Tuesday, August 11, 2015

Why Has the Federal Government Cut Funding for Chronic Wasting Disease Research?

 August 7, 2015


Why Has the Federal Government Cut Funding for Chronic Wasting Disease Research?


by Craig Dougherty 13


 Photograph by USFWS


Ask any deer biologist to list the top threats to the future of deer and deer hunting and you can be almost certain that Chronic Wasting Disease (CWD) will be somewhere near the top. CWD is the always-fatal deer disease that has been steadily spreading across the country. Twenty-two states and two provinces are now reporting outbreaks of chronic wasting disease. In some states, like New York, it is but a blip on the radar. In other states, like Wisconsin, it is leaving an ever-growing and very large footprint. Small blip or large footprint, the threat of CWD sends chills down the spine of professional deer managers. So why has the federal government cut funding to fight this disease?


 *2012 and 2013 numbers are estimates as no amount was specifically identified for CWD. 2015 total is aslo an estimate. Data is from Bryan Richards, USGS.


Bryan Richards, Emerging Disease Coordinator at the USGS National Wildlife Center, offered this perspective on CWD research: “With the outbreak of CWD in Wisconsin, the USDA declared CWD a national emergency. In 2002 Congress began to appropriate large amounts of monies to states for research. At first we were worried that CWD would spread to humans, so we spent money on humans, and then we shifted our attention to cattle. The US government was appropriating over $18 million per year in the early 2000s for research. Now we are seeing appropriations in the range of $1 million to $3 million per year for CWD. With humans and cattle no longer a concern, the funding has all but disappeared.”


The other experts and researchers I spoke to did not know of any other major federal funding sources for CWD research. They said it was now mostly up to the state budgets to fund CWD prevention and research.


Yet chronic wasting disease continues to spread, and little by little consume the backbone of the hunting industry (i.e. whitetail deer). “It’s as though we have CWD fatigue,” said Richards. But the problem persists, and if anything, it’s getting worse.


Dr. David Clausen, a veterinarian, former Chair of the Wisconsin Department of Natural Resources Board and well-respected CWD expert recently gave a presentation that pointed out that the number of deer tested for CWD in Wisconsin has declined drastically even though CWD has increased exponentially. He cites budgetary reasons for the decline. But even more alarming was his contention that the worst may lie just ahead. He cited recent research from Colorado State University, which indicates that plants will take up prions from infected earth, (where prions can live almost indefinitely) and now CWD prions are found to bind on grains and other plants. As far as research goes, according to Clausen, some excellent institutions are still doing research but, “as the science of CWD continues to evolve. It raises more questions than it answers and points to the need for more research.”


The Great Unknown


I recently did some research on how states are attempting to control the spread of CWD. For the most part, they are trying to isolate and eliminate known carriers of CWD. They have instituted all kinds of restrictions, which appear primarily preventative in nature. And who can blame them? Who among them wants to be the one known to ignore the threat of CWD? The deeper I dug into the issue, the more I learned about what we know and more to the point, what we think we know about the disease. Now I’m the one with chills running down my spine. State agencies are making all kinds of decisions on best guesses and and leaps of faith. Even the Chronic Wasting Alliance is forced to admit how little we actually know: “It is not completely understood how CWD is spread.”


This has lead to a standoff of sorts between the various factions of the deer community. I made a list of what the best research scientists in the country believe we actually know about CWD and compared it to a list of what we sort of know about CWD. The sort-of-know list was a whole lot longer. That’s right, all things considered we don’t know all that much about CWD.


The more I dug, the madder I got. Not because we don’t know all that much about CWD, but it almost looks like we have given up figuring this thing out. Or, at least the federal government has given up on it. If we are going to have deer to hunt 50 years from now, we need some answers and we need them fast. Answers come from good research and research takes both time and money.


Science moves slowly and by all accounts this is tough science. But, it is also science that is critical to our deer hunting future. Take a look at the graph above. Congress channeled CWD funds through the USDA. Experts are calling for increased CWD research but policy makers and politicians continue to ignore their calls. Funds for CWD research averaged a little over $18.5 million from 2004-2006 then started to steadily drop. They are now hovering around $2.0 million (2012 – 2014).


Where has our federal government gone? Has it pulled the plug on the disease that many believe has the potential to all but wipe out our deer herds?


As someone who loves whitetail deer, I think that federal funding for CWD research is not something that we can afford to cut. Maybe it’s time that hunters start demanding that our government takes up the battle against CWD once again.




