DNR view of CWD

Discussion in 'Whitetail Deer Disease' started by Joe Archer, Jan 8, 2016.

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  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 Banned

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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 Banned

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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
     
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  5. terry

    terry Banned

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    *** WDA 2016 NEW YORK ***

    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.

    Student Presentations Session 2

    The species barriers and public health threat of CWD and BSE prions

    Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University

    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.

    Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders

    http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf

    From: TSS (216-119-163-189.ipset45.wt.net)

    Subject: CWD aka MAD DEER/ELK TO HUMANS ???

    Date: September 30, 2002 at 7:06 am PST

    From: "Belay, Ermias"

    To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

    Sent: Monday, September 30, 2002 9:22 AM

    Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

    Dear Sir/Madam,

    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.

    Ermias Belay, M.D. Centers for Disease Control and Prevention

    -----Original Message-----

    From: Sent: Sunday, September 29, 2002 10:15 AM

    To: [email protected]; [email protected]; [email protected]

    Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

    Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

    Thursday, April 03, 2008

    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.

    snip...

    *** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

    snip... full text ;

    http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html

    I urge everyone to watch this video closely...terry

    *** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***

    https://histodb11.usz.ch/Images/videos/video-004/video-004.html

    *** 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.

    http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf

    BSE INQUIRY

    *** 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). ***

    *** There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

    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).

    snip...

    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).

    snip...

    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. ...

    snip...

    ***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)

    snip...see full report ;

    https://web.archive.org/web/2017012...einquiry.gov.uk/files/yb/1994/08/00004001.pdf

    you can see more evidence here ;

    http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html


    kind regards, terry
     
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  6. terry

    terry Banned

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    Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque

    ''On secondary and tertiary transmissions, however, the proportion of PrPres positive animals gradually increased to almost 100%.

    ''Recent communications suggest that a similar situation might exist in other models of experimental exposure to prions involving swine32 and cattle33.''

    ''Experimental transfusion of variant CJD-infected blood reveals previously uncharacterised prion disorder in mice and macaque''

    http://vcjd.blogspot.com/2017/11/experimental-transfusion-of-variant-cjd.html

    i am thinking of that 10,000,000 POUNDS OF BLOOD LACED MEAT AND BONE MEAL IN COMMERCE WARNING LETTER back in 2007, see;

    SATURDAY, NOVEMBER 4, 2017

    FDA 589.2000, Section 21 C.F.R. Animal Proteins Prohibited in Ruminant Feed WARNING Letters and FEED MILL VIOLATIONS OBSERVATIONS 2017 to 2006

    http://bovineprp.blogspot.com/2017/11/fda-5892000-section-21-cfr-animal.html

    FRIDAY, NOVEMBER 3, 2017

    BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW

    ''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.''

    IN CONFIDENCE

    http://madcowfeed.blogspot.com/2017/11/bse-mad-cow-tse-prion-disease-pet-food.html


    kind regards, terry
     
  7. motdean

    motdean

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    Can I ask your background?

    By the way thanks for taking the time to post all of this. I haven't read it all, but am as I can.

    Dean
     
  8. terry

    terry Banned

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    December 14, 1997 my mother died from heidenhain variant creutzfeldt Jakob disease hvCJD confirmed. About 12 14 weeks from 1st onset of clinical symptoms to death. She did everything Linda Blair did in the exercists, except spin her head 360 degrees. Just to have our fine federal officials tell me it was not here, all a spontaneous event. My reply back today would be the same. Bullsh!t. Since then, pretty much everything I said back in 1997 have come to pass. Wish I had been wrong. In short, just made a promise to mom, never forget, and never let them forget. ..
     
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  9. ridgewalker

    ridgewalker

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    Terry, I believe that more of us would read your information if you could put it into a synopsis. The above posts, as are some others by you, are a long technical read. I believe that you sincerely want to pass helpful information to us and I am just trying to make a suggestion that would get the most folks on here reading it.
     
  10. terry

    terry Banned

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    yes sir, i get that from some folks, but then i have others that want the science. then you have the ones that say my posts are too long. i thought by posting a short sentence or two and then posting the science in blogs (no advertisements and have made no money from them, just for education), i thought that would work. but then you have folks that says it's junk science coming from blogs, claiming i am sitting here in my tin foil hat making this stuff up. bottom line, it does not matter what i say, it's the science, show me the transmission studies, i have said that from day one, show me the science. i think that what folks need. the old science that was, and what has happened along the way, all of it, to the latest science. then they can make their own minds up, without just taking my word for it...or not.

    kind regards, terry
     
  11. motdean

    motdean

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    My condolences. Sincerely.

    Again, thanks for joining the conversation.

    Dean
     
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  12. 357Maximum

    357Maximum Banned

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    Short and concise is your desire? WE ARE SCREWED, when is the only question, not if.............. there ya go.
     
  13. Waif

    Waif

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    I read that quite a while back where mentioned on a link.
    To present information in an unbiased manner is not easy ,but you cover the bases by showing your sources well enough.
     
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  14. ridgewalker

    ridgewalker

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    Thank you for your reply. I agree that it is impossible to please everyone. As one that some scientists have said that I have a prion disease, PD, I do appreciate your efforts. I do not know what to believe or not to believe about my circumstances but I often do feel like a lab rat. :)
     
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  15. bioactive

    bioactive Tornado Jim Premium Member

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    Of course you can please everyone. Post a short synopsis with a link for those who want more detail. Or confuse the hell out of people with too many words, and a potpourri of real science (published, peer reviewed data) and goofy, unsubstantiated stuff from websites and the lay press.
     
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