: arial, helvetica; font-size: 12px; line-height: 1.22em; margin: 0in 0in 0.0001pt;">
<a href="http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html</a></div>
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<span style="font-family: Georgia;">WEDNESDAY, MARCH 13, 2019 </span></div>
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<span style="font-family: Georgia;">CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood</span></div>
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<span style="font-family: Georgia;"><a href="https://chronic-wasting-disease.blogspot.com/2019/03/cwd-tse-prion-maternal-mother-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/03/cwd-tse-prion-maternal-mother-to.html</a></span></div>
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<span style="font-family: Georgia; font-size: x-small;">MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</span></div>
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<a href="https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a></div>
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<a href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html</a></div>
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<span style="font-family: Georgia; font-size: x-small;">PUBLIC HEALTH U of M launches Chronic Wasting Disease Program to address potential health crisis</span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/public-health-u-of-m-launches-chronic.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/public-health-u-of-m-launches-chronic.html</a></div>
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cattle, pigs, sheep, cwd, tse, prion, oh my!</div>
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***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). </div>
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<span style="font-family: arial, helvetica; font-size: x-small;">Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.</span><div style="font-family: arial, helvetica; font-size: small;">
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<a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/733407/DEFRA_QRA_TSE_in_cervids_June2018_v1.pdf</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2012/08/susceptibility-of-cattle-to-agent-of.html</a></div>
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cwd scrapie pigs oral routes</div>
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***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** </div>
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>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** </div>
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***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). </div>
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***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. </div>
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This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. </div>
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Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. </div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091</a></div>
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<a href="https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017</a></div>
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<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-size: 10pt; line-height: 1.22em;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Animals considered at high risk for CWD include:</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div>
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<a href="https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">TUESDAY, APRIL 18, 2017 </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***</span></div>
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<a href="http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://usdameatexport.blogspot.com/2017/04/extreme-usa-fda-part-589-tse-prion-feed.html</a></div>
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Prion Conference 2018</div>
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O5 Prion Disease in Dromedary Camels </div>
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Babelhadj B (1), Di Bari MA (2), Pirisinu L (2), Chiappini B (2), Gaouar SB (3), Riccardi G (2), Marcon S (2), Agrimi U (2), Nonno R (2), Vaccari G (2) (1) École Normale Supérieure Ouargla. Laboratoire de protection des écosystèmes en zones arides et semi arides University Kasdi Merbah Ouargla, Ouargla, Algeria; (2) Istituto Superiore di Sanità, Department of Food Safety, Nutrition and Veterinary Public Health, Rome, Italy (3) University Abou Bekr Bélkaid, Tlemcen, Algeria. </div>
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Prions are responsible for fatal and transmissible neurodegenerative diseases including CreutzfeldtJakob disease in humans, scrapie in small ruminants and bovine spongiform encephalopathy (BSE). Following the BSE epidemic and the demonstration of its zoonotic potential, general concerns have been raised on animal prions. </div>
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Here we report the identification of a prion disease in dromedary camels (Camelus dromedarius) in Algeria and designate it as Camel Prion Disease (CPD). In the last years, neurological symptoms have been observed in adult male and female dromedaries presented for slaughter at the Ouargla abattoir. The symptoms include weight loss, behavioral abnormalities and neurological symptoms such as tremors, aggressiveness, hyper-reactivity, typical down and upwards movements of the head, hesitant and uncertain gait, ataxia of the hind limbs, occasional falls and difficult getting up. During 2015 and 2016, symptoms suggestive of prion disease were observed in 3.1% of 2259 dromedaries presented at ante-mortem examination. Laboratory diagnosis was obtained in three symptomatic dromedaries, sampled in 2016 and 2017, by the detection of typical neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues. </div>
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Histopathological examination revealed spongiform change, gliosis and neuronal loss preferentially in grey matter of subcortical brain areas. Abundant PrPSc deposition was detected in the same brain areas by immunohistochemistry and PET-blot. Western blot analysis confirmed the presence of PK-resistant PrPSc, whose N-terminal cleaved PK-resistant core was characterized by a mono-glycosylated dominant form and by a distinctive N-terminal cleavage, different from that observed in BSE and scrapie. </div>
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PrPSc was also detected, by immunohistochemistry, in all sampled lymph nodes (cervical, prescapular and lumbar aortic) of the only animal from which they were collected. </div>
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The PRNP sequence of the two animals for which frozen material was available, showed 100% nucleotide identity with the PRNP sequence already reported for dromedary camel. </div>
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Overall, these data demonstrate the presence of a prion disease in dromedary camelswhose nature, origin and spread need further investigations. However, our preliminary observations on the rather high prevalence of symptomatic dromedaries and the involvement of lymphoid tissues, are consistent with CPD being an infectious disease. In conclusion, the emergence of a new prion disease in a livestock species of crucial importance for millions of people around the world, makes urgent to assess the risk for humans and to develop policies able to control the spread of the disease in animals and to minimize human exposure. </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Volume 24, Number 6—June 2018 Research </span></div>
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Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.</div>
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The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.</div>
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Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (<a class="yiv1512629044aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r27" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="27"><em style="line-height: 1.22em;">27</em></a>) should be investigated to trace the possible origin of CPD from other countries.</div>
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Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (<a class="yiv1512629044aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r28" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="28"><em style="line-height: 1.22em;">28</em></a>). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (<a class="yiv1512629044aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc..cdc.gov/eid/article/24/6/17-2007_article#r28" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="28"><em style="line-height: 1.22em;">28</em></a>).</div>
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On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (<a class="yiv1512629044aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r29" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="29"><em style="line-height: 1.22em;">29</em></a>). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (<a class="yiv1512629044aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r30" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="30"><em style="line-height: 1.22em;">30</em></a>).</div>
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Such genetic homogeneity also might be reflected in <em style="line-height: 1.22em;">PRNP</em>. Studies on <em style="line-height: 1.22em;">PRNP</em> variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep.</div>
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In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (<a class="yiv1512629044aolmail_aolmail_aolmail_tp-link-policy" href="https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article#r13" rel="noopener noreferrer" shape="rect" style="color: #075290; cursor: pointer; line-height: 1.22em;" target="_blank" title="13"><em style="line-height: 1.22em;">13</em></a>). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.</div>
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The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock.</div>
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<span style="font-size: 13.3333px;">***> IMPORTS AND EXPORTS <***</span></div>
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<span style="font-size: 13.3333px; line-height: 1.22em;">***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***</span></div>
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<a href="http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html</a></div>
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ZOONOSIS OF SCRAPIE TSE PRION</div>
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O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***thus questioning the origin of human sporadic cases*** </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">=============== </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">============== </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></div>
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***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div>
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PRION 2016 TOKYO</div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Saturday, April 23, 2016</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Taylor & Francis</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">WS-01: Prion diseases in animals and zoonotic potential</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div>
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***> why do we not want to do TSE transmission studies on chimpanzees $</div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">R. BRADLEY</span></div>
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<a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></div>
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Title: Transmission of scrapie prions to primate after an extended silent incubation period) </div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a> </span></div>
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***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***</div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmission of scrapie prions to primate after an extended silent incubation period </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Abstract </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.</span></div>
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<a href="https://www.nature.com/articles/srep11573" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.nature.com/articles/srep11573</a></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">Docket No. APHIS-2013-0044] COMMENT SUBMISSION TERRY S. SINGELTARY SR..pdf: success</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">November 2013...TSS</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">Singeltary Submission Environmental Impact Statements; Availability, etc.: Animal Carcass Management [Docket No. APHIS-2013-0044]</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">Sunday, November 3, 2013</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">Environmental Impact Statements; Availability, etc.: Animal Carcass Management [Docket No. APHIS-2013-0044]</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question... </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">''IN PARTICULAR THE US DATA DO NOT CLEARLY EXCLUDE THE POSSIBILITY OF HUMAN (SPORADIC OR FAMILIAL) TSE DEVELOPMENT DUE TO CONSUMPTION OF VENISON. THE WORKING GROUP THUS RECOGNIZES A POTENTIAL RISK TO CONSUMERS IF A TSE WOULD BE PRESENT IN EUROPEAN CERVIDS.'' SCIENTIFIC OPINION ON CHRONIC WASTING DISEASE (II)</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors </span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">First published: 17 January 2018 <a href="https://doi.org/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.2903/j.efsa.2018.5132</a> ;</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">also, see; 8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.</span></span></div>
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<a href="https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132</a></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm</span></span></div>
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<span style="font-family: arial, helvetica;"><span style="font-size: 12px;">***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116***</span></span></div>
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<a href="https://www.tandfonline.com/doi/pdf/10.4161/pri.29237" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.tandfonline.com/doi/pdf/10.4161/pri.29237</a></div>
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Scientific Advisors and Consultants Staff 2001 Advisory Committee TSE PRION Singeltary Submission </div>
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Freas </div>
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Monday, January 08,2001 3:03 PM </div>
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FDA Singeltary submission 2001 </div>
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Greetings again Dr. Freas and Committee Members, </div>
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I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here: </div>
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fda link is dead in the water; </div>
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snip...see full text </div>
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<a href="https://bseusa.blogspot.com/2019/03/scientific-advisors-and-consultants.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bseusa.blogspot.com/2019/03/scientific-advisors-and-consultants.html</a></div>
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CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002</div>
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CHRONIC WASTING DISEASE</div>
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JOINT OVERSIGHT HEARING BEFORE THE SUBCOMMITTEE ON FORESTS AND FOREST HEALTH JOINT WITH THE SUBCOMMITTEE ON FISHERIES CONSERVATION, WILDLIFE AND OCEANS OF THE COMMITTEE ON RESOURCES U.S. HOUSE OF REPRESENTATIVES ONE HUNDRED SEVENTH CONGRESS SECOND SESSION</div>
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May 16, 2002</div>
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Serial No. 107-117</div>
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snip...</div>
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Mr. MCINNIS. Today, this joint Subcommittee hearing will explore an issue of immeasurable importance to the growing number of communities in wide-ranging parts of this country, the growing incidence of Chronic Wasting Disease in North America’s wild and captive deer and elk populations. In a matter of just a few months, this once parochial concern has grown into something much larger and much more insidious than anyone could have imagined or predicted.</div>
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As each day passes, this problem grows in its size, scope, and consequence. One thing becomes clear. Chronic Wasting Disease is not a Colorado problem. It is a Wisconsin problem or a Nebraska or Wyoming problem. It is a national problem and anything short of a fully integrated, systematic national assault on this simply will not do, which is precisely why we brought our group together here today.</div>
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So this is a disease that is spreading throughout the continent and it is going to require a national response as well as the efforts that are currently taking place in States like Wisconsin, Colorado, Nebraska, Wyoming, the interest they now have down in Texas and some of the neighboring States that have large white-tailed deer population and also elk.</div>
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This is a huge issue for us, Mr. Chairman, in the State of Wisconsin. I want to commend Governor McCallum and your staff and the various agencies for the rapid response that you have shown, given the early detection of CWD after the last deer hunting season. The problem that we have, though, is just a lack of information, good science in regards to what is the best response, how dangerous is this disease. We cannot close the door, quite frankly, with the paucity of scientific research that is out there right now in regards to how the disease spreads, the exposure of other livestock herds—given the importance of our dairy industry in the State, that is a big issue—and also the human health effects.</div>
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<a href="https://www.govinfo.gov/content/pkg/CHRG-107hhrg79658/pdf/CHRG-107hhrg79658.pdf?fbclid=IwAR1-dMPpYLher4m8SyMICwoGXNyQcVjcinPvAw8CvIys1lEG7hxgzWplJlk" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://www.govinfo.gov/content/pkg/CHRG-107hhrg79658/pdf/CHRG-107hhrg79658.pdf?fbclid=IwAR1-dMPpYLher4m8SyMICwoGXNyQcVjcinPvAw8CvIys1lEG7hxgzWplJlk</a></div>
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<span style="font-family: arial, helvetica;">FRIDAY, MARCH 30, 2018</span></div>
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<span style="font-family: arial, helvetica;">Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018</span></div>
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<a href="https://www.regulations.gov/document?D=APHIS-2018-0011-0003" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.regulations.gov/document?D=APHIS-2018-0011-0003</a></div>
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<br /></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/03/docket-no-aphis-2018-0011-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/03/docket-no-aphis-2018-0011-chronic.html</a></div>
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<span style="font-family: arial, helvetica;">THURSDAY, JUNE 07, 2018 </span></div>
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<span style="font-family: arial, helvetica;">Michigan DNR to present chronic wasting disease recommendations to Natural Resources Commission Singeltary submission</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2018/06/michigan-dnr-to-present-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/06/michigan-dnr-to-present-chronic-wasting.html</a></div>
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<span style="font-family: arial, helvetica;">WEDNESDAY, NOVEMBER 08, 2017 </span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">Montana Chronic Wasting Disease CWD TSE Prion Response Plan Singeltary Submission</span></div>
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<div>
<a href="http://chronic-wasting-disease.blogspot.com/2017/11/montana-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/11/montana-chronic-wasting-disease-cwd-tse.html</a></div>
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<span style="font-family: arial, helvetica;">SATURDAY, AUGUST 05, 2017 </span></div>
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<span style="font-family: arial, helvetica;">CWD PLAN Singeltary Submission Comment New York State DEC</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2017/08/cwd-plan-singeltary-submission-comment.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/08/cwd-plan-singeltary-submission-comment.html</a></div>
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<br /></div>
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<span style="font-family: arial, helvetica;">TUESDAY, AUGUST 02, 2016</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas with CWD Rule Terry S. Singeltary Sr. comment submission</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/08/texas-tpwd-sets-public-hearings-on-deer.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/08/texas-tpwd-sets-public-hearings-on-deer.html</a></div>
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<span style="font-family: arial, helvetica;">Wednesday, November 09, 2016</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">Chronic Wasting Disease (CWD) Program Standards - Review and Comment By Terry S Singeltary Sr. November 9, 2016</span></div>
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<div>
<a href="http://chronic-wasting-disease.blogspot.com/2016/11/chronic-wasting-disease-cwd-program_9.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/11/chronic-wasting-disease-cwd-program_9.html</a></div>
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<br /></div>
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<div>
Singeltary submission ;</div>
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<br /></div>
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Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose</div>
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<br /></div>
<div>
DOCUMENT ID: APHIS-2006-0118-0411</div>
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<br /></div>
<div>
***Singeltary submission</div>
<div>
<br /></div>
<div>
<a href="http://www.regulations.gov/#!documentDetail;D=APHIS-2006-0118-0411" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.regulations.gov/#!documentDetail;D=APHIS-2006-0118-0411</a></div>
<div>
<br /></div>
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2014/03/docket-no-00-108-10-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/03/docket-no-00-108-10-chronic-wasting.html</a></div>
</div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">Singeltary Submissions to EU on CWD TSE Prion</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">Friday, November 22, 2013</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">Wasting disease is threat to the entire UK deer population CWD TSE PRION disease in cervids</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">***SINGELTARY SUBMISSION</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">The Scottish Parliament's Rural Affairs, Climate Change and Environment Committee has been looking into deer management, as you can see from the following press release,</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">***and your email has been forwarded to the committee for information:</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<a href="http://www.scottish.parliament.uk/parliamentarybusiness/CurrentCommittees/29878.aspx" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.scottish.parliament.uk/parliamentarybusiness/CurrentCommittees/29878.aspx</a></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html</a></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">Friday, November 22, 2013</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Wasting disease is threat to the entire UK deer population</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html</a></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Sunday, July 21, 2013</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">Welsh Government and Food Standards Agency Wales Joint Public Consultation on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations 2013</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
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<span style="font-family: arial, helvetica;">*** Singeltary Submission WG18417</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/welsh-government-and-food-standards.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/welsh-government-and-food-standards.html</a></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">Sunday, June 23, 2013</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">National Animal Health Laboratory Network Reorganization Concept Paper (Document ID APHIS-2012-0105-0001)</span></div>
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<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">***Terry S. Singeltary Sr. submission</span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/06/national-animal-health-laboratory.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2013/06/national-animal-health-laboratory.html</a></div>
<div>
<br /></div>
<div>
<div>
Scientific Advisors and Consultants Staff 2001 Advisory Committee TSE PRION Singeltary Submission Freas Monday, January 08,2001 3:03 PM FDA Singeltary submission 2001 </div>
<div>
<br /></div>
<div>
Greetings again Dr. Freas and Committee Members, </div>
<div>
<br /></div>
<div>
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here: </div>
<div>
<br /></div>
<div>
fda link is dead in the water; </div>
<div>
<br /></div>
<div>
<a href="http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf</a></div>
<div>
<br /></div>
<div>
snip...see full text </div>
<div>
<br /></div>
<div>
<a href="https://bseusa.blogspot.com/2019/03/scientific-advisors-and-consultants.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bseusa.blogspot.com/2019/03/scientific-advisors-and-consultants.html</a></div>
<div>
<br /></div>
<div>
<a href="http://creutzfeldt-jakob-disease.blogspot.com/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/</a></div>
<div>
<br /></div>
<div>
Harvard BSE Risk Assessment Singeltary et al</div>
<div>
<br /></div>
<div>
<div>
Owens, Julie</div>
<div>
<br /></div>
<div>
From: Terry S. Singeltary Sr. [<a href="mailto:flounder9@verizon.net" rel="noopener noreferrer" style="color: blue; cursor: pointer;">flounder9@verizon.net</a>]</div>
<div>
<br /></div>
<div>
Sent: Monday, July 24, 2006 1:09 PM</div>
<div>
<br /></div>
<div>
To: FSIS RegulationsComments</div>
<div>
<br /></div>
<div>
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)</div>
<div>
<br /></div>
<div>
Page 1 of 98</div>
<div>
<br /></div>
<div>
8/3/2006</div>
<div>
<br /></div>
<div>
Greetings FSIS, </div>
<div>
<br /></div>
<div>
I would kindly like to comment on the following ;</div>
<div>
<br /></div>
<div>
[Federal Register: July 12, 2006 (Volume 71, Number 133)] [Notices] [Page 39282-39283] From the Federal Register Online via GPO Access [<a href="http://wais.access.gpo.gov/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">wais.access.gpo.gov</a>] [DOCID:fr12jy06-35] </div>
</div>
<div>
<br /></div>
<div>
<a href="http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.230.8886&rep=rep1&type=pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.230.8886&rep=rep1&type=pdf</a></div>
<div>
<br /></div>
<div>
Response to Singeltary et al</div>
<div>
<br /></div>
<div>
<a href="https://www.fsis.usda.gov/wps/wcm/connect/a4b69cec-0233-49bb-b5fa-d198876bad90/BSE_Risk_Assess_Response_Public_Comments.pdf?MOD=AJPERES" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.fsis.usda.gov/wps/wcm/connect/a4b69cec-0233-49bb-b5fa-d198876bad90/BSE_Risk_Assess_Response_Public_Comments.pdf?MOD=AJPERES</a></div>
<div>
<br /></div>
</div>
<div>
<div>
<span style="font-family: arial, helvetica;">SUNDAY, FEBRUARY 14, 2010 [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Suppressed peer review of Harvard study October 31, 2002. </span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;">October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024 </span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;"><a href="http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf</a> </span></div>
<div>
<span style="font-family: arial, helvetica;"><br /></span></div>
<div>
<span style="font-family: arial, helvetica;"><a href="http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html</a></span></div>
</div>
</div>
<div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 Singeltary et al</span></div>
<div>
<span style="font-size: x-small;"><br /></span></div>
<div>
<a href="http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div>
<div>
<br /></div>
<div>
<div style="font-size: small;">
<div>
<span style="font-size: 13.3333px;">THURSDAY, FEBRUARY 28, 2019 </span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">BSE infectivity survives burial for five years with only limited spread</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/02/bse-infectivity-survives-burial-for.html</a></div>
<div>
<br /></div>
<div>
<div style="line-height: 1.22em;">
<span style="font-family: Georgia;"><span style="font-size: 13px;">SATURDAY, MARCH 2, 2019 </span></span></div>
<div style="line-height: 1.22em;">
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<span style="font-family: Georgia;"><span style="font-size: 13px;">MAD COW TSE PRION DISEASE AND THE PEER REVIEW PROCESS OF BSe Science $$$</span></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;"><a href="https://bovineprp.blogspot.com/2019/03/mad-cow-tse-prion-disease-and-peer.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/03/mad-cow-tse-prion-disease-and-peer.html</a></span></span></div>
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<span style="font-size: 13.3333px;">MONDAY, FEBRUARY 25, 2019 </span></div>
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<span style="font-size: 13.3333px;">MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</span></div>
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<span style="font-size: 13.3333px;"><a href="https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a></span></div>
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<span style="font-family: Georgia; font-size: x-small;">Cervid to human prion transmission 5R01NS088604-04 Update</span></div>
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<a href="http://grantome.com/grant/NIH/R01-NS088604-04" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://grantome.com/grant/NIH/R01-NS088604-04</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html</a></div>
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<span style="font-family: Georgia; font-size: x-small;">MONDAY, APRIL 01, 2019 </span></div>
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<span style="font-family: Georgia; font-size: x-small;">PUBLIC HEALTH U of M launches Chronic Wasting Disease Program to address potential health crisis</span></div>
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<a href="https://chronic-wasting-disease.blogspot.com/2019/04/public-health-u-of-m-launches-chronic.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/public-health-u-of-m-launches-chronic.html</a></div>
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<span style="font-family: Georgia; line-height: 1.22em;">Estimating the amount of Chronic Wasting Disease infectivity passing through abattoirs and field slaughter</span></div>
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<span style="font-family: Georgia; line-height: 1.22em;"><a href="https://chronic-wasting-disease.blogspot.com/2019/04/estimating-amount-of-chronic-wasting.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://chronic-wasting-disease.blogspot.com/2019/04/estimating-amount-of-chronic-wasting.html</a></span></div>
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<span style="font-size: 13.3333px;">Saturday, December 15, 2018 </span></div>
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<span style="font-size: 13.3333px;">***> ADRD Summit RFI Singeltary COMMENT SUBMISSION BSE, SCRAPIE, CWD, AND HUMAN TSE PRION DISEASE December 14, 2018</span></div>
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<a href="https://prionprp.blogspot.com/2018/12/adrd-summit-rfi-singeltary-comment.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://prionprp.blogspot.com/2018/12/adrd-summit-rfi-singeltary-comment.html</a></div>
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<em style="color: #333333; font-family: arial; font-size: 13px; line-height: inherit;">PLOS ONE Journal </em></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">IBNC Tauopathy or TSE Prion disease, it appears, no one is sure </span></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT</span></span></div>
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***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" />***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" />*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***<br style="line-height: 1.22em;" /><br style="line-height: 1.22em;" /><a href="http://www.plosone.org/annotation/listThread.action?root=86610" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; line-height: 1.22em;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=86610</a></div>
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<span style="font-family: arial, helvetica; font-size: 10pt;">*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;</span></div>