>>> Why Has the Federal Government Cut Funding for Chronic Wasting Disease Research? <<<


same reason with all the other TSE prion disease in all the other species and humans in the USA, they have lost control of this slow and long incubating disease, which once clinical, is 100 % fatal, and will not admit it due to the many industries and lies there from it will curtail, from the dead and dying. for something they say is not here, why fund it then. don’t believe me, just think back to asbestos and tobacco. just saying.


>>> Bryan Richards, emerging disease coordinator at the USGS National Wildlife Center, suggested that "with humans and cattle no longer a concern, the funding has all but disappeared." <<<


LOL...with sad tears in my eyes, if they only knew.


who gives a damn about the truth right $$$


what is the truth anyway, or does anyone care anymore.


mom dod 12/14/97 confirmed hvCJD...just made a promise to mom, never forget, and never let them forget. ...carry on///


20097 Section Contents Menu Recalls, Market Withdrawals, & Safety Alerts8


Archive for Recalls, Market Withdrawals & Safety Alerts9 200910 Recall -- Firm Press Release .


Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease


Contact: Exotic Meats USA 1-800-680-4375


FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah’s Ark Processors LLC.


Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease found in elk and deer. The disease is caused by an abnormally shaped protein called a prion, which can damage the brain and nerves of animals in the deer family. Currently, it is believed that the prion responsible for causing CWD in deer and elk is not capable of infecting humans who eat deer or elk contaminated with the prion, but the observation of animal-to-human transmission of other prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has raised a theoretical concern regarding the transmission of CWD from deer or elk to humans. At the present time, FDA believes the risk of becoming ill from eating CWD-positive elk or deer meat is remote. However, FDA strongly advises consumers to return the product to the place of purchase, rather than disposing of it themselves, due to environmental concerns.



Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.



now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”


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




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: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV




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.




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


snip... full text ;





*** 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).***





*** 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.









Zoonotic Potential of CWD Prions


Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA


Chronic wasting disease (CWD) is a widespread and expanding prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern. Current literature generated with in vitro methods and in vivo animal models (transgenic mice, macaques and squirrel monkeys) reports conflicting results. The susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. In our earlier bioassay experiments using several humanized transgenic mouse lines, we detected protease-resistant PrPSc in the spleen of two out of 140 mice that were intracerebrally inoculated with natural CWD isolates, but PrPSc was not detected in the brain of the same mice. Secondary passages with such PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient prion transmission with clear clinical and pathological signs in both humanized and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD isolates in a new humanized transgenic mouse line led to clinical prion infection in 2 out of 20 mice.


*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.




P.105: RT-QuIC models trans-species prion transmission


Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA


***This insinuates that, at the level of protein: protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.




P.157: Uptake of prions into plants


Christopher Johnson1, Christina Carlson1, Matthew Keating1,2, Nicole Gibbs1, Haeyoon Chang1, Jamie Wiepz1, and Joel Pedersen1 1USGS National Wildlife Health Center; Madison, WI USA; 2University of Wisconsin - Madison; Madison, WI USA


 ***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.







*** P.126: Successful transmission of chronic wasting disease (CWD) into mice over-expressing bovine prion protein (TgSB3985)


Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1 1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA


Keywords: chronic wasting disease, transmission, transgenic mouse, bovine prion protein


Background. CWD is a disease affecting wild and farmraised cervids in North America. Epidemiological studies provide no evidence of CWD transmission to humans. Multiple attempts have failed to infect transgenic mice expressing human PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal human PrPC in vitro provides additional evidence that transmission of CWD to humans cannot be easily achieved. However, a concern about the risk of CWD transmission to humans still exists. This study aimed to establish and characterize an experimental model of CWD in TgSB3985 mice with the following attempt of transmission to TgHu mice.


Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse (CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD) or elk (CWD/Elk). Animals were observed for clinical signs of neurological disease and were euthanized when moribund. Brains and spleens were removed from all mice for PrPCWD detection by Western blotting (WB). A histological analysis of brains from selected animals was performed: brains were scored for the severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain regions.


Results. Clinical presentation was consistent with TSE. More than 90% of TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres in the brain but only mice in the latter group carried PrPCWD in their spleens. We found evidence for co-existence or divergence of two CWD/ Tga20 strains based on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen by WB. However, on neuropathological examination we found presence of amyloid plaques that stained positive for PrPCWD in three CWD/WTD- and two CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and CWD/Elkinfected mice were similar but unique as compared to profiles of BSE, BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM mice tested positive for PrPCWD by WB or by immunohistochemical detection.


Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.






CWD to cattle figures CORRECTION




I believe the statement and quote below is incorrect ;


"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."


Please see ;


Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.



" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "


shouldn't this be corrected, 86% is NOT a low rate. ...


kindest regards,


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518


Thank you!


Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.



re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations


1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu



Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures.





