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post #1 of 5 (permalink) Old 02-03-2016, 01:10 PM Thread Starter
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Consuming a deer with CWD

Maybe this should be added to the Banning Scents thread but I was wondering what happens, or could happen, to a person who ate a deer that had CWD?
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post #2 of 5 (permalink) Old 02-03-2016, 03:43 PM
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Re: Consuming a deer with CWD

Quote:
Originally Posted by irishxc
Maybe this should be added to the Banning Scents thread but I was wondering what happens, or could happen, to a person who ate a deer that had CWD?
Currently they have no definitive evidence that eating the meat from a CWD positive deer can lead to a TSE disease in people. But, they also have no definitive evidence that it can't happen either.

There is a TSE disease that affects people known as Creutzfeldt-Jakob Disease. Some of those human TSE disease cases have involved people who ate a lot of deer meat while other have died of the disease with no known evidence of having eaten deer meat. It is known though that TSE diseases have crossed barriers in other species in the past.

Currently though no one has proven that CWD infected meat can cross over to a TSE disease in people or in any way be harmful they also tell you NOT to eat the meat from a CWD positive deer or any other deer that doesn't appear to be healthy.

Here is a link to a study on some of the human TSE barriers;

http://wwwnc.cdc.gov/eid/article/15/12/pdfs/09-0194.pdf

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post #3 of 5 (permalink) Old 02-03-2016, 10:03 PM
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Re: Consuming a deer with CWD

We probably have people here in PA who have consumed infected deer, hard to really tell. Probably no human exposure experiments going on. But when the first case is confirmed of a human getting it from eating deer , elk or what ever, then you will see hunter numbers drop drastically. The prions also are in plant tissue. Who knows maybe deer can get CWD by eating plants with prions. This CWD is worse than any other illness. It was not taken seriously enough and has spread around the country.
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post #4 of 5 (permalink) Old 02-04-2016, 02:15 PM
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Re: Consuming a deer with CWD

Quote:
Originally Posted by bpottorff
It was not taken seriously enough and has spread around the country.
I think it has been taken very seriously, it's just that even with all the research, doctors, biologist, game managers, researchers still know very little on what causes it.

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post #5 of 5 (permalink) Old 12-25-2016, 10:19 PM
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Quote:
Originally Posted by irishxc View Post
Maybe this should be added to the Banning Scents thread but I was wondering what happens, or could happen, to a person who ate a deer that had CWD?
only time will tell. but now that cwd has mutated into more than one strain, there are many scientist around the world very concerned about cwd zoonosis, and some say it might look like sporadic cjd. some might be interested in ;

*** WDA 2016 NEW YORK ***
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-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.
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-Student Presentations Session 2
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-The species barriers and public health threat of CWD and BSE prions
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-Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University
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-Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. 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. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD.
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Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
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http://www.wda2016.org/uploads/5/8/6...gs_low_res.pdf


PRION 2016 TOKYO
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Zoonotic Potential of CWD Prions: An Update
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Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6 1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. 4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, 2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
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Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.
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PRION 2016 TOKYO In Conjunction with Asia Pacific Prion Symposium 2016 PRION 2016 Tokyo Prion 2016
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http://prion2016.org/dl/newsletter_03.pdf
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Cervid to human prion transmission
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Kong, Qingzhong
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Case Western Reserve University, Cleveland, OH, United States
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Abstract
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Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that:
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(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
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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;
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(3) Reliable essays can be established to detect CWD infection in humans;and
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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.
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Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3.
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Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
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Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
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Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
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Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
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Funding Agency Agency National Institute of Health (NIH)
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Institute National Institute of Neurological Disorders and Stroke (NINDS)
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Type Research Project (R01)
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Project # 1R01NS088604-01A1
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Application # 9037884
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Cervid to human prion transmission - Qingzhong Kong

Monday, May 02, 2016
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*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
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Chronic Wasting Disease: Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo

Saturday, April 23, 2016
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PRION 2016 TOKYO
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Saturday, April 23, 2016
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-SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
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-Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
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Taylor & Francis
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Prion 2016 Animal Prion Disease Workshop Abstracts
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WS-01: Prion diseases in animals and zoonotic potential
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Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
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Natalia Fernandez-Borges a. and Alba Marin-Moreno a
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"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
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-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.
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-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.
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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.
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-Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with ef?ciency comparable to that of cattle BSE. While the ef?ciency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 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. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
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http://www.tandfonline.com/doi/abs/1...nalCode=kprn20
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-why do we not want to do TSE transmission studies on chimpanzees $
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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.
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-snip...
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-R. BRADLEY
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http://collections.europarchive.org/...9/23001001.pdf
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Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES-
-----------------------------
Location: Virus and Prion Research
-------------------------------
Title: Transmission of scrapie prions to primate after an extended silent incubation period)----------
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-*** 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.
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-*** 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.
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-*** 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.-
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http://www.ars.usda.gov/research/pub..._NO_115=313160
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
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Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
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SCRAPIE USA: SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article

Wednesday, December 21, 2016

TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH

Transmissible Spongiform Encephalopathy: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH --

Thursday, December 08, 2016

USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie

SCRAPIE USA: USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie

SCRAPIE USA: Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

Chronic Wasting Disease: Chronic Wasting Disease CWD cervids interspecies transmission
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kind regards, terry
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