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<a href="http://www.plosone.org/annotation/listThread.action;jsessionid=635CE9094E0EA15D5362B7D7B809448C?root=7143" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.plosone.org/annotation/listThread.action;jsessionid=635CE9094E0EA15D5362B7D7B809448C?root=7143</a></div>
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<span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">MONDAY, MAY 20, 2019 </span></span></div>
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<span style="font-family: Georgia; line-height: 1.22em;"><span style="font-size: 13px; line-height: 1.22em;">Tracking and clarifying differential traits of classical- and atypical L-type bovine spongiform encephalopathy prions after transmission from ca</span></span><span style="font-family: Georgia; font-size: 13px; line-height: 1.22em;">ttle to cynomolgus monkeys</span></div>
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<span style="font-family: Georgia; font-size: 13px; line-height: 1.22em;"><a href="https://bse-atypical.blogspot.com/2019/05/tracking-and-clarifying-differential.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://bse-atypical.blogspot.com/2019/05/tracking-and-clarifying-differential.html</a></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;">SUNDAY, APRIL 14, 2019 </span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;">Estimation of prion infectivity in tissues of cattle infected with atypical BSE by real time-quaking induced conversion assay</span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 12px;"><a href="https://bse-atypical.blogspot.com/2019/04/estimation-of-prion-infectivity-in.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2019/04/estimation-of-prion-infectivity-in.html</a></span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 13.3333px;">WEDNESDAY, APRIL 24, 2019 </span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 13.3333px;">USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019</span></span></div>
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<a href="https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bse-atypical.blogspot.com/2019/04/usda-announces-atypical-bovine.html</a></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Diagnosis and Reporting of Creutzfeldt-Jakob Disease </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">To the Editor: </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Terry S. Singeltary, Sr Bacliff, Tex </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. </span></div>
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<a href="http://jama.jamanetwork.com/article.aspx?articleid=1031186" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://jama.jamanetwork.com/article.aspx?articleid=1031186</a></div>
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<span style="font-family: arial, helvetica;">doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Available online 29 July 2003. </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Volume 3, Issue 8, August 2003, Page 463 </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem..” ............................ </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><a href="http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://download.thelancet..com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf</a> </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">January 28, 2003; 60 (2) VIEWS & REVIEWS</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Ermias D. Belay, Ryan A. Maddox, Pierluigi Gambetti, Lawrence B. Schonberger</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;"><span style="line-height: 1.22em;">First published January 28, 2003, DOI: <a href="https://doi.org/10.1212/01.WNL.0000036913.87823.D6" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://doi.org/10.1212/01.WNL.0000036913.87823.D6</a></span></span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Transmissible spongiform encephalopathies (TSEs) attracted increased attention in the mid-1980s because of the emergence among UK cattle of bovine spongiform encephalopathy (BSE), which has been shown to be transmitted to humans, causing a variant form of Creutzfeldt-Jakob disease (vCJD). The BSE outbreak has been reported in 19 European countries, Israel, and Japan, and human cases have so far been identified in four European countries, and more recently in a Canadian resident and a US resident who each lived in Britain during the BSE outbreak. To monitor the occurrence of emerging forms of CJD, such as vCJD, in the United States, the Centers for Disease Control and Prevention has been conducting surveillance for human TSEs through several mechanisms, including the establishment of the National Prion Disease Pathology Surveillance Center. Physicians are encouraged to maintain a high index of suspicion for vCJD and use the free services of the pathology center to assess the neuropathology of clinically diagnosed and suspected cases of CJD or other TSEs.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Received May 7, 2002. Accepted August 28, 2002.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Terry S. Singeltary, retired (medically) </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Published March 26, 2003</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">26 March 2003</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Terry S. Singeltary, retired (medically) CJD WATCH</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Reply to Singletary Ryan A. Maddox, MPH Other Contributors: Published March 26, 2003 </span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD surveillance.[1] In addition, because CJD is least accurately diagnosed early in the course of illness, notifiable-disease surveillance could be less accurate than, if not duplicative of, current mortality surveillance.[1] However, in states where making CJD officially notifiable would meaningfully facilitate the collection of data to monitor for variant CJD (vCJD) or other emerging prion diseases, CDC encourages the designation of CJD as a notifiable disease.[1] Moreover, CDC encourages physicians to report any diagnosed or suspected CJD cases that may be of special public health importance (e.g...., vCJD, iatrogenic CJD, unusual CJD clusters).</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">As noted in our article, strong evidence is lacking for a causal link between chronic wasting disease (CWD) of deer and elk and human disease,[2] but only limited data seeking such evidence exist. Overall, the previously published case-control studies that have evaluated environmental sources of infection for sporadic CJD have not consistently identified strong evidence for a common risk factor.[3] However, the power of a case-control study to detect a rare cause of CJD is limited, particularly given the relatively small number of subjects generally involved and its long incubation period, which may last for decades. Because only a very small proportion of the US population has been exposed to CWD, a targeted surveillance and investigation of unusual cases or case clusters of prion diseases among persons at increased risk of exposure to CWD is a more efficient approach to detecting the possible transmission of CWD to humans. In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Mr. Singletary also expresses concern over a recent publication by Asante and colleagues indicating the possibility that some sporadic CJD cases may be attributable to bovine spongiform encephalopathy (BSE).[4] The authors reported that transgenic mice expressing human prion protein homozygous for methionine at codon 129, when inoculated with BSE prions, developed a molecular phenotype consistent with a subtype of sporadic CJD. Although the authors implied that BSE might cause a sporadic CJD-like illness among persons homozygous for methionine, the results of their research with mice do not necessarily directly apply to the transmission of BSE to humans. If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication)..</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Diagnosis and reporting of Creutzfeldt-Jakob disease. JAMA 2001;285:733-734.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">2. Belay ED, Maddox RA, Gambetti P, Schonberger LB. Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States. Neurology 2003;60:176-181.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">3. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol 1999;53:283-314.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">4. Asante EA, Linehan JM, Desbruslais M, et al. BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J 2002;21:6358-6366.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">5. The UK Creutzfeldt-Jakob Disease Surveillance Unit. CJD statistics. Available at: <a href="http://www.cjd.ed.ac.uk/figures.htm" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.cjd.ed.ac.uk/figures.htm</a>. Accessed February 18, 2003.</span></div>
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<span style="font-family: arial, helvetica; line-height: 1.22em;">Competing Interests: None declared.</span></div>
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Volume 2: Science </div>
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Summary 4.29 The evidence discussed above that vCJD is caused by BSE seems overwhelming. Uncertainties exist about the cause of CJD in farmers, their wives and in several abattoir workers. It seems that farmers at least might be at higher risk than others in the general population. 1 Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrPSc found in vCJD. </div>
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***>It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people...end</div>
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BSE INQUIRY</div>
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SATURDAY, JUNE 23, 2018</div>
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***> Diagnosis of Methionine/Valine Variant Creutzfeldt-Jakob Disease by Protein Misfolding Cyclic Amplification </div>
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Volume 24, Number 7—July 2018 Dispatch </div>
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<span style="font-size: x-small;">15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S. </span></div>
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<a href="http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us</a></div>
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<span style="font-family: arial;">MONDAY, FEBRUARY 25, 2019 </span></div>
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<span style="font-size: 13.3333px;">MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</span></div>
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BSE INQUIRY EVIDENCE</div>
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Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the<span class="yiv6419974778text_exposed_show" style="display: inline; font-family: inherit;"> PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.</span></div>
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TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..</div>
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see references:</div>
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DEER BRAIN SURVEY</div>
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<a href="https://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf</a></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY </span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Date: Fri, 18 Oct 2002 23:12:22 +0100 </span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">From: Steve Dealler </span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member </span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">To: BSE-L@ References: <3daf5023 .4080804=""<a class="yiv6419974778linkified" href="http://wt.net/" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">WT.NET</a>""></span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Dear Terry,</span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">An excellent piece of review as this literature is desparately difficult to get back from Government sites.</span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!</span></span></div>
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<span style="color: #1d2129; font-family: Helvetica, Arial, sans-serif;"><span style="font-size: 14px;">Steve Dealler =============== </span></span></div>
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<a href="https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html</a></div>
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<span style="background-color: #fef9f5; color: #121212; font-size: 17px;">Stephen Dealler is a consultant medical microbiologist</span><span style="background-color: #fef9f5; color: #121212; font-size: 17px;"><span style="font-family: Arial, Helvetica, sans-serif;"> </span></span><span style="color: #121212; font-family: Arial, Helvetica, sans-serif;"><span style="font-size: 17px;"> <a class="yiv6419974778linkified" href="mailto:deal@airtime.co.uk" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank" ymailto="mailto:deal@airtime.co.uk">deal@airtime.co.uk</a> </span></span></div>
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BSE Inquiry Steve Dealler</div>
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Management In Confidence</div>
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BSE: Private Submission of Bovine Brain Dealler</div>
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reports of sheep and calf carcasses dumped...</div>
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<span style="font-size: 13.3333px;">re-scrapie to cattle GAH Wells BSE Inquiry</span></div>
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Dr. Dealler goes rogue to confirm BSE</div>
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Confirmation BSE Dealler's mad cow</div>
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BSE vertical transmission</div>
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1993 cjd report finds relationship with eat venison and cjd increases 9 fold, let the cover up begin...tss</div>
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FINDINGS</div>
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<span style="font-family: arial, helvetica;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span></div>
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<span style="font-family: arial, helvetica;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span></div>
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<span style="font-family: arial, helvetica;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span></div>
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<span style="font-family: arial, helvetica;">There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02)..</span></div>
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<span style="font-family: arial, helvetica;">The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</span></div>
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<span style="font-family: arial, helvetica;">It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</span></div>
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<span style="font-family: arial, helvetica;">In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</span></div>
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<span style="font-family: arial, helvetica;">In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including </span><span style="font-size: 10pt;">liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</span></div>
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<span style="font-family: arial, helvetica;">snip...see full report ; </span></div>
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<a href="https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/2</a><a href="https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer; font-size: 10pt;" target="_blank">0170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a></div>
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GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID</div>
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<span style="font-family: arial, helvetica;">October 1994</span></div>
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<span style="font-family: arial, helvetica;">Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane </span></div>
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<span style="font-family: arial, helvetica;">BerksWell Coventry CV7 7BZ</span></div>
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<span style="font-family: arial, helvetica;">Dear Mr Elmhirst,</span></div>
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<span style="font-family: arial, helvetica;">CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT</span></div>
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<span style="font-family: arial, helvetica;">Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.</span></div>
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<span style="font-family: arial, helvetica;">The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.</span></div>
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<span style="font-family: arial, helvetica;">The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.</span></div>
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<span style="font-family: arial, helvetica;">The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.</span></div>
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<span style="font-family: arial, helvetica;">I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all. </span></div>
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<span style="font-family: arial, helvetica;"><a href="http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf</a></span></div>
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snip...see full text;</div>
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MONDAY, FEBRUARY 25, 2019</div>
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MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019</div>
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<a href="https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html" rel="noopener noreferrer" shape="rect" style="background-color: inherit; color: #222222; cursor: pointer; transition: all 0s ease-in-out 0s;" target="_blank">https://bseinquiry.blogspot.com/2019/02/mad-dogs-and-englishmen-bse-scrapie-cwd.html</a></div>
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<span style="font-family: Georgia;">SATURDAY, MARCH 2, 2019 </span></div>
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<span style="font-family: Georgia;">MAD COW TSE PRION DISEASE AND THE PEER REVIEW PROCESS OF BSe Science $$$</span></div>
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<span style="font-family: Georgia;"><a href="https://bovineprp.blogspot.com/2019/03/mad-cow-tse-prion-disease-and-peer.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/03/mad-cow-tse-prion-disease-and-peer.html</a></span></div>
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friendly fire, pass it forward, they call it iatrogenic cjd, or what i call 'tse prion poker', are you all in $$$</div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">SATURDAY, MARCH 16, 2019 </span></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;">Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary Submission</span></span></div>
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<span style="font-family: Georgia;"><span style="font-size: 13px;"><a href="https://bovineprp.blogspot.com/2019/03/medical-devices-containing-materials.html" rel="noopener noreferrer" shape="rect" style="color: blue; cursor: pointer;" target="_blank">https://bovineprp.blogspot.com/2019/03/medical-devices-containing-materials.html</a></span></span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">TUESDAY, APRIL 09, 2019 </span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;">Horizon Health Network Moncton Hospital notified more than 700 patients after two cases of CJD were diagnosed both patients had undergone cataracts surgery before being diagnosed</span></div>
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<span style="font-family: Arial, Helvetica, sans-serif;"><a href="https://creutzfeldt-jakob-disease.blogspot.com/2019/04/horizon-health-network-moncton-hospital.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://creutzfeldt-jakob-disease.blogspot.com/2019/04/horizon-health-network-moncton-hospital.html</a></span></div>
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MONDAY, APRIL 8, 2019 </div>
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Studies Further Support Transmissibility of Alzheimer Disease–Associated Proteins</div>
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<a href="https://betaamyloidcjd.blogspot.com/2019/04/studies-further-support.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://betaamyloidcjd.blogspot.com/2019/04/studies-further-support.html</a></div>
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Thursday, December 1, 2016 </div>
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PRION2017 DECIPHERING NEURODEGENERATIVE DISORDERS 23 – 26 May 2017 Edinburgh</div>
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<a href="http://prionprp.blogspot.com/2016/12/prion2017-deciphering-neurodegenerative.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://prionprp.blogspot.com/2016/12/prion2017-deciphering-neurodegenerative.html</a></div>
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First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </div>
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Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </div>
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University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </div>
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This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </div>
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Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </div>
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At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </div>
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PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </div>
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Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO</div>
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PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS</div>
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PRION 2017 CONFERENCE VIDEO</div>
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<a href="https://www.youtube.com/embed/Vtt1kAVDhDQ" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ</a></div>
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<a href="http://prion2017.org/programme/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://prion2017.org/programme/</a></div>
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Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?</div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE </div>
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ABSTRACT </div>
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First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a></div>
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FRIDAY, JUNE 16, 2017</div>
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P55 Susceptibility of human prion protein to in vitro conversion by chronic wasting disease prions</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/p55-susceptibility-of-human-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/p55-susceptibility-of-human-prion.html</a></div>
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TUESDAY, JUNE 13, 2017</div>
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PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html</a></div>
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TUESDAY, JULY 04, 2017</div>
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*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html</a></div>
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PRION 2017 CONFERENCE ABSTRACT </div>
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P61 vCJD strain properties in a Spanish mother and son replicate as those of a young UK case</div>
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<a href="http://vcjd.blogspot.com/2017/06/prion-2017-conference-abstract-p61-vcjd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://vcjd.blogspot.com/2017/06/prion-2017-conference-abstract-p61-vcjd.html</a></div>
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TUESDAY, JUNE 20, 2017 </div>
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Prion 2017 Conference Transmissible prions in the skin of Creutzfeldt-Jakob disease patients</div>
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/06/prion-2017-conference-transmissible.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/06/prion-2017-conference-transmissible.html</a></div>
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Wednesday, May 24, 2017 </div>
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PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1 </div>
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Subject: PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh</div>
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*see archives of previous Prion Conferences, the ones that are still available, scroll down towards bottom in this link.</div>
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<a href="http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html</a></div>
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MONDAY, MAY 02, 2016 </div>
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Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html</a></div>
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<a href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a></div>
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ALSO SEE;</div>
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<a href="http://www.prions2016bcn.com/assets/abstract-book.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.prions2016bcn.com/assets/abstract-book.pdf</a></div>
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PRION 2015</div>
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<a href="http://www.tandfonline.com/action/doSearch?AllField=PRION+2015&SeriesKey=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/action/doSearch?AllField=PRION+2015&SeriesKey=kprn20</a></div>
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<a href="http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1123372" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1123372</a></div>
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<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29371" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29371</a></div>
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PRION 2015 ORAL ABSTRACTS</div>
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<a href="http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248?src=recsys</a></div>
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<a href="http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1033248?needAccess=true" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1033248?needAccess=true</a></div>
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<a href="http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1036655?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1036655?src=recsys</a></div>
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Saturday, May 30, 2015</div>
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PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS</div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2015/05/prion-2015-oral-and-poster.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2015/05/prion-2015-oral-and-poster.html</a></div>
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PRION 2014</div>
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<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29371?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29371?src=recsys</a></div>
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<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29370?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29370?src=recsys</a></div>
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<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29368?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29368?src=recsys</a></div>
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<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29365" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29365</a></div>
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PRION 2013</div>
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<a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.26105?needAccess=true" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.26105?needAccess=true</a></div>
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PRION 2012</div>
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<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.20605" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.20605</a></div>
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<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.20615?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.20615?src=recsys</a></div>
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PRION 2011</div>
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Seven main threats for the future linked to prions</div>
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The NeuroPrion network has identified seven main threats for the future linked to prions.</div>
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First threat</div>
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The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed. Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.</div>
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Second threat</div>
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In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.</div>
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Third threat</div>
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The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.</div>
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Fourth threat</div>
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Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy, whereas other countries, including the US, Brazil, and Argentine do not have these constraints. However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.</div>
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Fifth threat</div>
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The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.</div>
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Sixth threat</div>
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The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.</div>
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Seventh Threat</div>
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The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.</div>
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<div>
<a href="http://www.neuroprion.org/en/np-neuroprion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/en/np-neuroprion.html</a></div>
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<a href="http://www.neuroprion.org/en/np-news.html#63731832" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/en/np-news.html#63731832</a></div>
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PRION 2010</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf</a></div>
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<a href="http://tandfonline.com/toc/kprn20/4/3?nav=tocList" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://tandfonline.com/toc/kprn20/4/3?nav=tocList</a></div>
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PRION 2009</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf</a></div>
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PRION2008 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a></div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/programme.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/programme.pdf</a></div>
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SUNDAY, NOVEMBER 23, 2008 </div>
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PRION October 8th - 10th 2008 Book of Abstracts </div>
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<a href="http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.html</a></div>
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PRION2007 NEWSLETTER</div>
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<a href="http://www.neuroprion.org/en/np-event-prion-2007.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/en/np-event-prion-2007.html</a></div>
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PRION2007 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf</a> </div>
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PRION2006 NEWSLETTER</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/newsletters/neuroprion-newsletter-prion-2006-special-issue.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/newsletters/neuroprion-newsletter-prion-2006-special-issue.pdf</a></div>
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PRION2006 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2006/abstract_book.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2006/abstract_book.pdf</a></div>
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PRION2005 PRESS RELEASE</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/pressrelease_eng.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/pressrelease_eng.pdf</a></div>
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PRION2005 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/abstract_book.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/abstract_book.pdf</a></div>
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PRION2004 PRESS RELEASE</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/dossier_de_presse.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/dossier_de_presse.pdf</a></div>
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PRION2004 BOOK OF ABSTRACTS</div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/abstract_book.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/abstract_book.pdf</a></div>
