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DNR view of CWD

Discussion in 'Wildlife Diseases' started by Joe Archer, Jan 8, 2016.

  1. Joe Archer

    Joe Archer Staff Member Mods

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    Since I refer to this literature on a semi-regular basis I am posting it as a sticky to aid in the understanding of the current science on CWD.
    From http://www.michigan.gov/documents/e...ngencyPlan_2012Update_FinalDraft_391020_7.pdf

    Guiding principles drawn from the current state of the science
    1
    . CWD is an infectious prion disease, and claims to the contrary are not scientifically credible.
    2. CWD is transmitted between animals by direct contact with infectious saliva, respiratory aerosols, urine, and feces. Infected animals are infectious for other animals before they appear sick. Infected animals inevitably succumb, although the amount of time that takes to happen can vary from months to years.
    3. CWD is also transmitted indirectly from contaminated items in the environment such as soils where it persists for decades. Where the disease becomes established, environmental contamination likely drives CWD outbreaks perpetually, and may be the most critical factor limiting their control. Substantial environmental contamination with CWD may effectively define the threshold for when the disease is 'established'.
    4. There is essentially no evidence that CWD can infect humans. While recognizing that some members of the public may perceive it as a risk, management of CWD need not assume it is a substantial threat to human health.
    5. As CWD prevalence and perceived threats to human health increase, abandonment of hunting in infected areas may seriously limit the most practical approaches by which agencies may control the disease and deer populations, and have a potentially catastrophic impact on hunter recruitment.
    6. The public supports lethal management to control wildlife disease when that control achieves desired ends. Non-hunters are largely unconcerned with CWD and its management. Hunters are mainly concerned with the effect of CWD on deer hunting and the safety of venison for human consumption.
    7. CWD surveillance based solely on testing of hunter-harvested cervids has a low probability of detecting the disease, and may not be representative of the broader population. By the time cervids with clinical disease are detected, the prevalence of CWD in the population is likely to be over 1 %, and the disease already effectively established.
    8. Effective CWD management relies on preventing establishment of the disease in the first place. Once CWD is established in an area, all methods tried to date have failed to eradicate the disease. Current evidence suggests that in those Michigan Surveillance and Response Plan for CWD of Free-ranging and Privately owned Cervids, Rev. July 18, 2012 3 situations, cervid density reduction is no longer likely to be helpful. Nonetheless, density reductions in surrounding areas may help limit geographic spread.
    9. Density reductions should target entire family groups (does and their fawns) to minimize the probability of disease persistence, and yearling bucks to minimize the probability of disease spread via dispersal. Hunter harvest decisions depend most heavily on personal attitudes and are relatively unaffected by agency educational efforts. For these reasons, agency culling is likely to be more effective for controlling CWD than hunter harvest.
    10. Management practices that increase biological carrying capacity (such as supplemental feeding by humans) may cause CWD to persist and spread, just as they do with other diseases such as bovine tuberculosis. Alternative strategies for allowing supplemental feeding to continue in a restricted manner do not mitigate the potential for CWD transmission.
    11. Once established, CWD outbreaks (and the substantial costs of their management) can be expected to last for decades.
    <----<<<
     
  2. back40

    back40

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    can this information (dated 1/8/16) be considered current?
     

  3. terry

    terry

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    i would say it is extremely wrong or extremely out of date here ;

    4. There is essentially no evidence that CWD can infect humans. While recognizing that some members of the public may perceive it as a risk, management of CWD need not assume it is a substantial threat to human health.


    see once again;

    2017

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

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

    Chronic Wasting Disease (CWD)

    Prevention

    If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people.

    Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat.

    Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD.

    To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD:

    Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD.

    Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)

    https://www.cdc.gov/prions/cwd/prevention.html

    > 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

    2017 PRION CONFERENCE

    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

    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

    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.

    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.

    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.

    PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS

    Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO

    PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS

    *** PRION 2017 CONFERENCE VIDEO



    http://prion2017.org/programme/

    TUESDAY, JUNE 13, 2017

    PRION 2017 CONFERENCE ABSTRACT

    First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

    http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html

    TUESDAY, JULY 04, 2017

    *** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***

    http://chronic-wasting-disease.blogspot.com/2017/07/prion-2017-conference-abstracts-on.html

    TUESDAY, JUNE 13, 2017

    PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD

    http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-chronic.html

    Wednesday, May 24, 2017

    PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1

    http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html

    SATURDAY, JULY 29, 2017

    Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC

    http://chronic-wasting-disease.blogspot.com/2017/07/risk-advisory-opinion-potential-human.html


    kind regards, terry
     
  4. terry

    terry

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    2015

    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

    Tuesday, December 16, 2014

    *** Evidence for zoonotic potential of ovine scrapie prions

    Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics

    Abstract

    Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE.

    ***The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans.

    ***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

    Subject terms: Biological sciences• Medical research At a glance

    http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html

    see more here ;

    http://www.nature.com/ncomms/2014/141216/ncomms6821/extref/ncomms6821-s1.pdf

    ***The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans.***

    ***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.***

    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