CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018

Discussion in 'Wildlife Diseases' started by terry, Jan 27, 2018.

  1. terry

    terry

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  2. otcarcher

    otcarcher

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  3. terry

    terry

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    What is sad is that cdc refuse to update science.

    > However, to date, no CWD infections have been reported in people.
    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

    LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$

    *** 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).***

    http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys

    http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true

    Molecular Barriers to Zoonotic Transmission of Prions

    *** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

    *** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.

    http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm

    TUESDAY, SEPTEMBER 12, 2017

    CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat

    http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html

    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.

    *** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

    ***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),

    ***is the third potentially zoonotic PD (with BSE and L-type BSE),

    ***thus questioning the origin of human sporadic cases.
    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.

    ===============

    ***thus questioning the origin of human sporadic cases***

    ===============

    ***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.

    ==============

    https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
     
  4. terry

    terry

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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. 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.

    http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

    http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

    PRION 2016 TOKYO

    Saturday, April 23, 2016

    SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
    Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
    Taylor & Francis

    Prion 2016 Animal Prion Disease Workshop Abstracts

    WS-01: Prion diseases in animals and zoonotic potential

    Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
    Natalia Fernandez-Borges a. and Alba Marin-Moreno a
    "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

    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.

    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.
    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.

    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. 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.

    http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

    why do we not want to do TSE transmission studies on chimpanzees $

    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.

    snip...

    R. BRADLEY

    https://web.archive.org/web/2017012...einquiry.gov.uk/files/yb/1990/09/23001001.pdf

    Title: Transmission of scrapie prions to primate after an extended silent incubation period)

    *** 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.

    *** 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.

    *** 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.

    http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
     
  5. otcarcher

    otcarcher

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    Flounder9, it's not just the CDC. The WHO (World Health Organization), and National Institute of Health, are not succumbing to this fear-mongering either. Warnings have been issued by them, which is exactly what you want.

    What better way to end hunting than to convince the general population that venison is unfit to eat? Isn't that right "Terry"? I mean, you spend an exorbitant amount of time in various hunting forums across the country with the same cut and paste posts. I think your motivations have become quite clear.
     
    Last edited: Jan 28, 2018
  6. otcarcher

    otcarcher

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    Just so everyone else is aware of the motivations......

    Terry has frequented multiple forums across the country under various names, at least until the forum catches on. He works in tandem with anti-meat, pro-vegetarian activist groups spreading sensationalist ideas and theories and completely ignores the scientific community when his outlandish claims are refuted by science. The MSF is just his next target audience for sensationalist ideas and unproven claims looking to convince hunters that venison is unsafe to eat.

    Considering this is a hunting and outdoors forum, these motivations should be taken seriously.
     
    jr28schalm and HUBBHUNTER2 like this.
  7. Luv2hunteup

    Luv2hunteup

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    I have not researched it. Which scientific organization advocates eating CWD contaminated meat?
     
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  8. stickbow shooter

    stickbow shooter

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    Link ?
     
    357Maximum likes this.
  9. otcarcher

    otcarcher

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    PM sent....
     
  10. GRUNDY

    GRUNDY

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    Just link it here so everyone can know if this Terry individual is blowing smoke with a anti hunting agenda.

    I've done alot of research of my own about CWD jumping to humans. It hasn't been officially documented, but there are a lot of possibilities. It can be done in a lab. There are also links to alzheimers and protein mutation. This could suggest that CWD may not immediately get ya, but could increase your risk of alzheimers.

    Consuming animals from a CWD infected population certainly carries a level of risk not seen before in MI.

    I know I can't help but think about it just a little when eating my allegan county doe...
     
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  11. otcarcher

    otcarcher

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    I have no interest in publicly destroying the man, but enough is enough. I've sent the links in private to Steve. He can decide for himself.
     
  12. Luv2hunteup

    Luv2hunteup

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    While we are waiting for that can you provide the link to which scientific organization is advocating eating CWD contaminated meat?
     
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  13. otcarcher

    otcarcher

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    I never said there was. Quite the opposite actually.

    What I said......

     
  14. terry

    terry

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    LOL!

    otcarcher, that's exactly what you wanted to do, and your now a coward for saying otherwise.

    nice try though.

    facts are;

    Subject: Mad Cow Fear Mongers, or Truth Tellers

    i just love it when folks are grasping for straws and fake news trying to cover up the truth. this old article has been proven so terribly wrong, and they just don't get it, still. every thing i said back then has come true...sadly.

    SO, just who are The Center for Consumer Freedom ;

    http://www.consumerfreedom.com/index.cfm

    https://www.consumerfreedom.com/articles/138-mad-cow-scaremongers/

    let's take a closer look shall we ;

    The Center for Consumer Freedom (CCF) (formerly called the "Guest Choice Network (GCN)") is a front group for the restaurant, alcohol and tobacco industries. It runs media campaigns which oppose the efforts of scientists, doctors, health advocates, environmentalists and groups like Mothers Against Drunk Driving, calling them "the Nanny Culture -- the growing fraternity of food cops, health care enforcers, anti-meat activists, and meddling bureaucrats who 'know what's best for you.'"

    CCF is registered as a tax-exempt, non-profit organization under the IRS code 501(c)(3). Its advisory board is comprised mainly of representatives from the restaurant, meat and alcoholic beverage industries.

    http://www.sourcewatch.org/index.php?title=Center_for_Consumer_Freedom

    http://en.wikipedia.org/wiki/Center_for_Consumer_Freedom

    snip...SEE FULL TEXT HERE ;

    http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html

    Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011

    http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html

    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.

    *** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

    ***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),

    ***is the third potentially zoonotic PD (with BSE and L-type BSE),

    ***thus questioning the origin of human sporadic cases.
    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.

    ===============

    ***thus questioning the origin of human sporadic cases***

    ===============

    ***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.

    ==============

    https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

    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. 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.
    http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

    http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

    continued
     
  15. terry

    terry

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    PRION 2016 TOKYO

    Saturday, April 23, 2016

    SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

    Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
    Taylor & Francis

    Prion 2016 Animal Prion Disease Workshop Abstracts

    WS-01: Prion diseases in animals and zoonotic potential

    Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
    Natalia Fernandez-Borges a. and Alba Marin-Moreno a
    "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

    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.

    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.
    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.
    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. 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.

    http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

    why do we not want to do TSE transmission studies on chimpanzees $

    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.

    snip...

    R. BRADLEY

    https://web.archive.org/web/2017012...einquiry.gov.uk/files/yb/1990/09/23001001.pdf

    Title: Transmission of scrapie prions to primate after an extended silent incubation period)

    *** 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.

    *** 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.

    *** 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.

    http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160

    continued