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<a href="http://tandfonline.com/loi/kprn20?open=1&year=2007&repitition=0#vol_1_2007" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://tandfonline.com/loi/kprn20?open=1&year=2007&repitition=0#vol_1_2007</a></div>
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*see archives of previous Prion Conferences, the ones that are still available, scroll down towards bottom in this link.</div>
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<a href="http://www.neuroprion.org/en/np-news.html#42417828" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/en/np-news.html#42417828</a></div>
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<a href="http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html</a></div>
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<span style="font-size: 10pt;">i do not advertise or make money from this, these blogs of tse prion science are for educational use. when i started to try and figure all this out was back in 1997, and the only available science for the lay public was from </span></div>
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<a href="http://mad-cow.org/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://mad-cow.org/</a> </div>
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and </div>
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<a href="http://www.mad-cow.org/00/archive_frame.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.mad-cow.org/00/archive_frame.html</a> </div>
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God Bless Dr. Tom Pringle. </div>
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<span style="font-size: 10pt;">SO, i made a promise back then, i just made a promise to mom dod 12/14/97 confirmed Heidenhain Variant of Creutzfeldt Jakob Disease, never forget, and never let them forget.</span></div>
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<span style="font-size: 10pt;">this science on the tse prion should be made easy for the lay public to educate on the transmissible spongiform encephalopathy tse prion disease aka mad cow type disease.</span></div>
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wasted days and wasted nights...Freddy Fender</div>
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Terry S. Singeltary Sr.</div>
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Bacliff, Texas USA 77518 Galveston Bay, flounder9@verizon.net ...on the bottom!</div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0tag:blogger.com,1999:blog-5783466110981773845.post-88943086755369150472018-02-25T10:08:00.001-08:002018-07-14T11:39:08.718-07:00PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW<div style="font-family: arial; font-size: small;">
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<span style="font-size: 13.3333px;"><span style="background-color: white; font-family: arial, helvetica; text-align: start;">-----Original Message-----</span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /><span style="background-color: white; font-family: arial, helvetica; text-align: start;">From: Terry Singeltary <flounder9@verizon.net></span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /><span style="background-color: white; font-family: arial, helvetica; text-align: start;">To: xestioneventos <xestioneventos@usc.es></span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /><span style="background-color: white; font-family: arial, helvetica; text-align: start;">Sent: Fri, Jun 22, 2018 9:14 am</span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /><span style="background-color: white; font-family: arial, helvetica; text-align: start;">Subject: Re: PRION 2018 CONGRESSIONAL ABSTRACTS AND POSTERS</span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /></span><br />
<div id="AOLMsgPart_2_baa428db-3866-45a3-a27f-4d8cbce3744d" style="background-color: white; font-family: arial, helvetica; font-size: 13.3333px; text-align: start;">
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<span style="color: black; font-family: arial; font-size: x-small; position: relative !important;">very sad for those that donated their loved ones brains for this research, and very disturbing that you will not share this information with them. this is the first year of ALL PRION CONFERENCE that this information was/is not shared...very sad...thank you, kind regards, terry<br /><br /><br /><div style="font-family: arial, helvetica; font-size: 10pt;">
-----Original Message-----<br />From: Oficina de Congresos USC <<a href="mailto:xestioneventos@usc.es" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">xestioneventos@usc.es</a>><br />To: 'Terry Singeltary' <<a href="mailto:flounder9@verizon.net" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">flounder9@verizon.net</a>><br />Sent: Fri, Jun 22, 2018 2:20 am<br />Subject: RE: PRION 2018 CONGRESSIONAL ABSTRACTS AND POSTERS<br /><br /><div id="aolmail_AOLMsgPart_2_a25bc8ab-7b7a-42de-9fdf-a88dcdbeaa3f">
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<span style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;">Dear friend,</span></div>
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<span style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;"> </span></div>
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<span lang="EN-GB" style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;">we are not allowed to share this information. As long as I know, this information is just available for the conference attendants.</span></div>
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<span lang="EN-GB" style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;">best regards,</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">Olga Gutiérrez Méndez</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">Oficina de Congresos da USC</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">Complexo CEA-CE</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">Parque Vista Alegre - Rua Salvadas s/n</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">15705 Santiago de Compostela</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">tel 881816329 ext 16329</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">E-mail: <a href="mailto:xestioneventos@usc.es" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"></a><a href="mailto:xestioneventos@usc.es" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">xestioneventos@usc.es</a></span></div>
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<b><span style="font-family: Tahoma, sans-serif; font-size: 10pt;">De:</span></b><span style="font-family: Tahoma, sans-serif; font-size: 10pt;"> Terry Singeltary [<a href="mailto:flounder9@verizon.net?" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">mailto:flounder9@verizon.net</a>]<br /><b>Enviado el:</b> jueves, 21 de junio de 2018 18:19<br /><b>Para:</b> <a href="mailto:xestioneventos@usc.es" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">xestioneventos@usc.es</a><br /><b>Asunto:</b> PRION 2018 CONGRESSIONAL ABSTRACTS AND POSTERS</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt;">Hello Again,</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt;">a kind greetings from Bacliff, Texas. </span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt;">is there any way now that the conference is over, that i can get a copy of the PRION 2018 CONGRESSIONAL ABSTRACTS AND POSTERS. i have followed the tse prion science with great interest following the demise of my mother to the heidenhain variant of creutzfeldt jakob disease hvCJD. i have no access to the full conference pdf files, but it would be most appreciative i you might send them to me...</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt;">with kindest regards, terry</span></div>
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<span style="font-size: 13.3333px;">PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW</span></div>
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<span style="font-size: 13.3333px;">“Prion 2018: Back to basics, understanding the biology of prions”</span></div>
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<span style="font-size: 13.3333px;">O</span><span style="font-size: 10pt;">n behalf of the Prion 2018 Congress Local Organizing Committee, and the NeuroPrion Association, we heartily invite you to join us in Santiago de Compostela for the international conference Prion 2018. Since the Paris 2004 international conference, fostered by NeuroPrion, the yearly international Prion meetings have become the reference events for the prion research community, gathering the leading scientists and breaking news about the latest discoveries in the field. With Prion 2011 Montreal, the conference crossed the Atlantic for the first time; and with Prion 2016 Tokyo, it became definitively global. Last year, the successful Prion 2017 Edinburgh left a very high standard to follow. Initially focused on PrPSc alone, the conferences have more recently reached out to other neurodegenerative diseases in which protein misfolding, and prion (or is it prion-like…?) mechanisms play a central role. In Prion 2018, we aim at putting an emphasis in structural biology, hence our subtitle: “Prion 2018: Back to basics, understanding the biology of prions”. Without neglecting other very important aspects of human and animal prion disease, the Scientific Committee has put together a program that highlights an update and a discussion of what we know -and still ignore-, about the molecular underpinnings of prion transmission. In the last few years, important breakthroughs in this area, such as generation of recombinant PrPSc, generalization of PMCA as a useful tool to model all aspects of the propagation of PrPSc, or elucidation of the global architecture of PrPSc, and of the structure of PrP23-144 prions at a nearly atomic resolution, leave a final understanding of prion propagation and transmission barriers at the reach of our fingertips. And, very significantly, allow us for the first time to embark in the design of anti-prion drugs using rational approaches. Therefore, exciting times lie ahead.</span></div>
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<span style="font-size: 13.3333px;">But, as mentioned, we will also pay close attention to the lingering threat of CWD, now present in Europe: are we about to repeat the errors of BSE?, to the rest of animal prion diseases, and, of course, to CJD…and Alzheimer´s disease, Parkinson´s disease, tauopathies…</span></div>
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<span style="font-size: 13.3333px;">The program has some novelties with respect to previous meetings. In particular, we will have three round tables in which a small group of speakers will discuss three central topics in prion research, with ample opportunities for the public to intervene. The titles of these round tables are: 1) The structure of PrPSc; 2) A β, tau, synuclein, SOD1, TDP43, FUS…: are they prions, prion-like proteins, or what?; and 3) Prion therapy: where do we stand?</span></div>
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<span style="font-size: 13.3333px;">The historic city of Santiago de Compostela, home of Prion 2018, is a truly remarkable and attractive place, providing a fantastic back-drop to the congress. The venue of the conference will be the city Congress Center, that provides first class facilities. Santiago de Compostela started in the IX Century as a small shrine attracting pilgrims from all over Europe. As the final destination of the medieval St. James pilgrimage trail, it has a tradition of receiving visitors from all over the world since its very beginnings as a city. With an impressive medieval cathedral, numerous churches and stately homes and colleges of its XVI century-old university in characteristic stone architecture, it is a place definitively worth visiting.</span></div>
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<span style="font-size: 13.3333px;">Finally, we should mention that Prion 2018 will be a great opportunity for young scientists at the start of their careers to speak and present their work. We have allocated considerable space for oral communications selected among those submitted</span></div>
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<span style="font-size: 13.3333px;">We look forward to seeing you in Santiago de Compostela.</span></div>
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<span style="font-size: 13.3333px;"><a href="https://prion2018.org/" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://prion2018.org/</a></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Program</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Tuesday 22: AI-APRI Workshop: Structural biology of prions</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">8:30 Accreditation desk opens.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:30 Welcome and opening remarks: Holger Wille (University of Alberta) & Jesús Requena</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">(University of Santiago de Compostela).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:35 Tomas Sneideris (Vilnius University): Properties of prion self-replication.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:50 Vincent Béringue (INRA, Université Paris-Saclay): Dynamics of prion replication and</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">structural diversification.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:05 Patricia Aguilar-Calvo (UCSD): Heparan sulfate modulates the brain distribution of</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">fibrillar prions.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:20 Alejandro Sevillano (UCSD): Recombinant PrPSc as a surrogate of brain PrPSc for</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">structural studies.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:35 Byron Caughey (RML, NIH): Profound seeding selectivities of tau aggregates associated</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">with Alzheimer’s disease and other tauopathies.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:55 Additional Q&A time.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 11:00 Coffee break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:30 Ilia Baskakov (University of Maryland): Strain-specific PrPSc structures and N-linked</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">glycans.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:50 Witold Surewicz (Case Western Reserve University): Structural aspects of prion protein</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">conversion to the infectious form.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">12:10 Giovanni Spagnolli (University of Trento): A new structural model of PrPSc based on</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">recent experimental data and computational techniques.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">12:25 Holger Wille (University of Alberta): High-resolution structures from Aβ(1-42), αsynuclein,</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">PHF-tau, and HET-s(218-289) - why not from PrPSc?</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 12:45 Lunch</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">13:45 Antoine Loquet (CNRS, Bordeaux): A new solid-state NMR approach to determine 3D</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">structures of prion amyloid fibrils at atomic resolution.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:00 Michael Overduin (University of Alberta): Prion:lipid analysis using membrane</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">nanodiscs bounded by amphipathic polymers.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:15 Frederic Halgand (CNRS-Université Paris Sud): Prion protein conformational</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">landscape studied by mass spectrometry and ion mobility.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:30 Werner Kremer (University of Regensburg): Full-length human prion protein displays</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">a whole variety of conformational transitions as observed by high hydrostatic pressure</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">(HHP), xenon as a probe and spin labelling of the N-terminal domain.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:45 Michael Woodside (University of Alberta): Differences in the folding dynamics of prion</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">proteins from species with different disease susceptibility observed at the single-molecule</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">level.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:00 Lyudmyla Dorosh (University of Alberta): Structural biology of prions: Effects of</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">mutations, polymorphisms, and other variants of the PRND gene on the PrPC</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">structure </span></span><span style="font-family: "arial" , "helvetica"; font-size: 13.3333px;">from MD simulations analyzed with essential collective dynamics and machine learning</span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">methods.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:15 Dieter Willbold (Forschungszentrum Jülich): High resolution fibril structure of amyloidβ(1-42)</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">by cryoelectron microscopy.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:35 Additional Q&A time.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 15:45 Coffee break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:15 Boran Uluca (University of Düsseldorf): DNP-enhanced solid-state NMR at cryogenic</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">temperatures: a tool to snapshot conformational ensembles of -synuclein in different</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">states.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:30 Martin Margittai (University of Denver): Molecular basis for seeding barriers between</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">three- and four-repeat tau.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:45 Cristina Fernández (CIB-CSIC, Madrid): A bacterial prion-like protein as a synthetic</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">model to study amyloid toxicity.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:00 Reed Wickner (NIH, Bethesda): Five prion-curing systems in Saccharomyces cerevisiae:</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Upf proteins, inositol polyphosphates, Btn2p, Cur1p, and Hsp104p.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Additional Q&A time.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:20 Final remarks.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 17:45 Welcome cocktail (Conference center, hall)</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Tuesday 22: AI-APRI Workshop: Animal prion disease</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">8:30 Accreditation desk opens.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:30 Welcome and Opening Remarks: Judd Aiken (University of Alberta) and Debbie</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">McKenzie (University of Alberta).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:35 Candace Mathiason (Colorado State University): An Overview-Chronic Wasting</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Disease mother to offspring transmission studies conducted at Colorado State University.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:05 Hermann Schätzl/Sandor Dudas (University of Calgary): Oral transmission of CWD</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">macaques and bio-assayed transgenic mice.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:35 Sylvie Benestad (Norwegian Veterinary Institute): How is the CWD situation in</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Norway?</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:50 Additional Q&A time.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:00 Coffee Break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:30 Camilo Duque Velasquez (University of Alberta): Evolution of Chronic Wasting</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Disease prion conformers.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:45 Nate Denkers (Colorado State University): Assessing CWD prion neuro-invasion by</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">longitudinal CSF analysis in deer.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">12:00 Jifeng Bian (Colorado State University): Advances in CWD prion research.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">12:15 Judd Aiken (University of Alberta): Interaction of CWD prions with environmental</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">samples.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">12:30 Rodrigo Morales (University of Texas Health Science Center, Houston): PMCA as a</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">platform for pre-symptomatic CWD diagnosis. Validation in field samples.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">12:45 Lunch</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">13:45 Juan Carlos Espinosa (CISA-INIA, Madrid): Pig-PrP as a paradigm of resistance to</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">prion propagation.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:15 Gabriele Vaccari (Istituto Superiore di Sanitá, Rome): Prion disease in dromedary</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">camel.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:45 Anne Balkema-Buschmann (Friedrich-Loeffler-Institut): Absence of classical and</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">atypical (H- and L-Type) BSE prions in the blood of clinical bovine cases as confirmed</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">by cattle to cattle blood transfusions.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:00 Giuseppe Ru (Istituto Zooprofilattico Sperimentale Piemonte, Liguria e Valle d´Aosta,</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Turin): A scrapie cohort study shows the success of breeding for resistance.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:15 Khalid Salamat (The Roslin Institute): Detection of seeding activity in preclinical blood</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">samples from BSE-infected sheep using protein misfolding cyclic amplification (PMCA).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:30 Additional Q&A Time.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 15:45 Coffee Break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:15 Pierre Sibille (INRA-Université Paris-Saclay): Prion strain selection and evolution.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:30 Jo Moore (USDA, Ames): The agent of chronic wasting disease from pigs is infectious</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">in transgenic mice expressing human PRNP.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:45 Ermias Belay (CDC, Atlanta): Monitoring potential CWD transmission to Humans.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:00 Hermann Schätzl (University of Calgary): Vaccination of transgenic elk PrP mice and</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">reindeer with recombinant prion protein overcomes self-tolerance and protects mice</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">against CWD infection.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:15 Final remarks.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 17:45 Welcome cocktail (Conference center hall)</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Wednesday 23</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">8:30 Accreditation desk opens.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:30 Opening Plenary: Chairs: Jesús Requena (University of Santiago de Compostela,</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Conference Chair) & Emmanuel Comoy (CEA.Université Paris-Saclay, NeuroPrion</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Association).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:30 Opening addresses.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:00 Plenary lecture: Stanley Prusiner (UCSF): A unified view of prion biology and diseases.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:00 Coffee break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:30 Session: PrPSc prions: animal disease (I), Chair: Juan María Torres (CISA-INIA,</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Madrid); Junior Co-chair: Alba Marín-Moreno (CISA-INIA, Madrid).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:30 Invited talk: Sylvie Benestad (Norwegian Veterinary Institute): Unusual types of CWD</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">in Norwegian cervids.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">12:30 Gabriele Vaccari (Istituto Superiore di Sanitá, Rome): Prion disease in dromedary</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">camels.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">12:45 Lunch buffet & poster viewing</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:15 Session: PrPSc prions: animal disease (II), Chair: Juan Badiola (University of</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Zaragoza); Junior co-Chair: Alba Marín-Moreno (CISA-INIA, Madrid)</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:15 Romolo Nonno (Istituto Superiore di Sanitá, Rome): Different chronic wasting disease</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">strains circulate in North America and Europe.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:30 Glenn Telling (Colorado State University): The strain properties of prions causing</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">chronic wasting disease in Norwegian cervids are distinct from those causing disease in</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">North America.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:45 Glenn Telling (Colorado State University): Gene targeted mice reveal an essential role</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">for PrP residue 226 and an accurate means to model CWD peripheral pathogenesis.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:00 Alvina Huor (INRA, Toulouse): Permeability of the bovine transmission barrier to</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Atypical / Nor98 scrapie.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:15 Alba Marín-Moreno (CISA-INIA, Madrid): Zoonotic potential of atypical BSE prions:</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">a systematic evaluation.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 15:30 Coffee break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 16:00 Poster session: poster presenting authors will be at their posters</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:00 Session: PrPSc prions: animal disease (III), Chairs: Juan Badiola (University of</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Zaragoza) and Juan María Torres (CISA-INIA, Madrid).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:00 Wen-Quan Zou (Case Western Reserve University): Preclinical detection of prions in</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">skin samples of scrapie-infected animals by serial PMCA and RT-QuIC assays.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:15 Invited talk: Rosa Bolea (University of Zaragoza): Experimental studies on prion</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">transmission barrier and TSE pathogenesis in large animals.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:45 End of scientific sessions for the day</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Thursday 24</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:00 Session: Structure and basic biology of PrPSc and other mammalian, and fungal</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">prions. Chair: Jesús Requena (University of Santiago de Compostela); Junor Co-chair:</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Alejandro Sevillano (UCSD).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:00 Discussion table: The structure of PrPSc; Chair: Jesús Requena; Junior Co-chair:</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Alejandro Sevillano (UCSD). Experts: Holger Wille (University of Alberta), Witold</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Surewicz (Case Western Reserve University), Byron Caughey (RML-NIH), Ilia</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Baskakov (University of Maryland).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:30 Ilaria Vanni (Istituto Superiore di Sanitá, Rome): Purified 7 kDa PrPres aggregates from</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">GSS-A117V are infectious.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:45 Christina Sigurdson (UCSD): Generation of novel neuroinvasive prions following</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">intravenous challenge.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 11:00 Coffee break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:30 Invited talk: Sven Saupe (CNRS, Bordeaux): Prion forming domains in cell death</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">signaling.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">12:30 Sarah Kane (Colorado State University): a novel means of epitope unmasking due to</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">incomplete N-glycan attachment establishes that PrPSc is underglycosylated relative to</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">PrPC </span></span><span style="font-family: "arial" , "helvetica"; font-size: 13.3333px;">and affords prion detection.</span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 12:45 Lunch buffet & poster viewing</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:15 Session: Aβ, tau, -synuclein, SOD1, TDP43, FUS…and other prion and/or prionlike</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">proteins causing human disease. Chair: Mathias Jucker (DZNE-Tübingen); Junior</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Co-chair: Hasier Eraña (CIC-bioGUNE, Bilbao).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:15 Discussion table: are they prions, prion-like proteins, or what? Chair: Mathias Jucker</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">(DZNE, Tübingen); Junior Co-chair: Hasier Eraña (CIC-bioGUNE, Bilbao). Experts:</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Stanley Prusiner (UCSF), Claudio Soto (University of Texas Houston Medical School),</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Erdem Tamguney (DZNE, Bonn), Corinne Lasmezas (Scripps, Florida).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 15:45 Coffee break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:15 Natalie Beschorner (DZNE, Tübingen): Amyloid polymorphisms constitute distinct</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">clouds of conformational variants in different etiological subtypes of Alzheimer´s</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">disease.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:00 Amanda Woerman (UCSF): Multiple system atrophy prions replicate in</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Tg(SNCAA53T) mice and induce glial pathology throughout the limbic system.</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:15 Jacob Ayers (University of Florida, Gainesville): Prion strain-like properties of</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">misfolded superoxide dismutase-1 (SOD1).</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">17:30 Poster competition winner announced</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 17:35 End of scientific sessions of the day</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">19:30 Cultural event: visit to the cathedral and botafumeiro</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">20:30 Gala Dinner & Neurovision dance extravaganza (Pazo de San Lourenzo)</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Friday 25</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:00 Session: PrPSc prions: human disease (I). Chair: George Carlson (UCSF); Junior Cochair:</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Aušrinė Areškevičiūtė (University Hospital, Copenhaguen).</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:00 Emmanuelle Viré (University College, London): Epigenetics in prion diseases:</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">identification of novel markers for misfolded protein-associated neurodegenerative</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">disorders.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:15 Emmanuel Comoy (CEA-Université Paris-Saclay): Experimental transfusion of variant</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">CJD-infected blood reveals novel class of prion disorders.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:30 Jean-Yves Douet (INRA, Toulouse): Evaluation of iatrogenic risk of CJD transmission</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">associated with corneal transplantation.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:45 Session: Patients & families: a dialogue with scientists; Chair: Raffaella Robello</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">(Italian Association on Prion Diseases).</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">9:45 Suzanne Solvyns & Deana Simpson (CJD-ISA): Reflections and testimonials.</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:20 Debbie Yobs (CJD Foundation-USA): Announcement of the CJDF 2018 call for research</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">projects.</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">10:25 Alice Anane (CJD Foundation-Israel): Creating a large database of gCJD samples in</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Israel.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 10:30 Coffee break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:00 Session: PrPSc prions: human disease (II). Chair: George Carlson (UCSF); Junior Cochair:</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Aušrinė Areškevičiūtė (University Hospital, Copenhaguen).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:00 Cécile Voisset (INSERM-Brest University): AP326, a new FDA-approved drug active</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">against PrPSc</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">11:15 Discussion table: Prion therapy: where do we stand? Chair: Joaquín Castilla (CICbioGUNE,</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Bilbao); Junior Co-chair: Akin Nihat (University College, London); Experts:</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">John Collinge (University College, London), Fabrizio Tagliavini (Carlo Besta Institute,</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Milan), Kurt Giles (UCSF), Kenta Teruya (Tohoku University).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 12:45 Lunch buffet & poster viewing</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:15 Session: special, hot and/or late-breaking. Chair: Jiyan Ma (Van Andel Institute);</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Junor Co-chair: Alzbeta Cardova (Cambridge University).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:15 Brain junk clearing mechanisms: Hermann Schätzl (University of Calgary): Autophagy</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">has various roles in the life cycle of prions.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:30 Prion precursor biology & functions: Cathryn Haigh (University of Melbourne): Redox</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">regulation of adult neurogenesis by PrP and PrP N-terminal cleavage fragments.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">14:45 Joaquín Castilla (CIC-BioGUNE, Bilbao): Shaken, not sonicated: A strategy to generate</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">large amounts of recombinant bona fide prions for definitive structural studies.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:00 Andrew Fang (University of Alberta): Rationally designed, structure-based vaccine</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">candidates targeting Chronic Wasting Disease.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">15:15 Giuseppe Legname (SISSA, Trieste): Serpina3n plays a critical role in prion infection.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 15:30 Coffee break</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:00 Closing plenary</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:00 Winning poster presentation.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:15 Presentation: Iberian Prion Meeting 2018, Laguardia, Spain, Joaquín Castilla (CICBioGUNE,</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Bilbao).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:25 Presentation: PRION 2019 Edmonton: Hermann Schätzl (University of Calgary) &</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">David Westaway (University of Alberta).</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:40 Concluding remarks from NeuroPrion: Emmanuel Comoy.</span></span><br />
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><br /></span></span>
<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">16:50 Concluding remarks: Jesús Requena.</span></span><br />
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"> 17:00 Farewell</span></span><br />
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<a href="https://prion2018.org/wp-content/uploads/2018/05/program.pdf">https://prion2018.org/wp-content/uploads/2018/05/program.pdf</a></div>
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PRION 2018 MAY, 22-25</div>
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Program (Status: Draft – Version: 08/01/2018) </div>
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TUESDAY 22</div>
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AI-APRI Workshops: Animal prion diseases & Structural biology of prions Specific Program to be announced soon. The two parallel monographic workshops will focus on these two aspects of prion research and will be an excellent opportunity for Ph.D. students and postdocs to present and discuss their work in the company of more senior specialists in their fields.</div>
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• Animal prion diseases: The recent discovery of Chronic Wasting Disease (CWD) in Europe has expanded the range of animal prion diseases. CWD is the most contagious of the prion diseases and naturally infects at least 5 cervid species. The hosts for CWD are, in general, free-ranging animals which makes management and surveillance more challenging than managing the other animal prion diseases, BSE and scrapie. In this workshop, we will provide a general introduction to CWD biology and will discuss current research on spread, abundance and impact of disease in North America and Europe, genetic susceptibility, environmental contamination as well as management strategies. The diferent strains of CWD, BSE and scrapie provide an excellent opportunity to understand strain properties and how they impact transmission and spread of these diseases within and between species. The latest findings in CWD, BSE and scrapie will also be welcome.This workshop will also provide trainees a forum for sharing their research on the animal TSEs and provide an opportunity for wildlife managers, policy makers etc to gain expertise on the biology of CWD.</div>
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• Structural biology of prions: The transition from α-helix rich PrPC to predominantly β- sheeted PrPSc is the underlying event for all prion diseases. Therefore, the structural biology of this transition and the structures of all involved molecules are of fundamental interest. Similar misfolding events have been described for other protein misfolding diseases, indicating the general need to understand the structural biology principles that determine protein stability and conversion mechanisms. Functional amyloids and fungal prions provide unique insights through their greater accessibility and easier to determine structures. In this workshop, we will discuss the latest findings regarding the structures of PrPSc, PrPC , PrP amyloid in general and of any misfolding mechanisms that may facilitate the conversion from PrPC to PrPSc. Results on the proteins from other protein misfolding diseases, functional amyloids, and fungal prions are also welcome. Special emphasis will be given to short oral presentations by trainees (all levels) to encourage young structural biologists in their quest to analyze these difcult to study proteins.</div>
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17:45 Reception cocktail WEDNESDAY 23</div>
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Opening Plenary</div>
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9:30 Opening addresses</div>
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10:00 Plenary lecture Stanley Prusiner (to be confirmed)</div>
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11:00 Cofee break</div>
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11:30 PrPSc prions: animal disease (I) Chair: Juan María Torres</div>
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11:30 Invited talk Sylvie Benestad</div>
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12:30 Oral communication Selected from submissions</div>
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12:45 Lunch bufet & poster viewing</div>
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14:15 PrPSc prions: animal disease (cont.)</div>
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14:15 Oral communication Selected from submissions</div>
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14:30 Oral communication Selected from submissions</div>
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14:45 Oral communication Selected from submissions</div>
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15:00 Oral communication Selected from submissions</div>
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15:15 Oral communication Selected from submissions</div>
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15:30 Cofee break</div>
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16:00 Prion precursor conformers: cell biology and functions. Chair: TBA</div>
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16:00 Oral communication Selected from submissions</div>
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16:15 Oral communication Selected from submissions</div>
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16:30 Oral communication Selected from submissions</div>
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16:45 Oral communication Selected from submissions</div>
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17:00 Poster & beer jam & pizza (soft drinks also available)</div>
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THURSDAY 24</div>
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9:00 Structure and basic biology of PrPSc and other mammalian, yeast and fungal prions. Chair: Jesús Requena</div>
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9:00 Round table: The structure of PrPSc Chair: Jesús Requena Experts: Holger Wille, Witold Surewicz, Byron Caughey, Ilia Baskakov</div>
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10:30 Oral communication Selected from submissions</div>
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11:00 Cofee break</div>
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11:30 Invited talk Sven Saupe</div>
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12:30 Oral communication Selected from submissions</div>
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12:45 Lunch bufet & poster viewing</div>
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14:15 A, tau, synuclein, SOD1, TDP43, FUS…and other prion and/or prion-like proteins causing human disease (II). Chair: TBA</div>
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14:15 Round table: Are they prions, prion-like proteins, or what? Chair: Mathias Jucker Experts: Adriano Aguzzi, Claudio Soto</div>
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15:45 Cofee break</div>
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16:15 Oral communication Selected from submissions</div>
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17:00 Oral communication Selected from submissions</div>
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17:15 Oral communication Selected from submissions</div>
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17:30 End of day scientific sessions</div>
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18:30 Social event & gala dinner</div>
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FRIDAY 25</div>
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9:00 PrPSc prions: human disease (I). Chair: TBA</div>
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9:00 Round table: Prion therapy: where do we stand?</div>
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Chair: Joaquín Castilla</div>
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Experts: John Collinge, Fabrizio Tagliavini, Kurt Giles</div>
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10:30 Cofee break</div>
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11:00 Oral communication Selected from submissions</div>
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11:15 Oral communication Selected from submissions</div>
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11:30 Oral communication Selected from submissions</div>
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11:45 Oral communication Selected from submissions</div>
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12:00 CJD International support association. Chair: Suzanne Solvyns</div>
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12:45 Lunch bufet & poster viewing</div>
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14:15 Brain protein-junk cleaning mechanisms. Chair: TBA</div>
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14:15 Invited talk TBA</div>
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14:45 Oral communication</div>
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15:00 Late breaking communications. Chair: TBA</div>
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15:00 Late breaking communication Selected from submissions</div>
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15:15 Late breaking communication Selected from submissions</div>
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15:30 Poster winners announced Selected from submissions</div>
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15:35 Cofee break</div>
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16:05 Winning poster presentation Selected among posters</div>
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16:20 Winning poster presentation Selected among posters</div>
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16:35 Presentation: Prion 2019 Edmonton</div>
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16:50 Concluding remarks from NeuroPrion Jean-Philippe Deslys</div>
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17:00 Farewell Jesús Requena</div>
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<a href="https://prion2018.org/wp-content/uploads/2017/12/program.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://prion2018.org/wp-content/uploads/2017/12/program.pdf</a></div>
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WHO'S WHO?</div>
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<a href="https://prion2018.org/scientific-program/" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://prion2018.org/scientific-program/</a><br />
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WORKSHOPS<br />
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<span style="font-family: "arial"; font-size: 10pt;">''But, as mentioned, we will also pay close attention to the lingering threat of CWD, now present in Europe: are we about to repeat the errors of BSE?, to the rest of animal prion diseases, and, of course, to CJD…and Alzheimer´s disease, Parkinson´s disease, tauopathies…''</span></div>
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Greetings Prion 2018 et al, </div>
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Sadly, those 'errors' have already been made, that is why cwd tse prion has spread from USA to Canada to Korea, and now Norway. To insinuate anything but another colossal failure, just as the BSE debacle, would be foolish, and you would only kidding yourselves. the mad cow follies in the USA are far from over, USDA et al just got better at covering up, by not testing enough for BSE both typical and atypical, imo. i have tried since 2013 to get the EU et al prepared for the Chronic Wasting Disease CWD TSE Prion. i think i have failed in every aspect of my 20 year endeavor to warn the world about the tse prion mad cow type disease...</div>
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GOOD LUCK WITH THIS YEARS PRION 'ROUND TABLE' CONFERENCE!<br />
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<span style="font-size: 13.3333px;">cwd and scrapie transmits to pigs orally and the USA Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed ban WARNING</span></div>
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<span style="font-size: 13.3333px;">Posted by flounder on 08 Jul 2018 at 21:05 GMT</span></div>
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<span style="font-size: 13.3333px;">>>>Although no prion transmission has been reported in pigs following oral BSE challenge, our data support the continuation of the Feed Ban measure implemented to prevent entry of the BSE agent into the feed chain.<<<</span></div>
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<span style="font-size: 13.3333px;">I would kindly like to bring urgent awareness to PLOS and the authors of this study, and the globe, the USA Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed ban has been a failed policy since inception imo (see DEFRA report below), also, cervid that are potentially at risk of Chronic Wasting Disease CWD TSE Prion, are still allowed to be used as protein feed for livestock. But foremost, CWD and Scrapie TRANSMITS TO PIGS BY ORAL ROUTE. please see many many more tonnages of 589.2000, Animal Proteins Prohibited in Ruminant Feed right up to 2017. this is an extremely dangerous situation for the globe, especially with this new outbreak of TSE Prion disease in a new livestock species, i.e. camels in Nigeria, this is an extremely dangerous situation that has global ramifications and needs to be addressed asap, or risk spreading cwd tse prion from the USA and Canada further around the globe. please see;</span></div>
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<a href="http://journals.plos.org/plosone/article/comment?id=10.1371/annotation/a02528e2-6b60-49b2-8719-17927c1a2d60" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://journals.plos.org/plosone/article/comment?id=10.1371/annotation/a02528e2-6b60-49b2-8719-17927c1a2d60</a></div>
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<span style="font-size: 13.3333px;">WEDNESDAY, JULY 11, 2018</span></div>
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<span style="font-size: 13.3333px;">CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000</span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/07/confidential-in-confidence-spongiform.html</a></div>
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<span style="font-family: Arial, sans-serif;"><span style="font-size: 16px;">WEDNESDAY, JULY 11, 2018 </span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="font-size: 16px;">Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions CDC AHEAD OF PRINT</span></span></div>
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<span style="font-family: Arial, sans-serif;"><span style="font-size: 16px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/07/susceptibility-of-human-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/07/susceptibility-of-human-prion-protein.html</a></span></span></div>
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<span style="font-family: arial, helvetica;">TUESDAY, JULY 03, 2018 </span></div>
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<span style="font-family: arial, helvetica;">Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news</span></div>
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<span style="font-family: arial, helvetica;"><a href="http://chronic-wasting-disease.blogspot.com/2018/07/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/07/chronic-wasting-disease-cwd-tse-prion.html</a></span></div>
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Terry S. Singeltary Sr.</div>
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<span style="font-size: 13.3333px;"><span style="background-color: white; font-family: arial, helvetica; text-align: start;">-----Original Message-----</span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /><span style="background-color: white; font-family: arial, helvetica; text-align: start;">From: Terry Singeltary <flounder9@verizon.net></span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /><span style="background-color: white; font-family: arial, helvetica; text-align: start;">To: xestioneventos <xestioneventos@usc.es></span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /><span style="background-color: white; font-family: arial, helvetica; text-align: start;">Sent: Fri, Jun 22, 2018 9:14 am</span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /><span style="background-color: white; font-family: arial, helvetica; text-align: start;">Subject: Re: PRION 2018 CONGRESSIONAL ABSTRACTS AND POSTERS</span><br style="background-color: white; font-family: arial, helvetica; text-align: start;" /></span></div>
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<span style="color: black; font-family: arial; font-size: x-small; position: relative !important;">very sad for those that donated their loved ones brains for this research, and very disturbing that you will not share this information with them. this is the first year of ALL PRION CONFERENCE that this information was/is not shared...very sad...thank you, kind regards, terry<br /><br /><br /><div style="font-family: arial, helvetica; font-size: 10pt;">
-----Original Message-----<br />From: Oficina de Congresos USC <<a href="mailto:xestioneventos@usc.es" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">xestioneventos@usc.es</a>><br />To: 'Terry Singeltary' <<a href="mailto:flounder9@verizon.net" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">flounder9@verizon.net</a>><br />Sent: Fri, Jun 22, 2018 2:20 am<br />Subject: RE: PRION 2018 CONGRESSIONAL ABSTRACTS AND POSTERS<br /><br /><div id="aolmail_AOLMsgPart_2_a25bc8ab-7b7a-42de-9fdf-a88dcdbeaa3f">
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<span style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;">Dear friend,</span></div>
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<span style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;"> </span></div>
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<span lang="EN-GB" style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;">we are not allowed to share this information. As long as I know, this information is just available for the conference attendants.</span></div>
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<span lang="EN-GB" style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;"> </span></div>
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<span lang="EN-GB" style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;">best regards,</span></div>
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<span lang="EN-GB" style="color: #1f497d; font-family: Calibri, sans-serif; font-size: 11pt;"> </span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">Olga Gutiérrez Méndez</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">Oficina de Congresos da USC</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">Complexo CEA-CE</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">Parque Vista Alegre - Rua Salvadas s/n</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">15705 Santiago de Compostela</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">tel 881816329 ext 16329</span></div>
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<span style="color: navy; font-family: Arial, sans-serif; font-size: 10pt;">E-mail: <a href="mailto:xestioneventos@usc.es" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank"></a><a href="mailto:xestioneventos@usc.es" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">xestioneventos@usc.es</a></span></div>
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<b><span style="font-family: Tahoma, sans-serif; font-size: 10pt;">De:</span></b><span style="font-family: Tahoma, sans-serif; font-size: 10pt;"> Terry Singeltary [<a href="mailto:flounder9@verizon.net?" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">mailto:flounder9@verizon.net</a>]<br /><b>Enviado el:</b> jueves, 21 de junio de 2018 18:19<br /><b>Para:</b> <a href="mailto:xestioneventos@usc.es" rel="noopener noreferrer" style="color: purple; cursor: pointer;" target="_blank">xestioneventos@usc.es</a><br /><b>Asunto:</b> PRION 2018 CONGRESSIONAL ABSTRACTS AND POSTERS</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt;">Hello Again,</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt;">a kind greetings from Bacliff, Texas. </span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt;">is there any way now that the conference is over, that i can get a copy of the PRION 2018 CONGRESSIONAL ABSTRACTS AND POSTERS. i have followed the tse prion science with great interest following the demise of my mother to the heidenhain variant of creutzfeldt jakob disease hvCJD. i have no access to the full conference pdf files, but it would be most appreciative i you might send them to me...</span></div>
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<span style="font-family: Arial, sans-serif; font-size: 10pt;">with kindest regards, terry</span></div>
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see;</div>
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Friday, November 22, 2013</div>
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Wasting disease is threat to the entire UK deer population CWD TSE PRION disease in cervids</div>
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***SINGELTARY SUBMISSION</div>
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The Scottish Parliament's Rural Affairs, Climate Change and Environment Committee has been looking into deer management, as you can see from the following press release,</div>
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***and your email has been forwarded to the committee for information:</div>
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<a href="http://www.scottish.parliament.uk/parliamentarybusiness/CurrentCommittees/29878.aspx" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.scottish.parliament.uk/parliamentarybusiness/CurrentCommittees/29878.aspx</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html</a></div>
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Friday, November 22, 2013</div>
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Wasting disease is threat to the entire UK deer population</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2013/11/wasting-disease-is-threat-to-entire-uk.html</a></div>
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Sunday, July 21, 2013</div>
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Welsh Government and Food Standards Agency Wales Joint Public Consultation on the Proposed Transmissible Spongiform Encephalopathies (Wales) Regulations 2013</div>
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*** Singeltary Submission WG18417</div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/welsh-government-and-food-standards.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/welsh-government-and-food-standards.html</a></div>
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<span style="color: #29303b; font-family: "georgia" , "times new roman" , sans-serif; font-size: x-small;">FRIDAY, FEBRUARY 23, 2018 </span></div>
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<span style="color: #29303b; font-family: "georgia" , "times new roman" , sans-serif; font-size: x-small;">Norwegian Food Safety Authority that two new cases of Skrantesjuke Chronic Wasting Disease (CWD) TSE Prion in Nordfjella have been confirmed</span></div>
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<span style="color: #29303b; font-family: "georgia" , "times new roman" , sans-serif; font-size: x-small;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/norwegian-food-safety-authority-that.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/norwegian-food-safety-authority-that.html</a></span></div>
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sadly i failed to stop cwd tse prion from being shipped back to Europe. </div>
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i tried to warn the USDA/OIE inc about CWD starting back around 2001, was laughed at there too. see;</div>
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*** URGENT CWD UPDATE Friday, January 17, 2014</div>
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FINALLY, 12 years later, the OIE becomes concerned with CWD to humans, not that I did not try and warn them 12 years ago. ...kind regards, terry</div>
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Friday, January 17, 2014</div>
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Annual report of the Scientific Network on BSE-TSE EFSA, Question No EFSA-Q-2013-01004, approved on 11 December 2013</div>
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*** Further, it was addressed that recently discussions have being held at OIE level on Chronic Wasting Disease of cervids.</div>
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2002 Singeltary vs O.I.E. on CWD to human risk factor ;</div>
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Subject: Re: CWD AMERICA ???</div>
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Date: Fri, 12 Jul 2002 19:10:18 +0200</div>
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From: "INFORMATION DEPT"</div>
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Organization: O.I.E</div>
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To: "Terry S. Singeltary Sr."</div>
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References: <<a href="mailto:3D2F0169.3@wt.net" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">3D2F0169.3@wt.net</a>> <012901c229b2$ad43bb90$7f00000a@HPKB> <a href="mailto:3D2F2358.5010700@wt.net" style="color: #0096ef; cursor: pointer; text-decoration-line: none;">3D2F2358.5010700@wt.net</a></div>
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I agree with you Dr Terry. The OIE, namely the International Animal Health Code Commission is working on making proposals to Member Countries to change the OIE lists so to avoid some the problems mentioned in you e-mail. This will take at least two years before adoption by the International Committee. For BSE, countries asked the OIE to post information on BSE on the OIE web site.</div>
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Personally, I am interested in Chronic Wasting Disease and I follow what is distributed through ProMed. Delegates of OIE Member Countries can propose diseases to be added to the list.</div>
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Kind regards.</div>
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<div style="color: #1d2129; font-family: Helvetica, Arial, sans-serif; font-size: 14px; margin-bottom: 6px; margin-top: 6px;">
Karim Ben Jebara</div>
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<br />
<a href="https://transmissiblespongiformencephalopathy.blogspot.com/2012/07/oie-bse-cwd-scrapie-tse-prion-disease.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2012/07/oie-bse-cwd-scrapie-tse-prion-disease.html</a></div>
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<br />
----- Original Message -----</div>
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<div style="color: #1d2129; font-family: Helvetica, Arial, sans-serif; font-size: 14px; margin-bottom: 6px; margin-top: 6px;">
From: "Terry S. Singeltary Sr."</div>
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To: "INFORMATION DEPT"</div>
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Sent: Friday, July 12, 2002 8:43 PM</div>
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Subject: Re: CWD AMERICA ???</div>
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>>> *** Further, it was addressed that recently discussions have being held at OIE level on Chronic Wasting Disease of cervids. <<<</div>
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<br />
> hello Dr. Jebara,<br />
><br />
> many thanks for your swift and kind reply.<br />
><br />
> if i am not mistaken, it was the same email address.<br />
> it was 3 or 4 weeks ago i wrote, as it is, i don't<br />
> save 'sent' emails anymore, unless very important.<br />
><br />
> my main concern (besides the fact that a potential TSE<br />
> has been in the USA cattle for some time, but the APHIS<br />
> do not test to find), is that the CWD could very well be<br />
> transmitting to humans, and i just did not see to much<br />
> posted about it on OIE site.<br />
><br />
> > Coming back to your question, Chronic Wasting Disease is not an OIE<br />
><br />
> > listed disease. Please see OIE disease lists at<br />
><br />
> <a href="https://l.facebook.com/l.php?u=http%3A%2F%2Fwww.oie.int%2Feng%2Fmaladies%2Fen_classification.htm%23ListeA&h=ATPCfwzq6Yw-9U6htnuiTNv0Ok0ECJDAij2BRHRkzrjcAZ5mxGih8S7ypK8TgcaK33ev6Gtv3XOdOSsWg7fzvkliaLaDneQ0nIx6TZn0qvEZK_IiFiyXA1KbljQb-FtxjXyY6CBpApyuXU75Nw" rel="noopener noreferrer" style="color: #365899; cursor: pointer; font-family: inherit; text-decoration-line: none;" target="_blank">http://www.oie.int/eng/maladies/en_classification.htm#ListeA</a>).<br />
><br />
> why is this TSE (CWD) not listed and followed as with BSE ?<br />
><br />
> Article 1.1.3.2.<br />
> 1. Countries shall make available to other countries, through the<br />
> OIE, whatever information is necessary to minimise the spread of<br />
> important animal diseases and to assist in achieving better worldwide<br />
> control of these diseases.<br />
><br />
> <a href="http://www.oie.int/eng/normes/MCode/A_00005.htm" rel="noopener noreferrer" style="color: #365899; cursor: pointer; font-family: inherit; text-decoration-line: none;" target="_blank">http://www.oie.int/eng/normes/MCode/A_00005.htm</a><br />
><br />
> The USA CWD is an important animal disease.<br />
><br />
> why is it not followed?<br />
><br />
> > The decision to add or delete a disease from the OIE lists, come<br />
><br />
> > through proposals made by Member Countries and it has to be adopted by<br />
><br />
> > the International Committee.<br />
><br />
> i _urgently_ suggest a proposal to the OIE to follow this disease very<br />
> closely, and to propose _more_ testing in the USA for TSEs in the USA<br />
> cattle...<br />
><br />
> kindest regards,<br />
> terry<br />
><br />
> INFORMATION DEPT wrote:<br />
><br />
> > Dear Sir,<br />
> ><br />
> > This is the first time that I receive your e-mail. To whom have you written<br />
> > in the OIE or to which address?<br />
> ><br />
> > Coming back to your question, Chronic Wasting Disease is not an OIE listed<br />
> > disease. Please see OIE disease lists at<br />
> > <a href="https://l.facebook.com/l.php?u=http%3A%2F%2Fwww.oie.int%2Feng%2Fmaladies%2Fen_classification.htm%23ListeA&h=ATNuA5ho-qnxLcQwYtLe0hamBUA-IH1XobtPnthcf9GtymUpcBsUaaSIAPuhwy9FN06HV8WeiCiOxBETZuioODkMg4j1ECUaBHJI99L0s7gFYYQrbeu5WaHU8ZEwS003Mg6STy4H7NTOp--jXA" rel="noopener noreferrer" style="color: #365899; cursor: pointer; font-family: inherit; text-decoration-line: none;" target="_blank">http://www.oie.int/eng/maladies/en_classification.htm#ListeA</a>).<br />
> ><br />
> > Countries should report to the OIE any disease even is not listed in the<br />
> > OIE's lists in some conditions (example: an exceptional epidemiological<br />
> > event). Please read Chapter 1.1.3 of the International animal health code to<br />
> > have more information on disease notification and epidemiological<br />
> > information agreed by OIE Member Countries at :<br />
> > <a href="https://l.facebook.com/l.php?u=http%3A%2F%2Fwww.oie.int%2Feng%2Fnormes%2FMCode%2FA_00005.htm&h=ATNfUvQza91hIxVGypi8B3UhdckbH0EwbYVmW1Alaxh9aRvv2on9LtLBM6EHhIQGTz-vwHDCvOf4cJUQOr6dv0tbMMNaa4gXM8pGB6r3_YfIFM-9r6Eut7CaEM3HTio8YW2LrftObvoc4uPTMg" rel="noopener noreferrer" style="color: #365899; cursor: pointer; font-family: inherit; text-decoration-line: none;" target="_blank">http://www.oie.int/eng/normes/MCode/A_00005.htm</a><br />
> ><br />
> > The decision to add or delete a disease from the OIE lists, come through<br />
> > proposals made by Member Countries and it has to be adopted by the<br />
> > International Committee.<br />
> ><br />
> > Hope that I answered to your question.<br />
> ><br />
> > Best regards.<br />
> ><br />
> > Dr Karim Ben Jebara<br />
> > Head<br />
> > Animal Health Information Department<br />
> > OIE<br />
> ><br />
> ><br />
> ><br />
> > ----- Original Message -----<br />
> > From: "Terry S. Singeltary Sr."<br />
> > To:<br />
> > Sent: Friday, July 12, 2002 6:18 PM<br />
> > Subject: CWD AMERICA ???<br />
> ><br />
> ><br />
> ><br />
> >>I WROTE TO OIE RECENTLY ASKING 'WHY OIE DOES NOT FOLLOW CWD IN<br />
> >>AMERICA' ? with no reply ? i am still seeking an answer ?<br />
> >><br />
> >>many thanks,<br />
> >>and kind regards,<br />
> >>terry<br />
=====================</div>
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<br />
<a href="https://transmissiblespongiformencephalopathy.blogspot.com/2012/07/oie-bse-cwd-scrapie-tse-prion-disease.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://transmissiblespongiformencephalopathy.blogspot.com/2012/07/oie-bse-cwd-scrapie-tse-prion-disease.html</a></div>
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MONDAY, MAY 05, 2014 </div>
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<span style="font-family: "georgia"; font-size: x-small;">Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing</span></div>
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<span style="font-family: "georgia"; font-size: x-small;"><a href="http://chronic-wasting-disease.blogspot.com/2014/05/member-country-details-for-listing-oie.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/05/member-country-details-for-listing-oie.html</a></span></div>
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<span style="font-size: 13.3333px;">In response to a Member Country’s detailed justification for listing of chronic wasting disease of cervids (CWD) against the criteria of Article 1.2.2., the Code Commission recommended this disease be reconsidered for listing. </span></div>
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<a href="http://www.oie.int/fileadmin/Home/eng/Internationa_Standard_Setting/docs/pdf/A_TAHSC_Feb_2013_Introduction.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.oie.int/fileadmin/Home/eng/Internationa_Standard_Setting/docs/pdf/A_TAHSC_Feb_2013_Introduction.pdf</a></div>
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REPORT OF THE MEETING OF THE OIE TERRESTRIAL ANIMAL HEALTH STANDARDS COMMISSION Paris, 17–26 September 2013</div>
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<span style="font-size: 13.3333px;">Item 5 Criteria for listing diseases (Chapter 1.2.)</span></div>
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<span style="font-size: 13.3333px;">Comments were received from Australia, EU, Japan, New Zealand, Switzerland, Thailand and AU-IBAR The Code Commission noted a Member Country’s comment suggesting that greater clarity was needed for the term ‘significant morbidity and mortality’. As noted in the February 2013 report, the Code Commission considered that the structured process of listing diseases, first by an expert group whose conclusions are documented and circulated for Member Countries’ review and comment, then consideration by the World Assembly of Delegates before final adoption, is sufficiently rigorous and transparent.</span></div>
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<a href="http://www.oie.int/fileadmin/Home/eng/Internationa_Standard_Setting/docs/pdf/A_TAHSC_Introduction_September_2013.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.oie.int/fileadmin/Home/eng/Internationa_Standard_Setting/docs/pdf/A_TAHSC_Introduction_September_2013.pdf</a></div>
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<span style="font-size: 13.3333px;"> greetings, what is criteria of Article 1.2.2. ??? curious as to what country detailed justification for listing ??? </span></div>
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<span style="font-size: 13.3333px;">kind regards, terry </span></div>
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<span style="font-size: 13.3333px;">*******UPDATE ON OIE ARTICLE 1.2.2******** </span></div>
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<span style="font-size: 13.3333px;"> OIE Article 1.2.2.</span></div>
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<span style="font-size: 13.3333px;">The criteria for the inclusion of a disease, infection or infestation in the OIE list are as follows:</span></div>
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<span style="font-size: 13.3333px;">1) International spread of the agent (via live animals or their products, vectors or fomites) has been proven.</span></div>
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<span style="font-size: 13.3333px;">AND</span></div>
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<span style="font-size: 13.3333px;">2) At least one country has demonstrated freedom or impending freedom from the disease, infection or infestation in populations of susceptible animals, based on the animal health surveillance provisions of the Terrestrial Code, in particular those contained in Chapter 1.4.</span></div>
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<span style="font-size: 13.3333px;">AND</span></div>
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<span style="font-size: 13.3333px;">3)</span></div>
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<span style="font-size: 13.3333px;">a) Natural transmission to humans has been proven, and human infection is associated with severe consequences. </span></div>
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<span style="font-size: 13.3333px;">OR</span></div>
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<span style="font-size: 13.3333px;">b) The disease has been shown to cause significant morbidity or mortality in domestic animals at the level of a</span></div>
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<span style="font-size: 13.3333px;">country or a zone.</span></div>
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<span style="font-size: 13.3333px;">OR</span></div>
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<span style="font-size: 13.3333px;">c) The disease has been shown to, or scientific evidence indicates that it would, cause significant morbidity or</span></div>
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<span style="font-size: 13.3333px;">mortality in wild animal populations.</span></div>
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<span style="font-size: 13.3333px;">AND</span></div>
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<span style="font-size: 13.3333px;">4) A reliable means of detection and diagnosis exists and a precise case definition is available to clearly identify cases</span></div>
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<span style="font-size: 13.3333px;">and allow them to be distinguished from other diseases, infections and infestations.</span></div>
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<span style="font-size: 13.3333px;">OR</span></div>
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<span style="font-size: 13.3333px;">5) The disease or infection is an emerging disease with evidence of zoonotic properties, rapid spread, or significant morbidity or mortality and a case definition is available to clearly identify cases and allow them to be distinguished from other diseases or infections.</span></div>
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<span style="font-size: 13.3333px;">2 2013 © OIE - Terrestrial Animal Health Code Chapter 1.2.- Criteria for the inclusion of diseases, infections and infestations on the OIE list</span></div>
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<a href="http://www.oie.int/fileadmin/Home/eng/Health_standards/tahc/2010/chapitre_1.1.2.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.oie.int/fileadmin/Home/eng/Health_standards/tahc/2010/chapitre_1.1.2.pdf</a></div>
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<span style="font-size: 13.3333px;"> *** URGENT CWD UPDATE </span></div>
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<span style="font-size: 13.3333px;">Friday, January 17, 2014 </span></div>
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<span style="font-size: 13.3333px;">FINALLY, 12 years later, the OIE becomes concerned with CWD to humans, not that I did not try and warn them 12 years ago. ...</span></div>
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<span style="font-size: 13.3333px;">kind regards, terry </span></div>
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<span style="font-size: 13.3333px;">Friday, January 17, 2014 </span></div>
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<span style="font-size: 13.3333px;">Annual report of the Scientific Network on BSE-TSE EFSA, Question No EFSA-Q-2013-01004, approved on 11 December 2013 </span></div>
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<span style="font-size: 13.3333px;">*** Further, it was addressed that recently discussions have being held at OIE level on Chronic Wasting Disease of cervids. </span></div>
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<span style="font-size: 13.3333px;">2002 Singeltary vs O.I.E. on CWD to human risk factor ;</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2014/05/member-country-details-for-listing-oie.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/05/member-country-details-for-listing-oie.html</a></span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2012/07/oie-bse-cwd-scrapie-tse-prion-disease.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2012/07/oie-bse-cwd-scrapie-tse-prion-disease.html</a></div>
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Greetings again <span style="font-size: 10pt;">Prion 2018 et al,</span></div>
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NOW, today, February 25, 2018, and i see little progress with the science to date, in terms of regulations, that will stop the spread of these TSE Prion disease (my greatest fear is iatrogenic gone undetected as sporadic cjd/alzheimer's). i have said it once, i have said it many times, until you get the industry, the politicians, and the lobbyist there from, out of the scientific decision makings, you will never stop this TSE Prion disease, it's the very reason we are at where we are today with cwd tse prion, imo. </div>
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Good Luck with the Prion 2018 Round Table Conference! i look forward to reading the science there from (i sure hope i can get a copy of this years congressional abstract book pdf and all posters, hint, hint). </div>
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a review to date of the chronic wasting disease cwd tse prion...</div>
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PRION CONFERENCE 2015, 2016, 2017, ON potential for CWD TSE PRION ZOONOSIS, if it has not happened already...</div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">***is the third potentially zoonotic PD (with BSE and L-type BSE), </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">***thus questioning the origin of human sporadic cases. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">=============== </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">***thus questioning the origin of human sporadic cases*** </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">=============== </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">============== </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><a href="https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf</a> </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;"><br /></span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></span></div>
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<span style="line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a> </span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">PRION 2016 TOKYO</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Saturday, April 23, 2016</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Taylor & Francis</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Prion 2016 Animal Prion Disease Workshop Abstracts</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">WS-01: Prion diseases in animals and zoonotic potential</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Natalia Fernandez-Borges a. and Alba Marin-Moreno a</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. </span></span></div>
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<span style="line-height: 1.22em;"><a href="http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: 10pt;" target="_blank">http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20</a></span></div>
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<span style="line-height: 1.22em;">why do we not want to do TSE transmission studies on chimpanzees $</span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">R. BRADLEY</span></span></div>
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<span style="line-height: 1.22em;"><a href="https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-size: 10pt;" target="_blank">https://web.archive.org/web/20170126051158/http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf</a></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">Title: Transmission of scrapie prions to primate after an extended silent incubation period) </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;">*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. </span></span></div>
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<span style="line-height: 1.22em;"><a href="http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160</a></span></div>
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<span style="line-height: 1.22em;"> <span style="font-size: 13.3333px;">*** WDA 2016 NEW YORK *** </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;"> *** We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. </span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: 13.3333px;"> Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders </span></span></div>
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<span style="line-height: 1.22em;">Volume 23, Number 9—September 2017 </span></div>
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<span style="line-height: 1.22em;"><span style="font-size: x-small;">Research Letter Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: x-small;">***Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.</span></span></div>
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<span style="line-height: 1.22em;"><span style="font-size: x-small;"><a href="https://wwwnc.cdc.gov/eid/article/23/9/16-1474_article" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://wwwnc.cdc.gov/eid/article/23/9/16-1474_article</a></span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat</span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat </span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">Chronic Wasting Disease (CWD) </span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">Prevention </span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">* Strongly consider having the deer or elk tested for CWD before you eat the meat. </span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">* If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. </span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">* If your animal tests positive for CWD, do not eat meat from that animal. </span></span></div>
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<span style="line-height: 1.22em;"><span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a href="https://www.cdc.gov/prions/cwd/prevention.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">https://www.cdc.gov/prions/cwd/prevention.html</a></span></span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">> However, to date, no CWD infections have been reported in people. </span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry </span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ </span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** </span></span></div>
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<span style="line-height: 1.22em;"><span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a href="http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys</a></span></span></span></div>
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<span style="line-height: 1.22em;"><span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true</a></span></span></span></div>
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<span style="line-height: 1.22em;"><span style="color: black;"><span style="background-color: rgba(255, 255, 255, 0);"><a href="http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm" rel="noopener noreferrer" style="color: blue; cursor: pointer; line-height: 1.22em;" target="_blank">http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm</a></span></span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">TUESDAY, SEPTEMBER 12, 2017 </span></span></div>
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<span style="line-height: 1.22em;"><span style="background-color: rgba(255, 255, 255, 0);">CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat </span></span></div>
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<span style="line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html" rel="noopener noreferrer" style="background-color: rgba(255, 255, 255, 0); color: blue; cursor: pointer; line-height: 1.22em;" target="_blank"><span style="color: black;"></span></a><span style="color: black;"><a href="http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html</a></span></span></div>
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<span style="line-height: 1.22em;"><span style="color: black; font-family: "arial"; font-size: x-small;"><span style="font-size: 13.3333px;">SATURDAY, JANUARY 27, 2018 </span></span></span></div>
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<span style="line-height: 1.22em;"><span style="color: black; font-family: "arial"; font-size: x-small;"><span style="font-size: 13.3333px;">CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018</span></span></span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html</a></div>
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<span style="font-size: 13.3333px;">Prion 2017 Conference Abstracts CWD</span></div>
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<span style="font-size: 13.3333px;"> 2017 PRION CONFERENCE </span></div>
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<span style="font-size: 13.3333px;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </span></div>
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<span style="font-size: 13.3333px;">Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </span></div>
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<span style="font-size: 13.3333px;">University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </span></div>
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<span style="font-size: 13.3333px;">This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </span></div>
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<span style="font-size: 13.3333px;">Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </span></div>
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<span style="font-size: 13.3333px;">At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">*** PRION 2017 CONFERENCE VIDEO </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<a href="https://www.youtube.com/embed/Vtt1kAVDhDQ" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<a href="http://prion2017.org/programme/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://prion2017.org/programme/</a></div>
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<br /></div>
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<span style="font-size: 13.3333px;">TUESDAY, JUNE 13, 2017</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">PRION 2017 CONFERENCE ABSTRACT </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a></div>
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<span style="font-size: 13.3333px;">TUESDAY, JULY 04, 2017</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html</a></div>
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<br /></div>
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<span style="font-size: 13.3333px;">***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.*** </span></div>
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<span style="font-size: 13.3333px;"><a href="http://www.nature.com/articles/srep11573" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/articles/srep11573</a> </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">SATURDAY, JULY 29, 2017 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html</a></div>
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<span style="line-height: 1.22em;">BSE INQUIRY</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">CJD9/10022</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">October 1994</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">BerksWell Coventry CV7 7BZ</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">Dear Mr Elmhirst,</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;"><a href="http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf</a></span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">snip...</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">snip...</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">snip...</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;">snip...see full report ;</span><br />
<span style="line-height: 1.22em;"><br /></span>
<span style="line-height: 1.22em;"><a href="https://web.archive.org/web/20170126073306/http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170126073306/http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf</a></span></div>
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<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">From: TSS (216-119-163-189.ipset45.wt.net)</span></span></div>
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<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">Subject: CWD aka MAD DEER/ELK TO HUMANS ???</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">Date: September 30, 2002 at 7:06 am PST</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">From: "Belay, Ermias"</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">Sent: Monday, September 30, 2002 9:22 AM</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">Dear Sir/Madam,</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">Ermias Belay, M.D. Centers for Disease Control and Prevention</span></span><br />
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;"><br /></span></span></div>
<div style="font-family: arial;">
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">-----Original Message-----</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">From: Sent: Sunday, September 29, 2002 10:15 AM</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">To: <a href="mailto:rr26k@nih.gov" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">rr26k@nih.gov</a>; <a href="mailto:rrace@niaid.nih.gov" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">rrace@niaid.nih.gov</a>; <a href="mailto:ebb8@CDC.GOV" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">ebb8@CDC.GOV</a></span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">Thursday, April 03, 2008</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">snip...</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,</span></span><br />
<span style="line-height: 1.22em;"><br style="color: #333333; font-family: "Trebuchet MS", Verdana, Arial, Helvetica, sans-serif; font-size: 14.6667px;" /></span>
<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">snip... full text ;</span></span><br />
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<span style="line-height: 1.22em;"><a href="http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html</a></span><br />
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<span style="line-height: 1.22em;"><span style="color: #333333; font-size: 14.6667px;"><span style="font-family: "arial" , "helvetica" , sans-serif;">*** </span></span><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">I urge everyone to watch this video closely...terry </span></span></div>
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<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***</span></span><br />
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<span style="line-height: 1.22em;"><a href="https://histodb11.usz.ch/Images/videos/video-004/video-004.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://histodb11.usz.ch/Images/videos/video-004/video-004.html</a></span><br />
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<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;">*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. </span></span><br />
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<span style="line-height: 1.22em;"><span style="color: #333333; font-family: "trebuchet ms" , "verdana" , "arial" , "helvetica" , sans-serif; font-size: 14.6667px;"><a href="http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf</a> </span></span></div>
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<span style="font-size: 13.3333px;">Friday, December 14, 2012</span></div>
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<span style="font-size: 13.3333px;">DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012</span></div>
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<span style="font-size: 13.3333px;">In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.</span></div>
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<span style="font-size: 13.3333px;">Animals considered at high risk for CWD include:</span></div>
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<span style="font-size: 13.3333px;">1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and</span></div>
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<span style="font-size: 13.3333px;">2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.</span></div>
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<span style="font-size: 13.3333px;">Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.</span></div>
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<span style="font-size: 13.3333px;">The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.</span></div>
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<span style="font-size: 13.3333px;">Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.</span></div>
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<span style="font-size: 13.3333px;">There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.</span></div>
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<span style="font-size: 13.3333px;">36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).</span></div>
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<span style="font-size: 13.3333px;">The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).</span></div>
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<span style="font-size: 13.3333px;">Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.</span></div>
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<span style="font-size: 13.3333px;">The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).</span></div>
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<span style="font-size: 13.3333px;">In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.</span></div>
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<span style="font-size: 13.3333px;">In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.</span></div>
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<span style="font-size: 13.3333px;">Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.</span></div>
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<span style="font-size: 13.3333px;"><a href="http://webarchive.nationalarchives.gov.uk/20130908115835/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://webarchive.nationalarchives.gov.uk/20130908115835/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf</a> </span></div>
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<span style="font-size: 13.3333px;">CWD TO PIGS</span></div>
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<span style="font-size: 13.3333px;">Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES</span></div>
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<span style="font-size: 13.3333px;">Location: Virus and Prion Research</span></div>
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<span style="font-size: 13.3333px;">Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></div>
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<span style="font-size: 13.3333px;">Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin</span></div>
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<span style="font-size: 13.3333px;">Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:</span></div>
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<span style="font-size: 13.3333px;">Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.</span></div>
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<span style="font-size: 13.3333px;">Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.</span></div>
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<span style="font-size: 13.3333px;">Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:</span></div>
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<span style="font-size: 13.3333px;">This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.</span></div>
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<span style="font-size: 13.3333px;">CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.</span></div>
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<span style="font-size: 13.3333px;">Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.</span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105</a> </span></div>
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<span style="font-size: 13.3333px;">CONFIDENTIAL</span></div>
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<span style="font-size: 13.3333px;">EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY</span></div>
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<span style="font-size: 13.3333px;">While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...</span></div>
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<a href="http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf</a></div>
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<span style="font-size: 13.3333px;">we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.</span></div>
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<a href="http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf</a></div>
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<span style="font-size: 13.3333px;">Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....</span></div>
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<a href="http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf</a></div>
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<span style="font-size: 13.3333px;">snip...see much more here ;</span></div>
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<span style="font-size: 13.3333px;">WEDNESDAY, APRIL 05, 2017</span></div>
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<span style="font-size: 13.3333px;">Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a></div>
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<span style="font-size: 13.3333px;">WEDNESDAY, APRIL 05, 2017</span></div>
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<span style="font-size: 13.3333px;">*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/04/disease-associated-prion-protein.html</a> </span></div>
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<span style="font-size: 13.3333px;">cattle are highly susceptible to white-tailed deer CWD and mule deer CWD</span></div>
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<span style="font-size: 13.3333px;">***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.</span></div>
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<span style="font-size: 13.3333px;">SNIP...</span></div>
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<a href="https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/514401/qra-chronic-wasting-disease.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/514401/qra-chronic-wasting-disease.pdf</a></div>
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<span style="font-size: 13.3333px;">price of prion poker goes up for cwd to cattle;</span></div>
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<span style="font-size: 13.3333px;">Monday, April 04, 2016</span></div>
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<span style="font-size: 13.3333px;">*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2016/04/limited-amplification-of-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/04/limited-amplification-of-chronic.html</a> </span></div>
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<span style="font-size: 13.3333px;">MONDAY, JUNE 12, 2017</span></div>
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<span style="font-size: 13.3333px;">Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/06/rethinking-major-grain-organizations.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/rethinking-major-grain-organizations.html</a></span></div>
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<span style="font-size: 13.3333px;">i am thinking of that 10,000,000 POUNDS OF BLOOD LACED MEAT AND BONE MEAL IN COMMERCE WARNING LETTER back in 2007, see;</span></div>
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<span style="font-size: 13.3333px;">SATURDAY, NOVEMBER 4, 2017 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">FDA 589.2000, Section 21 C.F.R. Animal Proteins Prohibited in Ruminant Feed WARNING Letters and FEED MILL VIOLATIONS OBSERVATIONS 2017 to 2006</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<a href="http://bovineprp.blogspot.com/2017/11/fda-5892000-section-21-cfr-animal.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/11/fda-5892000-section-21-cfr-animal.html</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">FRIDAY, NOVEMBER 3, 2017</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">IN CONFIDENCE</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://madcowfeed.blogspot.com/2017/11/bse-mad-cow-tse-prion-disease-pet-food.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://madcowfeed.blogspot.com/2017/11/bse-mad-cow-tse-prion-disease-pet-food.html</a> </span></div>
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</div>
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</div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"> WEDNESDAY, MAY 17, 2017</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/05/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/05/chronic-wasting-disease-cwd-tse-prion.html</a></span></div>
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</div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></span></div>
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</div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">snip...</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html</a></div>
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<br /></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">2012</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">snip...</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf</a></span></div>
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</div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">2011</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf</a></span></div>
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</div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">TUESDAY, MARCH 28, 2017 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/03/passage-of-scrapie-to-deer-results-in.html</a></span></div>
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</div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">SHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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<br /></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf</a></div>
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<br /></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">MONDAY, SEPTEMBER 25, 2017</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2017/09/colorado-chronic-wasting-disease-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/09/colorado-chronic-wasting-disease-cwd.html</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<div>
<span style="font-size: 13.3333px;">TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261</a></div>
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<br /></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"> *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION </span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article</a></div>
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<br /></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years *** </span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://jgv.sgmjournals.org/content/87/12/3737.full" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://jgv.sgmjournals.org/content/87/12/3737.full</a></div>
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<br /></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">=========================</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">========================</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. </span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="https://prion2015.files.wordpress.com/2015/05/programguide1.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://prion2015.files.wordpress.com/2015/05/programguide1.pdf</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
</div>
<div>
<span style="font-family: "arial"; font-size: 13.3333px;">the tse prion aka mad cow type disease is not your normal pathogen. </span></div>
<div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">you cannot cook the TSE prion disease out of meat. </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">the TSE prion agent also survives Simulated Wastewater Treatment Processes. </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">you can bury it and it will not go away. </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">it’s not your ordinary pathogen you can just cook it out and be done with. </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.</span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 </span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="font-family: arial;">
<span style="font-size: 13.3333px;">Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. </span></div>
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<span style="font-size: 13.3333px;">Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. </span></div>
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<span style="font-size: 13.3333px;">Laboratory of Central Nervous System Studies, National Institute of </span></div>
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<span style="font-size: 13.3333px;">Neurological Disorders and Stroke, National Institutes of Health, </span></div>
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<span style="font-size: 13.3333px;">Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. </span></div>
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<span style="font-size: 13.3333px;">PMID: 8006664 [PubMed - indexed for MEDLINE] </span></div>
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<a href="https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract</a> </div>
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<span style="font-size: 13.3333px;">New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication </span></div>
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<a href="http://www.pnas.org/content/97/7/3418.full" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.pnas.org/content/97/7/3418.full</a></div>
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<span style="font-size: 13.3333px;">Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production </span></div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/</a></div>
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<span style="font-size: 13.3333px;">Detection of protease-resistant cervid prion protein in water from a CWD-endemic area </span></div>
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<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802782/pdf/prion0303_0171.pdf</a></div>
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<span style="font-size: 13.3333px;">A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing </span></div>
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<a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract</a></div>
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<span style="font-size: 13.3333px;">Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals </span></div>
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<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html</a></div>
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<span style="font-size: 13.3333px;">PPo4-4: </span></div>
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<span style="font-size: 13.3333px;">Survival and Limited Spread of TSE Infectivity after Burial </span></div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf</a></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html</a></div>
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<span style="font-size: 13.3333px;">URINE</span></div>
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<span style="font-size: 13.3333px;">SUNDAY, JULY 16, 2017</span></div>
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<span style="font-size: 13.3333px;">*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/temporal-patterns-of-chronic-wasting.html</a> </span></div>
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<span style="font-size: 13.3333px;">Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). </span></div>
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<span style="font-size: 13.3333px;">Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). </span></div>
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<span style="font-size: 13.3333px;">Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). </span></div>
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<span style="font-size: 13.3333px;">Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. </span></div>
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<span style="font-size: 13.3333px;">Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. </span></div>
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<span style="font-size: 13.3333px;">Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). </span></div>
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<span style="font-size: 13.3333px;">The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. </span></div>
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<span style="font-size: 13.3333px;">When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. </span></div>
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<span style="font-size: 13.3333px;">This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. </span></div>
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<span style="font-size: 13.3333px;">Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. </span></div>
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<span style="font-size: 13.3333px;">It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. </span></div>
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<span style="font-size: 13.3333px;">Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. </span></div>
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<span style="font-size: 13.3333px;">Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. </span></div>
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<span style="font-size: 13.3333px;">Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. </span></div>
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<span style="font-size: 13.3333px;">PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. </span></div>
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<span style="font-size: 13.3333px;">In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. </span></div>
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<span style="font-size: 13.3333px;">In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). </span></div>
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<span style="font-size: 13.3333px;">As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. </span></div>
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<span style="font-size: 13.3333px;">False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). </span></div>
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<span style="font-size: 13.3333px;">This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. </span></div>
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<span style="font-size: 13.3333px;">This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. </span></div>
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<span style="font-size: 13.3333px;">In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. </span></div>
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<span style="font-size: 13.3333px;">Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. </span></div>
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<span style="font-size: 13.3333px;">The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. </span></div>
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<span style="font-size: 13.3333px;">In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). </span></div>
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<span style="font-size: 13.3333px;">A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). </span></div>
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<span style="font-size: 13.3333px;">This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. </span></div>
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<span style="font-size: 13.3333px;">Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. </span></div>
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<span style="font-size: 13.3333px;">In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. </span></div>
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<span style="font-size: 13.3333px;">These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. </span></div>
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<span style="font-size: 13.3333px;">Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification </span></div>
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<span style="font-size: 13.3333px;"><a href="http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full</a></span></div>
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<span style="font-size: 13.3333px;">Wednesday, December 16, 2015 </span></div>
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<span style="font-size: 13.3333px;">*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** </span></div>
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<a href="http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html</a></div>
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<span style="font-size: 13.3333px;">TSE Scrapie, CWD, BSE, Prion, Soil</span></div>
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<span style="font-size: 13.3333px;">Clay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern Illinois</span></div>
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<span style="font-size: 13.3333px;">Sheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-Pinilla</span></div>
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<span style="font-size: 13.3333px;">Scientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-x</span></div>
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<span style="font-size: 13.3333px;">Download Citation</span></div>
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<span style="font-size: 13.3333px;">Ecological epidemiology Ecological modelling Infectious diseases Prions</span></div>
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<span style="font-size: 13.3333px;">Received: 21 August 2017</span></div>
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<span style="font-size: 13.3333px;">Accepted: 08 December 2017</span></div>
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<span style="font-size: 13.3333px;">Published online: 22 December 2017</span></div>
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<span style="font-size: 13.3333px;">Abstract</span></div>
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<span style="font-size: 13.3333px;">Environmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.</span></div>
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<a href="https://www.nature.com/articles/s41598-017-18321-x" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.nature.com/articles/s41598-017-18321-x</a></div>
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<span style="font-size: 13.3333px;">Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles</span></div>
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<span style="font-size: 13.3333px;">Author Summary</span></div>
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<span style="font-size: 13.3333px;">Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.</span></div>
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<a href="https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson%20et%20al%20prions%20in%20soil.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson et al prions in soil.pdf</a></div>
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<span style="font-size: 13.3333px;">tse prion soil</span></div>
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<a href="http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630</a></div>
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<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf</a></div>
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<a href="http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217</a></div>
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<a href="http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4</a></div>
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<span style="font-size: 13.3333px;">cwd tse prion and soil, see more ;</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/01/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/01/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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USA MAD DEER ROUNDUP</div>
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Feb. 16, 2018<span style="font-size: 10pt;"><br /></span></div>
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<span style="font-size: 10pt;">Durkin: Stop private deer industry from trucking CWD across state </span></div>
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Patrick Durkin, For USA TODAY NETWORK-Wisconsin Published 10:13 a.m. CT Feb. 16, 2018 </div>
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A Waupaca County captive-deer shooting preserve that discovered its first two cases of chronic wasting disease in October found 10 more CWD cases last fall, with 11 of the deer coming from a breeding facility in Iowa County — Wisconsin’s most infected county.</div>
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Hunt’s End Deer Ranch near Ogdensburg is one of 376 fenced deer farms in Wisconsin, according to the Department of Agriculture, Trade and Consumer Protection. Hunt’s End bought the diseased deer from Windy Ridge Whitetails, a 15-acre, 110-deer breeding facility south of Mineral Point in Iowa County. Of Wisconsin’s 4,175 CWD cases in wild deer, 2,261 (54 percent) are in Iowa County.</div>
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Since CWD’s discovery in three wild deer shot during the November 2001 gun season, CWD has been detected on 18 Wisconsin deer farms, of which 11 were “depopulated.” DATCP has identified 242 CWD cases in captive facilities the past 16 years.</div>
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The state’s worst site remains the former Buckhorn Flats Game Farm near Almond in Portage County, where 80 deer tested positive for this always-fatal disease from 2002 to 2006. When the U.S. Department of Agriculture shot out the 70-acre pen in January 2006, 60 of the remaining 76 deer carried CWD, a nearly 80 percent infection rate. </div>
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The Department of Natural Resources bought the heavily contaminated site for $465,000 in 2011 and has kept it fenced and deer-free since.</div>
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The last time DATCP exterminated a captive herd was November 2015, when it killed 228 deer at Fairchild Whitetails, a 10-acre breeding facility in Eau Claire County, and paid its owner, Richard Vojtik, $298,770 in compensation. Tests revealed 34 of those deer carried CWD (15 percent), but two bucks had escaped earlier. Those bucks roamed five months before being shot and tested. They, too, had CWD.</div>
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Both operations were outside the endemic CWD region in southern Wisconsin; Buckhorn Flats by about 60 miles and Fairchild Whitetails by about 120. Wisconsin’s four most active CWD outbreaks on deer farms are north of U.S. 10, and farther away from the endemic region — basically the DNR’s Southern Farmlands district — which had 584 CWD cases 2017-18 and 4,148 since 2001.</div>
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Those businesses are:</div>
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• Wilderness Whitetails, near Eland in Marathon County: 68 CWD cases, including 43 in 2017-18. DATCP first reported CWD there in December 2013 in a 5-year-old buck shot by a facility client. The operation also found three cases in 2014, nine in 2015 and 12 in 2016. </div>
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The preserve held about 310 deer in its 351-acre pen last summer. Since beginning tests in 2002, the facility tested 373 deer before finding its first case 11 years later.</div>
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• Hunt’s End, Waupaca County: 12 cases, all in 2017-18. The owners, Dusty and Mandy Reid, didn’t detect CWD on the 84-acre shooting facility until two 4-year-old bucks tested positive last fall. DATCP announced those cases Oct. 20, and disclosed 10 additional cases in response to my open-records request in January.</div>
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Both Oct. 20 bucks originated from Windy Ridge Whitetails. Nine other bucks from Windy Ridge, owned by Steven and Marsh Bertram, tested positive for CWD after being shot by Hunt’s End clients.</div>
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Now DATCP records covering the past five years showed Hunt’s End acquired 31 deer from Windy Ridge, which also sent a combined 67 whitetails to nine other Wisconsin deer farms during that period.</div>
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Paul McGraw, DATCP’s state veterinarian and administrator in animal health, quarantined three Hunt’s End properties Oct. 20, but let its owners, continue selling hunts because “properly handled dead animals leaving the premises do not pose a disease risk.”</div>
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McGraw also quarantined Windy Ridge, but the specifications let the business move more deer to the Waupaca shooting facility. It made two more shipments to Hunt’s End, the last occurring Nov. 13.</div>
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• Apple Creek Whitetails, Oconto County: 11 cases. Since discovering CWD in September 2016 in an 18-month-old doe killed inside the facility near Gillett, DATCP has identified 10 more cases, including three in 2017-18. The preserve held about 1,850 deer on 1,363 acres, and tested 466 in 2016. After first testing for CWD in 2009, the business processed 1,192 deer before finding its first case 18 months ago.</div>
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• Three Lakes Trophy Ranch, Oneida County: Nine cases. Since discovering CWD in December 2015 in a 3-year-old buck at Three Lakes, DATCP has identified eight more cases, including two in 2017-18. The preserve held about 545 whitetails on 570 acres.</div>
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Although the Hunt’s End outbreak traces to Iowa County deer, Windy Ridge Whitetails sent even more deer, 42, to Vojtik’s American Adventures Ranch near Fairchild with no documented problems. DATCP reports no CWD cases there, and Vojtik, who also owned the 10-acre Fairchild Whitetails breeding facility, said he hasn’t bought Windy Ridge deer the past two years.</div>
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Vojtik said Wednesday that he and his clients shoot out his enclosure’s herd of about 200 deer each year to reduce CWD risks. And because he’s not in DATCP’s herd-status program, he must only test 50 percent of deer dying there.</div>
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Meanwhile, Wilderness Whitetails tests all of its dead deer. It leads the state with 68 CWD cases, even though it has maintained a “closed herd” since opening its Eland facility in 2004, said its owner, Greg Flees, when reached Wednesday. Flees said all deer in the 351-acre facility were born there or came from his family’s Portage County breeding pen, which began in the 1970s and has never had CWD.</div>
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Flees said the jump from 12 CWD cases in 2016 to 43 in 2017 is no mystery or surprise. “We shot more deer to lower our densities, so we found more CWD,” he said. He thinks CWD was in the facility’s soils when they enclosed it with an 8-foot-high fence 14 years ago, or it arrived in alfalfa bales brought in for feed.</div>
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Perhaps the bigger mystery is why DATCP allows any deer from Iowa County to be shipped anywhere. Windy Ridge Whitetails is one of eight captive-deer facilities in CWD-infected counties — Sauk, Dane, Iowa, Rock, Walworth and Richland — enrolled in DATCP’s herd-status program, which allows deer transfers if facilities follow specified guidelines.</div>
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That won’t change soon, either. In a letter Jan. 30 responding to my open records request, Paul Dedinsky, DATCP’s chief legal counsel, wrote, “The Department is not proposing any rule changes to prohibit movement from CWD endemic areas.”</div>
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No doubt Wisconsin’s wild deer provide a vast, mostly undocumented pool for spreading CWD, but sick deer can only carry disease as far as they walk. With DATCP’s approval, privately owned deer could spread CWD wherever they’re trucked.</div>
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Patrick Durkin is a freelance writer who covers outdoors for USA TODAY NETWORK-Wisconsin. Email him at <a href="mailto:patrickdurkin56@gmail.com" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">patrickdurkin56@gmail.com</a>.</div>
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<a href="https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/</a></div>
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<span style="font-size: 13.3333px;">FRIDAY, FEBRUARY 16, 2018 </span></div>
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<span style="font-size: 13.3333px;">Wisconsin Stop private deer industry from trucking CWD across state</span></div>
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<span style="font-size: 13.3333px;"><a href="https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://www.greenbaypressgazette.com/story/sports/outdoors/2018/02/16/durkin-stop-private-deer-industry-trucking-cwd-across-state/342532002/</a></span></div>
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<span style="font-size: 13.3333px;">FRIDAY, FEBRUARY 16, 2018 </span></div>
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<span style="font-size: 13.3333px;">Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/wisconsin-deer-from-now-quarantined-pa.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/wisconsin-deer-from-now-quarantined-pa.html</a></span></div>
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<span style="font-size: 13.3333px;">FRIDAY, JANUARY 26, 2018 </span></div>
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<span style="font-size: 13.3333px;">WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/wisconsin-reports-588-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/wisconsin-reports-588-cwd-tse-prion.html</a></span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">Tuesday, December 20, 2011</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;"><a href="http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf</a></span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">captive deer farmers breeders entitlement program, i.e. indemnity program</span><span style="font-family: "arial" , "helvetica";">, why?</span></div>
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<span style="font-family: "arial" , "helvetica";">how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms, and why do tax payers have to pay for it ???</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">For Immediate Release Thursday, October 2, 2014</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;"> Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or <a href="mailto:Dustin.VandeHoef@IowaAgriculture.gov" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">Dustin.VandeHoef@IowaAgriculture.gov</a></span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;"> *** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease ***</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;"> DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). </span></div>
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<a href="http://www.iowaagriculture.gov/press/2014press/press10022014.asp" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.iowaagriculture.gov/press/2014press/press10022014.asp</a></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">For Immediate Release</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">Thursday, October 2, 2014</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or <a href="mailto:Dustin.VandeHoef@IowaAgriculture.gov" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">Dustin.VandeHoef@IowaAgriculture.gov</a> Share on facebook Share on twitter Share on email Share on print More Sharing Services 1</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.</span></div>
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<a href="http://www.iowaagriculture.gov/press/2014press/press10022014.asp" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.iowaagriculture.gov/press/2014press/press10022014.asp</a></div>
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<span style="font-size: 13.3333px;">79.8 percent of the deer tested positive for the disease</span></div>
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<span style="font-size: 13.3333px;">DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.</span></div>
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<span style="font-size: 13.3333px;">The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.</span></div>
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<span style="font-size: 13.3333px;">The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.</span></div>
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<span style="font-size: 13.3333px;">Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.</span></div>
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<span style="font-size: 13.3333px;"><a href="http://www.iowaagriculture.gov/press/2014press/press10022014.asp" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.iowaagriculture.gov/press/2014press/press10022014.asp</a></span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">INFORM: Cervid Health and States Indemnity FY 2015</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">USDA Animal and Plant Health Inspection Service sent this bulletin at 09/19/2014 05:22 PM EDT</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS) received a total of $3 million in appropriated funding to support cervid health activities in fiscal year (FY) 2014, and made approximately $1.0 million of this funding available for indemnity of chronic wasting disease (CWD) positive, suspect, and exposed farmed cervids. All of the available FY2014 indemnity funding was used to depopulate three CWD-infected herds. However, several States have asked about the availability of Federal indemnity funds for CWD-exposed animals in the future.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">VS plans to offer Federal indemnity for CWD-exposed cervids beginning in FY2015. Briefly, we will prioritize the highest risk CWD-exposed animals for indemnity based on the availability of funding. Any newly reported CWD-positive herds will be considered for indemnity as they are identified, based first on funding availability and secondly on the risk presented by the herd.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">We will reassess our fiscal year funding on a quarterly basis so that providing indemnity for exposed animals does not exhaust available funding early in the fiscal year. By taking this fiscally cautious approach, we hope to provide indemnity for positive herds identified later in the fiscal year while removing high-risk animals from the landscape as soon as possible to minimize the risk for disease spread. Further, removal and testing of these exposed animals will provide a better understanding of the disease risk presented by these animals/herds.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">VS plans to work with our State and industry stakeholders on the criteria to assess the risk and on the process through which States can request this indemnity. These will be finalized in a VS Guidance Document in the near future. We look forward to working with you to implement this process in the coming year.</span></div>
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<span style="font-family: "arial" , "helvetica"; font-size: x-small;">***</span></div>
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<a href="http://content.govdelivery.com/accounts/USDAAPHIS/bulletins/d05806" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://content.govdelivery.com/accounts/USDAAPHIS/bulletins/d05806</a></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">FRIDAY, FEBRUARY 23, 2018</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;">Pennsylvania NEW CWD MANAGEMENT AREA TO BE ANNOUNCED</span></span></div>
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<span style="font-family: "arial" , "helvetica";"><span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/pennsylvania-new-cwd-management-area-to.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/pennsylvania-new-cwd-management-area-to.html</a></span></span></div>
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<span style="font-size: x-small;">MONDAY, FEBRUARY 12, 2018 </span></div>
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<span style="font-size: x-small;">Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties</span></div>
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<span style="font-size: x-small;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/pennsylvania-cwd-tse-prion-has-been.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/pennsylvania-cwd-tse-prion-has-been.html</a></span></div>
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<div class="aolmail_aolmail_aolmail_aolmail_aolmail_MsoNormal" style="background-attachment: initial; background-clip: initial; background-image: initial; background-origin: initial; background-position: initial; background-repeat: initial; background-size: initial; line-height: 14.65pt; margin: 0in 0in 0.0001pt;">
<span style="font-family: "arial" , sans-serif;"><span style="font-size: 13.3333px;">WEDNESDAY, FEBRUARY 21, 2018 </span></span></div>
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<span style="font-family: "arial" , sans-serif;"><span style="font-size: 13.3333px;">Maryland Chronic Wasting Disease CWD TSE Prion Found In Ten Deer Allegany and Washington Counties</span></span></div>
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<span style="font-family: "arial" , sans-serif;"><span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/maryland-chronic-wasting-disease-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/maryland-chronic-wasting-disease-cwd.html</a></span></span></div>
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<span style="font-size: 13.3333px;">SATURDAY, FEBRUARY 17, 2018 </span></div>
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<span style="font-size: 13.3333px;">Montana Special Hunts 9 more cases CWD TSE Prion to date, more samples still pending</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/montana-special-hunts-9-more-cases-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/montana-special-hunts-9-more-cases-cwd.html</a></span></div>
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<span style="font-size: 13.3333px;">FRIDAY, FEBRUARY 09, 2018 </span></div>
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<span style="font-size: 13.3333px;">Mississippi Chronic Wasting Disease confirmed in a White-tailed Deer</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-chronic-wasting-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-chronic-wasting-disease.html</a></span></div>
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<span style="font-size: 13.3333px;">TUESDAY, FEBRUARY 13, 2018 </span></div>
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<span style="font-size: 13.3333px;">*** MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations ***</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-state-department-of-health.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-state-department-of-health.html</a></span></div>
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<span style="font-size: 13.3333px;">WEDNESDAY, NOVEMBER 22, 2017 </span></div>
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<span style="font-size: 13.3333px;">Minnesota Chronic Wasting Disease discovered in Winona County farm</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/11/minnesota-chronic-wasting-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/11/minnesota-chronic-wasting-disease.html</a></span></div>
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<span style="font-size: 13.3333px;">FRIDAY, NOVEMBER 24, 2017 </span></div>
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<span style="font-size: 13.3333px;">Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting CWD TSE PRION DISEASE risk factors</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/11/todd-robbins-miller-president-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/11/todd-robbins-miller-president-of.html</a></span></div>
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<span style="font-size: x-small;">WEDNESDAY, FEBRUARY 21, 2018 </span></div>
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<span style="font-size: x-small;">TEXAS TPWD CWD TSE PRION 2 MORE FROM BREEDER RELEASE SITE TOTALS 81 CASES TO DATE </span></div>
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<span style="font-size: x-small;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/texas-tpwd-cwd-tse-prion-2-more-from.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/texas-tpwd-cwd-tse-prion-2-more-from.html</a> </span></div>
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<span style="font-size: 13.3333px;">WEDNESDAY, JANUARY 24, 2018</span></div>
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<span style="font-size: 13.3333px;">TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/texas-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/texas-chronic-wasting-disease-cwd-tse.html</a></span></div>
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<span style="font-size: 13.3333px;">FRIDAY, FEBRUARY 16, 2018 </span></div>
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<span style="font-size: 13.3333px;">Texas Deer Breeders Continue fight against the state’s wildlife agency and its regulations trying to contain CWD TSE Prion</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/texas-deer-breeders-continue-fight.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/texas-deer-breeders-continue-fight.html</a></span></div>
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<span style="font-size: 13.3333px;">WEDNESDAY, FEBRUARY 07, 2018 </span></div>
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<span style="font-size: 13.3333px;">New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/new-mexico-bans-all-live-cervid.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/new-mexico-bans-all-live-cervid.html</a></span></div>
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<span style="font-size: 13.3333px;">FRIDAY, FEBRUARY 09, 2018 </span></div>
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<span style="font-size: 13.3333px;">Virginia 2017 Hunt Confirms 16 Cases Chronic Wasting Disease CWD TSE Prion</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/virginia-2017-hunt-confirms-16-cases.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/virginia-2017-hunt-confirms-16-cases.html</a></span></div>
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<span style="font-size: 13.3333px;">MONDAY, FEBRUARY 05, 2018 </span></div>
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<span style="font-size: 13.3333px;">Nebraska Chronic Wasting Disease CWD TSE Prion 2017 Survey Confirms 203 Positives From 1,807 Deer Sampled</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/nebraska-chronic-wasting-disease-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/nebraska-chronic-wasting-disease-cwd.html</a></span></div>
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<span style="font-size: 13.3333px;">SATURDAY, FEBRUARY 03, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/arkansas-reports-346-positive-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/arkansas-reports-346-positive-cwd-tse.html</a></span></div>
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<span style="font-size: 13.3333px;">THURSDAY, FEBRUARY 08, 2018 </span></div>
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<span style="font-size: 13.3333px;">Utah Chronic Wasting Disease CWD TSE Prion Update to date from 2017 Hunting Season</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/utah-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/utah-chronic-wasting-disease-cwd-tse.html</a></span></div>
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<span style="font-size: 13.3333px;">TUESDAY, JANUARY 30, 2018 </span></div>
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<span style="font-size: 13.3333px;">Colorado Chronic Wasting Disease CWD TSE Prion 7/2015-6/2016 Results (2017?)</span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/colorado-chronic-wasting-disease-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/colorado-chronic-wasting-disease-cwd.html</a></span></div>
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<span style="font-size: 13.3333px;">THURSDAY, JANUARY 25, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Ohio Chronic Wasting Disease CWD TSE Prioin aka mad deer update 2016-2017 SEASON SUMMARY</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/ohio-chronic-wasting-disease-cwd-tse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/ohio-chronic-wasting-disease-cwd-tse.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">SATURDAY, JANUARY 20, 2018</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have tested positive for CWD majority of samples collected still are being analyzed</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/pennsylvania-cwd-tse-prion-cases.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/pennsylvania-cwd-tse-prion-cases.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">WEDNESDAY, JANUARY 24, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Illinois Chronic Wasting Disease CWD TSE Prion cases mounting with 75 confirmed 2017 and 685 total to date</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/illinois-chronic-wasting-disease-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/illinois-chronic-wasting-disease-cwd.html</a></span></div>
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<span style="font-size: 13.3333px;">THURSDAY, FEBRUARY 08, 2018</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/iowa-dnr-wayne-county-confirms-cwd-with.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/iowa-dnr-wayne-county-confirms-cwd-with.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">SATURDAY, FEBRUARY 10, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Chronic wasting disease management in ranched elk using rectal biopsy testing Research Paper 09 Feb 2018</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/02/chronic-wasting-disease-management-in.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/chronic-wasting-disease-management-in.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">January 14, 2018</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://www.michigan.gov/emergingdiseases/0,4579,7-186-81018_25806-357110--,00.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.michigan.gov/emergingdiseases/0,4579,7-186-81018_25806-357110--,00.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/michigans-chronic-wasting-disease.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/michigans-chronic-wasting-disease.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Michigan UPDATE, see also ;</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Contact: Dwayne Etter (DNR), 517-284-4725 or David Williams (MSU), 517-917-0716 Agency: Natural Resources</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Jan. 30, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Michigan State University and the Michigan Department of Natural Resources will be placing location-tracking collars on white-tailed deer in south-central Michigan as part of a multiyear study of deer disease, including chronic wasting disease.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://www.michigan.gov/som/0,4669,7-192-47796-458819--,00.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.michigan.gov/som/0,4669,7-192-47796-458819--,00.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">January 14, 2018</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Missouri MDC REPORTS 15 NEW CASES OF CWD TSE Prion in Deer</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/missouri-mdc-reports-15-new-cases-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/missouri-mdc-reports-15-new-cases-of.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">MONDAY, JANUARY 29, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Wyoming, Hanna, WGFD diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 161</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/wyoming-hanna-wgfd-diagnosed-chronic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/wyoming-hanna-wgfd-diagnosed-chronic.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">MONDAY, JANUARY 29, 2018 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">North Dakota CWD Confirmed whitetail buck and a mule deer doe 2017 deer gun season from unit 3F2</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2018/01/north-dakota-cwd-confirmed-whitetail.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/01/north-dakota-cwd-confirmed-whitetail.html</a></span></div>
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<br /></div>
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<div>
<span style="font-size: x-small;">SUNDAY, FEBRUARY 18, 2018 </span></div>
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<span style="font-size: x-small;"><br /></span></div>
<div>
<span style="font-size: x-small;">Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018</span></div>
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<span style="font-size: x-small;"><br /></span></div>
<div>
<a href="http://chronic-wasting-disease.blogspot.com/2018/02/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2018/02/chronic-wasting-disease-cwd-tse-prion.html</a></div>
</div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">TUESDAY, DECEMBER 12, 2017 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">*** Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017 ***</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">(zoonosis and environmental risk factors towards the bottom, after state by state reports)</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/12/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/12/chronic-wasting-disease-cwd-tse-prion.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">MONDAY, MARCH 13, 2017 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/03/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/03/chronic-wasting-disease-cwd-tse-prion.html</a></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">SATURDAY, JANUARY 14, 2017 </span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2017/01/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/01/chronic-wasting-disease-cwd-tse-prion.html</a></span></div>
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<br /></div>
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<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
Sunday, June 23, 2013</div>
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<br /></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
National Animal Health Laboratory Network Reorganization Concept Paper (Document ID APHIS-2012-0105-0001)</div>
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<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
***Terry S. Singeltary Sr. submission</div>
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<br /></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2013/06/national-animal-health-laboratory.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2013/06/national-animal-health-laboratory.html</a></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
<br /></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
Singeltary submission ;</div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
<br /></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose</div>
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<br /></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
DOCUMENT ID: APHIS-2006-0118-0411</div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
<br /></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
***Singeltary submission</div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
<br /></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
<a href="http://www.regulations.gov/#!documentDetail;D=APHIS-2006-0118-0411" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.regulations.gov/#!documentDetail;D=APHIS-2006-0118-0411</a></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
<br /></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
<a href="http://chronic-wasting-disease.blogspot.com/2014/03/docket-no-00-108-10-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/03/docket-no-00-108-10-chronic-wasting.html</a></div>
<div style="background-color: white; font-family: Georgia; line-height: 1.22em;">
<br /></div>
<div style="background-color: white; line-height: 1.22em;">
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<span style="font-size: 13.3333px;">Singeltary submission ;</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">*** DOCUMENT ID: APHIS-2006-0118-0411</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.regulations.gov/#!documentDetail;D=APHIS-2006-0118-0411" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.regulations.gov/#!documentDetail;D=APHIS-2006-0118-0411</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2014/03/docket-no-00-108-10-chronic-wasting.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2014/03/docket-no-00-108-10-chronic-wasting.html</a></span></div>
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<br /></div>
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<div class="aolmail_aolmail_aolmail_aolReplacedBody">
<div style="line-height: 1.22em;">
<div style="line-height: 1.22em;">
<div style="line-height: 1.22em;">
<div style="color: #29303b; font-family: Georgia, "Times New Roman", sans-serif;">
<span style="font-size: 13.3333px;">SUNDAY, FEBRUARY 11, 2018 </span></div>
<div style="color: #29303b; font-family: Georgia, "Times New Roman", sans-serif;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: #29303b; font-family: Georgia, "Times New Roman", sans-serif;">
<span style="font-size: 13.3333px;">Experimental sheep BSE prions generate the vCJD phenotype when serially passaged in transgenic mice expressing human prion protein</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: #29303b; font-family: Georgia, "Times New Roman", sans-serif;">
<span style="font-size: 13.3333px;"><a href="http://transmissiblespongiformencephalopathy.blogspot.com/2018/02/experimental-sheep-bse-prions-generate.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2018/02/experimental-sheep-bse-prions-generate.html</a></span></div>
<div style="color: #29303b; font-family: Georgia, "Times New Roman", sans-serif;">
<br /></div>
<div style="color: #29303b; font-family: Georgia, "Times New Roman", sans-serif;">
<a href="http://vcjd.blogspot.com/2018/02/experimental-sheep-bse-prions-generate.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://vcjd.blogspot.com/2018/02/experimental-sheep-bse-prions-generate.html</a></div>
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<br /></div>
<div style="color: #29303b; font-family: Georgia, "Times New Roman", sans-serif;">
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;">Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy</span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;">Ivett Ackermann, Anne Balkema-Buschmann, Reiner Ulrich, Kerstin Tauscher, James C. Shawulu, Markus Keller, Olanrewaju I. Fatola, Paul Brown and Martin H. GroschupEmail authorView ORCID ID profile</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;">Veterinary Research201748:88</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;"><a href="https://doi.org/10.1186/s13567-017-0495-5%C2%A9" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://doi.org/10.1186/s13567-017-0495-5©</a> The Author(s) 2017</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;">Received: 22 August 2017Accepted: 1 December 2017Published: 19 December 2017</span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;">Abstract</span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;">In classical bovine spongiform encephalopathy (C-BSE), an orally acquired prion disease of cattle, the ileal Peyer’s patch (IPP) represents the main entry port for the BSE agent. In earlier C-BSE pathogenesis studies, cattle at 4–6 months of age were orally challenged, while there are strong indications that the risk of infection is highest in young animals. In the present study, unweaned calves aged 4–6 weeks were orally challenged to determine the earliest time point at which newly formed PrPBSE and BSE infectivity are detectable in the IPP. For this purpose, calves were culled 1 week as well as 2, 4, 6 and 8 months post-infection (mpi) and IPPs were examined for BSE infectivity using a bovine PrP transgenic mouse bioassay, and for PrPBSE by immunohistochemistry (IHC) and protein misfolding cyclic amplification (PMCA) assays. For the first time, BSE prions were detected in the IPP as early as 2 mpi by transgenic mouse bioassay and PMCA and 4 mpi by IHC in the follicular dendritic cells (FDCs) of the IPP follicles. These data indicate that BSE prions propagate in the IPP of unweaned calves within 2 months of oral uptake of the agent.</span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;">snip...</span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;">In summary, our study demonstrates for the first time PrPBSE (by PMCA) and prion infectivity (by mouse bioassay) in the ileal Peyer’s patch (IPP) of young calves as early as 2 months after infection. From 4 mpi nearly all calves showed PrPBSE positive IPP follicles (by IHC), even with PrPBSE accumulation detectable in FDCs in some animals. Finally, our results confirm the IPP as the early port of entry for the BSE agent and a site of initial propagation of PrPBSE and infectivity during the early pathogenesis of the disease. Therefore, our study supports the recommendation to remove the last four metres of the small intestine (distal ileum) at slaughter, as designated by current legal requirements for countries with a controlled BSE risk status, as an essential measure for consumer and public health protection.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div style="color: black; font-family: arial;">
<span style="font-size: 13.3333px;"><a href="https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-017-0495-5" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">https://veterinaryresearch.biomedcentral.com/articles/10.1186/s13567-017-0495-5</a></span></div>
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<br /></div>
<div style="color: black; font-family: arial;">
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<span style="font-size: 13.3333px;">FRIDAY, DECEMBER 22, 2017 </span></div>
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<span style="font-size: 13.3333px;">Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy</span></div>
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<span style="font-size: 13.3333px;"><a href="http://bovineprp.blogspot.com/2017/12/detection-of-prpbse-and-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/12/detection-of-prpbse-and-prion.html</a></span></div>
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<span style="font-size: x-small;">Thursday, November 16, 2017 </span></div>
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<span style="font-size: x-small;">Texas Natural Meats Recalls Beef Products Due To Possible Specified Risk Materials Contamination</span></div>
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<span style="font-size: x-small;"><a href="http://specifiedriskmaterial.blogspot.com/2017/11/texas-natural-meats-recalls-beef.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://specifiedriskmaterial.blogspot.com/2017/11/texas-natural-meats-recalls-beef.html</a></span></div>
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<span style="font-size: 10pt;">*** Subject: USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS 2017</span></div>
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TUESDAY, DECEMBER 12, 2017 </div>
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Bovine Spongiform Encephalopathy BSE TSE Prion (aka mad cow disease) Report December 14, 2017 2017</div>
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<a href="http://bovineprp.blogspot.com/2017/12/bovine-spongiform-encephalopathy-bse.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://bovineprp.blogspot.com/2017/12/bovine-spongiform-encephalopathy-bse.html</a></div>
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Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017</div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/12/chronic-wasting-disease-cwd-tse-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/12/chronic-wasting-disease-cwd-tse-prion.html</a></div>
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<span style="font-size: 13.3333px;">FRIDAY, DECEMBER 15, 2017</span></div>
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<span style="font-size: 13.3333px;">Canada CFIA updating its national CWD TSE PRION efforts to eradicate disease farmed cervid NOT successful December 14, 2017</span></div>
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<a href="http://chronic-wasting-disease.blogspot.com/2017/12/canada-cfia-updating-its-national-cwd.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/12/canada-cfia-updating-its-national-cwd.html</a></div>
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TUESDAY, DECEMBER 12, 2017 </div>
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SCRAPIE TSE PRION UPDATE USA DECEMBER 14, 2017</div>
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<a href="http://scrapie-usa.blogspot.com/2017/12/scrapie-tse-prion-update-usa-december.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://scrapie-usa.blogspot.com/2017/12/scrapie-tse-prion-update-usa-december.html</a></div>
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USAHA 2017 RESOLUTIONS</div>
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RESOLUTION NUMBER: 23 </div>
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APPROVED AS AMENDED SOURCE: COMMITTEE ON WILDLIFE AND CAPTIVE WILDLIFE </div>
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SUBJECT MATTER: Annual Reporting on Chronic Wasting Disease Epidemiological Data </div>
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BACKGROUND INFORMATION: Chronic wasting disease (CWD) has been recognized in wild cervids since the 1980’s. Availability of complete epidemiological information is critical for evaluating the effectiveness of science-based disease control programs. Access to pertinent information from epidemiological investigations across the country in wild populations is imperative to developing success strategies for managing the disease. More comprehensive information is needed on CWD epidemiology in the affected wild populations. Analysis of data from CWD affected populations across the country will improve risk assessment. Comprehensive epidemiological data evaluation may potentially identify factors contributing to the detection of CWD, enhance mitigation strategies to reduce the likelihood of CWD in new populations, and facilitate its earliest detection when it is present. </div>
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RESOLUTION: The United States Animal Health Association (USAHA) requests the United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service, Veterinary Services and other appropriate federal and state agencies to work cooperatively to assemble, analyze, summarize, and make available annually to the Committee on Wildlife and Captive Wildlife at the USAHA meeting all pertinent information from epidemiological investigations of Chronic Wasting Disease (CWD) in cervid populations (including wild, free-ranging, and captive). </div>
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Specific information requested may include: </div>
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1) Compiled CWD testing data from each state to include: </div>
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a) Overall state testing numbers of each susceptible species tested; </div>
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b) Number of CWD positive tests found annually in each state; </div>
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c) Overall state testing in wild populations; </div>
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d) Prevalence of CWD in positive populations; </div>
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e) Population totals for each susceptible species of wild herds in each state; </div>
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f) Demography of positive and negative animals in infected herds; </div>
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g) Results from all tissues that were tested; </div>
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h) Duration of monitoring prior to detection of the first case - including numbers of animals in the herd, numbers tested, and numbers not tested; </div>
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i) Results of trace-forward and trace-back investigations; and </div>
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j) All other pertinent data that will enhance risk assessment of CWD in cervids and identification of effective mitigation measures. </div>
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<span style="font-size: x-small;">2) Compiled data should also be posted on the USDA website.</span><br />
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<a href="http://www.usaha.org/upload/Resolution/2017/Resolution_23_CWD_Data.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.usaha.org/upload/Resolution/2017/Resolution_23_CWD_Data.pdf</a><br />
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RESOLUTION NUMBER: 21 APPROVED SOURCE: COMMITTEE ON SHEEP, GOATS AND CAMELIDS SUBJECT MATTER: National Scrapie Eradication Program Funding </div>
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BACKGROUND INFORMATION: Due to the success of the cooperative National Scrapie Eradication Program, no new cases of scrapie have been identified in the United States (US) in the past 18 months. There are key components of the program that have been critical to this success and the effort to have the US be recognized internationally as free from scrapie, which would open new markets to US sheep and goat products. Surveillance and traceability are vital to this eradication program. Program use of sheep and goat official tags have demonstrated that official plastic tags are preferred over metal tags for readability and to reduce safety concerns. Funding for tags that are readable, acceptable to producers and efficient for regulators is essential to continue identification compliance and progress of the program. </div>
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<span style="font-size: 10pt;">RESOLUTION: The United States Animal Health Association urges the United States Secretary of Agriculture to request a congressional appropriation of five million additional dollars of new money to be added to the Equine, Cervid and Small Ruminant health line for the purpose of supporting Small Ruminant Health Programs to complete the eradication of scrapie and assure program success. It is vital that this new funding does not reduce other current United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services program funding lines. </span></div>
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<span style="font-size: 10pt;"><a href="http://www.usaha.org/upload/Resolution/2017/Resolution_21_NSEP_Funding.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.usaha.org/upload/Resolution/2017/Resolution_21_NSEP_Funding.pdf</a></span></div>
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<a href="http://www.usaha.org/usaha-resolutions" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://www.usaha.org/usaha-resolutions</a></div>
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lol, drop in the bucket and a band-aid approach to something that needed a tourniquet decades ago...</div>
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TUESDAY, DECEMBER 12, 2017 </div>
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Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017</div>
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html</a></div>
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<span style="font-size: 13.3333px;">THURSDAY, FEBRUARY 15, 2018 </span></div>
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<span style="font-size: 13.3333px;">Iatrogenic Creutzfeldt-Jakob disease with Amyloid-β pathology: an international study</span></div>
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2018/02/iatrogenic-creutzfeldt-jakob-disease.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2018/02/iatrogenic-creutzfeldt-jakob-disease.html</a></div>
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<span style="font-family: "georgia"; font-size: 13px;">WEDNESDAY, NOVEMBER 1, 2017 </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<a href="http://betaamyloidcjd.blogspot.com/2017/11/blood-derived-amyloid-protein-induces.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://betaamyloidcjd.blogspot.com/2017/11/blood-derived-amyloid-protein-induces.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ??? </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">>>> The only tenable public line will be that "more research is required’’ <<< </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">>>> possibility on a transmissible prion remains open<<< </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]</span><br />
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<a href="https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf</a><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<a href="https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf</a><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<a href="https://web.archive.org/web/20040315075058/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20040315075058/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf</a><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">snip...see full Singeltary Nature comment here; </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<a href="http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments</a><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">see Singeltary comments to Plos ; </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">BSE101/1 0136 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">IN CONFIDENCE </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">CMO </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">From: . Dr J S Metiers DCMO 4 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">November 1992 </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify. </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. what are the implications for public health? </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed. 1 </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">92/11.4/1.1 </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">BSE101/1 0137 4. </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical. </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2 </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<a href="https://web.archive.org/web/20160320084827/http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">https://web.archive.org/web/20160320084827/http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf</a><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">>>> The only tenable public line will be that "more research is required’’ <<< </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">>>> possibility on a transmissible prion remains open<<< </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ? </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015) </span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">snip...see full Singeltary Nature comment here; </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Alzheimer's disease</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease... </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy</span><br />
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<a href="http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d</a><br />
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<a href="https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">*** Singeltary comment PLoS *** </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ? </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Posted by flounder on 05 Nov 2014 at 21:27 GMT </span><br />
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<a href="http://www.plosone.org/annotation/listThread.action?root=82860" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://www.plosone.org/annotation/listThread.action?root=82860</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">Ann N Y Acad Sci. 1982;396:131-43. </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease). </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC. </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Abstract </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD. </span><br />
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<a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1982.tb26849.x/abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1982.tb26849.x/abstract</a><span style="font-family: "georgia"; font-size: 13px;"> </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Sunday, November 22, 2015 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Abstract </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans. </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00 </span><br />
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<a href="http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20</a><span style="font-family: "georgia"; font-size: 13px;"> </span><br />
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<a href="http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html</a><span style="font-family: "georgia"; font-size: 13px;"> </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery *** </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. </span><br />
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<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract</a><span style="font-family: "georgia"; font-size: 13px;"> </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">2012 Singeltary on CJD and Alzheimer’s and iatrogenic threat</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Proposal ID: 29403</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Background</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both disease, and it’s variants, in many cases are merely names of the people that first discovered them. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer than the TSE prion disease. Symptoms are very similar, and pathology is very similar. I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. today, there is enough documented science (some confidential), that shows that indeed Alzheimer’s is transmissible. The risk factor for friendly fire, and or the pass-it-forward mode i.e. Iatrogenic transmission is a real threat, and one that needs to be addressed immediately.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Methods</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Results</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease. TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. the TSE prion agent also survives Simulated Wastewater Treatment Processes. IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. TSE prion agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.. it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Conclusions</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">There should be a Global Congressional Science round table event (one of scientist and doctors et al only, NO CORPORATE, POLITICIANS ALLOWED) set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics let science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already. what’s the use of science progressing human life to the century mark, if your brain does not work?</span><br />
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<a href="http://aaic.scsubmissions.com/index.aspx" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://aaic.scsubmissions.com/index.aspx</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">combined cannot exceed 350 Words</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">shortened to proper word count ;</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Background</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Methods</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Results</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Conclusions</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">end...tss</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">source references ...end...tss </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Hello Nicole,</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">by all means, please do use my poster. but I thought this was already taken care of, and I could not attend for my poster presentation, therefore, it was not going to be presented. I have some health issues and could not make the trip.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">please see old correspondence below...</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">From: Nicole Sanders Sent: Tuesday, April 10, 2012 5:37 PM To: Terry S. Singeltary Sr. Subject: RE: re-submission</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Dear Terry,</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">The decline of proposal number 30756 is registered in the system. Thank you for your consideration.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Best Regards,</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Nicole</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Nicole Sanders</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Senior Specialist, Membership & Conference Programming</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">______________________________________</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Diagnosis and Reporting of Creutzfeldt-Jakob Disease </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">To the Editor: </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally. </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Terry S. Singeltary, Sr Bacliff, Tex </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. </span><br />
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<a href="http://jama.jamanetwork.com/article.aspx?articleid=1031186" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://jama.jamanetwork.com/article.aspx?articleid=1031186</a><span style="font-family: "georgia"; font-size: 13px;"> </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">From: xxxx </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">To: Terry Singeltary </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Sent: Saturday, December 05, 2009 9:09 AM </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Your preliminary abstract number: 670</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Dear Mr. Singeltary,</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">On behalf of the Scientific Committee, I am pleased to inform you that your abstract</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.</span><br />
<br style="font-family: Georgia; font-size: 13px; line-height: 1.22em;" />
<span style="font-family: "georgia"; font-size: 13px;">Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Author: T. Singeltary; Bacliff, TX/US</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">This abstract has been ACCEPTED.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Authors: T. Singeltary; Bacliff, TX/US</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Body: Background</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Methods</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">12 years independent research of available data</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Results</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Conclusion</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">page 114 ;</span><br />
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<a href="http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf</a><br />
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<a href="http://www.isid.org/14th_icid/" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://www.isid.org/14th_icid/</a><br />
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<a href="http://www.isid.org/publications/ICID_Archive.shtml" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://www.isid.org/publications/ICID_Archive.shtml</a><br />
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<a href="http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">TUESDAY, DECEMBER 12, 2017 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017</span><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">Tuesday, December 12, 2017 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Neuropathology of iatrogenic Creutzfeldt–Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology</span><br />
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<a href="http://tauopathies.blogspot.com/2017/12/neuropathology-of-iatrogenic.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://tauopathies.blogspot.com/2017/12/neuropathology-of-iatrogenic.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">MONDAY, OCTOBER 02, 2017 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species</span><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/10/creutzfeldt-jakob-disease-united-states.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/10/creutzfeldt-jakob-disease-united-states.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">THURSDAY, AUGUST 17, 2017 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Singeltary et al</span><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/08/monitoring-occurrence-of-emerging-forms.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/08/monitoring-occurrence-of-emerging-forms.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">TUESDAY, AUGUST 03, 2010 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Here we go folks. AS predicted. THIS JUST OUT !</span><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html</a><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2013/10/coexistence-of-distinct-prion-types.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2013/10/coexistence-of-distinct-prion-types.html</a><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2010/09/agent-strain-variation-in-human-prion.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2010/09/agent-strain-variation-in-human-prion.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">Saturday, June 13, 2009</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009 </span><br />
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<a href="http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://cjdusa.blogspot.com/2009/06/monitoring-occurrence-of-emerging-forms.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">Sunday, August 09, 2009</span><br />
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<span style="font-family: "georgia"; font-size: 13px;">CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009 </span><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html</a></div>
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<span style="font-family: "georgia"; font-size: 13px;">THURSDAY, AUGUST 10, 2017 </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">*** Minimise transmission risk of CJD and vCJD in healthcare settings Updated 10 August 2017</span><br />
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<a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/08/minimise-transmission-risk-of-cjd-and.html" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/08/minimise-transmission-risk-of-cjd-and.html</a><br />
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<span style="font-family: "georgia"; font-size: 13px;">Diagnosis and Reporting of Creutzfeldt-Jakob Disease </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">To the Editor: </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally. </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">Terry S. Singeltary, Sr Bacliff, Tex </span><br />
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<span style="font-family: "georgia"; font-size: 13px;">1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. </span><br />
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<a href="http://jama.jamanetwork.com/article.aspx?articleid=1031186" rel="noopener noreferrer" style="color: blue; cursor: pointer; font-family: Verdana; font-size: 13px; line-height: 1.22em;" target="_blank">http://jama.jamanetwork.com/article.aspx?articleid=1031186</a></div>
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<span style="font-size: 13.3333px;">Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.</span></div>
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<span style="font-size: 13.3333px;">To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.</span></div>
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<span style="font-size: 13.3333px;">Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.</span></div>
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<span style="font-size: 13.3333px;">Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.</span></div>
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<span style="font-size: 13.3333px;">"Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."</span></div>
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<span style="font-size: 13.3333px;">Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.</span></div>
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<span style="font-size: 13.3333px;">Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.</span></div>
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<span style="font-size: 13.3333px;">CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited". </span></div>
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<a href="http://infection.thelancet.com/" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://infection.thelancet.com/</a></div>
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<a href="http://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(03)00715-1.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(03)00715-1.pdf</a></div>
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<span style="font-size: 13.3333px;">26 March 2003 </span></div>
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<span style="font-size: 13.3333px;">Terry S. Singeltary, retired (medically) CJD WATCH </span></div>
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<span style="font-size: 13.3333px;">I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? </span></div>
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<a href="http://www.neurology.org/content/60/2/176/reply#neurology_el_535" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neurology.org/content/60/2/176/reply#neurology_el_535</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">2 January 2000 British Medical Journal U.S. </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Scientist should be concerned with a CJD epidemic in the U.S., as well </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well</a></div>
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<br /></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">15 November 1999 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">British Medical Journal hvCJD in the USA * BSE in U.S. </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us</a></div>
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<br /></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">2001 FDA CJD TSE Prion Singeltary Submission</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">*** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html</a></div>
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<br /></div>
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PRION CONFERENCE REPORTS</div>
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<div style="font-size: 10pt;">
Thursday, December 1, 2016 </div>
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<div style="font-size: 10pt;">
PRION2017 DECIPHERING NEURODEGENERATIVE DISORDERS 23 – 26 May 2017 Edinburgh</div>
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<div style="font-size: 10pt;">
<a href="http://prionprp.blogspot.com/2016/12/prion2017-deciphering-neurodegenerative.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://prionprp.blogspot.com/2016/12/prion2017-deciphering-neurodegenerative.html</a></div>
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</div>
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<div style="font-size: 10pt;">
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress </div>
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<div style="font-size: 10pt;">
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 </div>
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<div style="font-size: 10pt;">
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen </div>
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This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. </div>
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Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. </div>
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At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. </div>
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<div style="font-size: 10pt;">
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS </div>
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Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO</div>
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<div style="font-size: 10pt;">
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS</div>
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<div style="font-size: 10pt;">
PRION 2017 CONFERENCE VIDEO</div>
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<a href="https://www.youtube.com/embed/Vtt1kAVDhDQ" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">https://www.youtube.com/embed/Vtt1kAVDhDQ</a></div>
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<br /></div>
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<a href="http://prion2017.org/programme/" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://prion2017.org/programme/</a></div>
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<div style="font-size: 10pt;">
Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?</div>
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<div style="font-size: 10pt;">
TUESDAY, JUNE 13, 2017</div>
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<div style="font-size: 10pt;">
PRION 2017 CONFERENCE </div>
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<div style="font-size: 10pt;">
ABSTRACT </div>
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<br /></div>
<div style="font-size: 10pt;">
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress</div>
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<br /></div>
<div style="font-size: 10pt;">
<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html</a></div>
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FRIDAY, JUNE 16, 2017</div>
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<br /></div>
<div style="font-size: 10pt;">
P55 Susceptibility of human prion protein to in vitro conversion by chronic wasting disease prions</div>
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<br /></div>
<div style="font-size: 10pt;">
<a href="http://chronic-wasting-disease.blogspot.com/2017/06/p55-susceptibility-of-human-prion.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/p55-susceptibility-of-human-prion.html</a></div>
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TUESDAY, JUNE 13, 2017</div>
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<div style="font-size: 10pt;">
PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD</div>
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<br /></div>
<div style="font-size: 10pt;">
<a href="http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html</a></div>
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<div style="font-size: 10pt;">
TUESDAY, JULY 04, 2017</div>
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<div style="font-size: 10pt;">
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***</div>
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<br /></div>
<div style="font-size: 10pt;">
<a href="http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html</a></div>
<div style="font-size: 10pt;">
<br /></div>
<div style="font-size: 10pt;">
PRION 2017 CONFERENCE ABSTRACT </div>
<div style="font-size: 10pt;">
<br /></div>
<div style="font-size: 10pt;">
P61 vCJD strain properties in a Spanish mother and son replicate as those of a young UK case</div>
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<br /></div>
<div style="font-size: 10pt;">
<a href="http://vcjd.blogspot.com/2017/06/prion-2017-conference-abstract-p61-vcjd.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://vcjd.blogspot.com/2017/06/prion-2017-conference-abstract-p61-vcjd.html</a></div>
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<br /></div>
<div>
<span style="font-size: 13.3333px;">TUESDAY, JUNE 20, 2017 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Prion 2017 Conference Transmissible prions in the skin of Creutzfeldt-Jakob disease patients</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://creutzfeldt-jakob-disease.blogspot.com/2017/06/prion-2017-conference-transmissible.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://creutzfeldt-jakob-disease.blogspot.com/2017/06/prion-2017-conference-transmissible.html</a></span></div>
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<br /></div>
<div style="font-size: 10pt;">
<div>
Wednesday, May 24, 2017 </div>
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<br /></div>
<div>
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1 </div>
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<div>
Subject: PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh</div>
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<br /></div>
<div>
*see archives of previous Prion Conferences, the ones that are still available, scroll down towards bottom in this link.</div>
<div>
<br /></div>
<div>
<a href="http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html</a></div>
</div>
</div>
</div>
<div style="font-size: 10pt;">
<br /></div>
<div>
<div>
<span style="font-size: 13.3333px;">MONDAY, MAY 02, 2016 </span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html</a></span></div>
<div>
<br /></div>
<div>
<a href="http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html</a></div>
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<br /></div>
<div>
<div>
<span style="font-size: 13.3333px;">ALSO SEE;</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.prions2016bcn.com/assets/abstract-book.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.prions2016bcn.com/assets/abstract-book.pdf</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION 2015</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/action/doSearch?AllField=PRION+2015&SeriesKey=kprn20" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/action/doSearch?AllField=PRION+2015&SeriesKey=kprn20</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1123372" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1123372</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29371" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29371</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION 2015 ORAL ABSTRACTS</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248?src=recsys" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1033248?src=recsys</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1033248?needAccess=true" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/pdf/10.1080/19336896.2015.1033248?needAccess=true</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1036655?src=recsys" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1036655?src=recsys</a></div>
<div>
<br /></div>
<div>
<div>
Saturday, May 30, 2015</div>
<div>
<br /></div>
<div>
PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS</div>
<div>
<br /></div>
<div>
<a href="http://transmissiblespongiformencephalopathy.blogspot.com/2015/05/prion-2015-oral-and-poster.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://transmissiblespongiformencephalopathy.blogspot.com/2015/05/prion-2015-oral-and-poster.html</a></div>
</div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION 2014</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29371?src=recsys" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29371?src=recsys</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29370?src=recsys" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29370?src=recsys</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29368?src=recsys" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29368?src=recsys</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.29365" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.29365</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION 2013</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://www.tandfonline.com/doi/pdf/10.4161/pri.26105?needAccess=true" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/pdf/10.4161/pri.26105?needAccess=true</a></span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION 2012</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.20605" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.20605</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.tandfonline.com/doi/abs/10.4161/pri.20615?src=recsys" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.tandfonline.com/doi/abs/10.4161/pri.20615?src=recsys</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION 2011</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Seven main threats for the future linked to prions</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">The NeuroPrion network has identified seven main threats for the future linked to prions.</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">First threat</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed. Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Second threat</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Third threat</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Fourth threat</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy, whereas other countries, including the US, Brazil, and Argentine do not have these constraints. However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Fifth threat</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">Sixth threat</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">Seventh Threat</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/en/np-neuroprion.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/en/np-neuroprion.html</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/en/np-news.html#63731832" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/en/np-news.html#63731832</a></div>
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<br /></div>
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<span style="font-size: 13.3333px;">PRION 2010</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2010/prion_2010_programme.pdf</a></div>
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<br /></div>
<div>
<a href="http://tandfonline.com/toc/kprn20/4/3?nav=tocList" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://tandfonline.com/toc/kprn20/4/3?nav=tocList</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">PRION 2009</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf</a></div>
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<br /></div>
<div>
<span style="font-size: 13.3333px;">PRION2008 BOOK OF ABSTRACTS</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdf</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/programme.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/programme.pdf</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">SUNDAY, NOVEMBER 23, 2008 </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<span style="font-size: 13.3333px;">PRION October 8th - 10th 2008 Book of Abstracts </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://bse-atypical.blogspot.com/2008/11/prion-october-8th-10th-2008-book-of.html</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION2007 NEWSLETTER</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
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<a href="http://www.neuroprion.org/en/np-event-prion-2007.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/en/np-event-prion-2007.html</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION2007 BOOK OF ABSTRACTS</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;"><a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf</a> </span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION2006 NEWSLETTER</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/newsletters/neuroprion-newsletter-prion-2006-special-issue.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/newsletters/neuroprion-newsletter-prion-2006-special-issue.pdf</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION2006 BOOK OF ABSTRACTS</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2006/abstract_book.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2006/abstract_book.pdf</a></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION2005 PRESS RELEASE</span></div>
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<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/pressrelease_eng.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/pressrelease_eng.pdf</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION2005 BOOK OF ABSTRACTS</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/abstract_book.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2005/abstract_book.pdf</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION2004 PRESS RELEASE</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/dossier_de_presse.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/dossier_de_presse.pdf</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<span style="font-size: 13.3333px;">PRION2004 BOOK OF ABSTRACTS</span></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/abstract_book.pdf" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/resources/pdf_docs/conferences/prion2004/abstract_book.pdf</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://tandfonline.com/loi/kprn20?open=1&year=2007&repitition=0#vol_1_2007" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://tandfonline.com/loi/kprn20?open=1&year=2007&repitition=0#vol_1_2007</a></div>
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<div>
<br /></div>
<div>
<div>
<div>
*see archives of previous Prion Conferences, the ones that are still available, scroll down towards bottom in this link.</div>
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<br /></div>
<div>
<a href="http://www.neuroprion.org/en/np-news.html#42417828" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.neuroprion.org/en/np-news.html#42417828</a></div>
<div>
<span style="font-size: 13.3333px;"><br /></span></div>
<div>
<a href="http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html</a></div>
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<div>
<span style="font-size: 13.3333px;"><br /></span></div>
</div>
</div>
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<span style="font-size: 10pt;">i do not advertise or make money from this, these blogs of tse prion science are for educational use. when i started to try and figure all this out was back in 1997, and the only available science for the lay public was from </span></div>
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<br /></div>
<div style="font-size: 10pt;">
<a href="http://mad-cow.org/" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://mad-cow.org/</a> </div>
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<br /></div>
<div style="font-size: 10pt;">
and </div>
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<br /></div>
<div style="font-size: 10pt;">
<a href="http://www.mad-cow.org/00/archive_frame.html" rel="noopener noreferrer" style="color: #0096ef; cursor: pointer; text-decoration-line: none;" target="_blank">http://www.mad-cow.org/00/archive_frame.html</a> </div>
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<br /></div>
<div style="font-size: 10pt;">
God Bless Dr. Tom Pringle. </div>
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<span style="font-size: 10pt;"><br /></span></div>
<div style="font-size: 10pt;">
<span style="font-size: 10pt;">SO, i made a promise back then, i just made a promise to mom dod 12/14/97 confirmed Heidenhain Variant of Creutzfeldt Jakob Disease, never forget, and never let them forget.</span></div>
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<span style="font-size: 10pt;"><br /></span></div>
<div style="font-size: 10pt;">
<span style="font-size: 10pt;">this science on the tse prion should be made easy for the lay public to educate on the transmissible spongiform encephalopathy tse prion disease aka mad cow type disease.</span></div>
<div style="font-size: 10pt;">
<br /></div>
<div style="font-size: 10pt;">
wasted days and wasted nights...Freddy Fender</div>
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<span style="font-family: "arial"; font-size: x-small;"><br style="color: #191919; font-family: Verdana, Arial, sans-serif; font-size: 14px;" /><span style="color: #191919; font-family: "verdana" , "arial" , sans-serif; font-size: 14px;">Terry S. Singeltary Sr.</span></span></div>
<div class="aolmail_aolmail_aolmail_aolReplacedBody">
<span style="font-family: "arial"; font-size: x-small;"><span style="color: #191919; font-family: "verdana" , "arial" , sans-serif; font-size: 14px;">Bacliff, Texas USA 77518</span></span></div>
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<span style="font-family: "arial"; font-size: x-small;"><span style="color: #191919; font-family: "verdana" , "arial" , sans-serif; font-size: 14px;"><<a href="mailto:flounder9@verizon.net" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">flounder9@verizon.net</a>></span></span></div>
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<span style="font-family: "arial"; font-size: x-small;"><span style="color: #191919; font-family: "verdana" , "arial" , sans-serif; font-size: 14px;"><br /></span></span></div>
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Terry S. Singeltary Sr.http://www.blogger.com/profile/06986622967539963260noreply@blogger.com0