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


From: David Colby To: flounder9@verizon.net


Cc: stanley@XXXXXXXX


Sent: Tuesday, March 01, 2011 8:25 AM


Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations


Dear Terry Singeltary,


Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor Department of Chemical Engineering University of Delaware










Sunday, August 19, 2012


Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012





Thursday, November 21, 2013


*** Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy


The present study was designed to assess the susceptibility of the prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species barriers. Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a 90-100% attack rates, BSE from cattle failed to transmit, indicating agent adaptation in the deer.



Thus far, among domestic animals, CWDmd has been transmitted by the intracerebral route to a goat18 and cattle.5–7 The present findings demonstrate that it is also possible to transmit CWDmd agent to sheep via the intracerebral route.


Preliminary studies (Hamir et al., unpublished data, 2006) of intracerebral inoculation of CWD from white-tailed deer into cattle suggests that this source is much more efficient at causing disease (as indicated by the attack rate) than CWDmd.



these cattle ranchers supporting these shooting pens, if there are any, could be in terrible shape if a strain of cwd was to jump to cattle...just saying.


Title: Transmission of Chronic Wasting Disease of Mule Deer to Suffolk Sheep Following Intracerebral Inoculation




item Hamir, Amirali item Kunkle, Robert item Cutlip, Randall - ARS RETIRED item Miller, Janice - ARS RETIRED item Williams, Elizabeth - UNIVERSITY OF WYOMING item Richt, Juergen


Submitted to: Conference Research Workers Disease Meeting Publication Type: Abstract Only Publication Acceptance Date: December 3, 2006 Publication Date: December 3, 2006 Citation: Hamir, A.N., Kunkle, R.A., Cutlip, R.C., Miller, J.M., Williams, E.S., Richt, J.A. 2006. Transmission of chronic wasting disease of mule deer to Suffolk sheep following intracerebral inoculation [abstract]. Conference of Research Workers in Animal Diseases 87th Annual Meeting. Paper No. P34. p. 108.


Technical Abstract: To determine the transmissibility of chronic wasting disease (CWD) to sheep, 8 Suffolk lambs of various prion protein (PRNP) genotype (4 ARQ/ARR, 3 ARQ/ARQ, 1 ARQ/VRQ at codons 136, 154 and 171, respectively) were inoculated intracerebrally with brain suspension from mule deer with CWD (CWD**md). Two other lambs were kept as non inoculated controls. Within 36 months post inoculation (MPI), 2 inoculated animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in this sheep and its tissues were positive for the abnormal prion protein (PrP**res) by immunohistochemistry and Western blot. Three other inoculated sheep were euthanized (36 to 60 MPI) because of conditions unrelated to TSE. The 3 remaining inoculated sheep and the 2 control sheep were non clinical at the termination of the study (72 MPI) and were euthanized. One of the 3 remaining inoculated sheep revealed SE and its tissues were positive for PrP**res. The sheep with clinical prion disease (euthanized at 35 MPI) was of the heterozygous genotype (ARQ/VRQ) and the sheep with the sub clinical disease (euthanized at 72 MPI) was of the homozygous ARQ/ARQ genotype. These findings demonstrate that transmission of the CWD**md agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a significant part in successful transmission and incubation period of CWD**md.


Last Modified: 11/6/2014



I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...




In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.


***However, this recommendation is guidance and not a requirement by law.




31 Jan 2015 at 20:14 GMT


*** Ruminant feed ban for cervids in the United States? ***


Singeltary et al


31 Jan 2015 at 20:14 GMT



*** 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).




Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...


Table 9 presents the results of an analysis of these data.


There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).


Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.


There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).


*** 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).




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).




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. ...




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 ;



Saturday, May 30, 2015






***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.


Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.







The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.


RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.





For Immediate Release Thursday, October 2, 2014


Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov


*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease


DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).



*** see history of this CWD blunder here ;



On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.



The overall incidence of clinical CWD in white-tailed deer was 82%


Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)



*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.




the cwd tse prion aka mad cow type disease is not your normal pathogen.


The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.


you cannot cook the TSE prion disease out of meat.


you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.


Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.


the TSE prion agent also survives Simulated Wastewater Treatment Processes.


IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.


you can bury it and it will not go away.


The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.


it’s not your ordinary pathogen you can just cook it out and be done with. that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.


New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication


NOW, here is the most frightening aspect of all this, is the proven secondhand transmission, i.e. pass if forward mode, via iatrogenic (medical, surgical, dental, blood, tissue). you may never eat meat, but go to a hospital near you, it’s a proven risk factor, our hospitals have been exposed. I have countless articles on hospitals DEAR JOHN mad cow letters i.e. you have been exposed via surgery).


Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.


Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.


Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.


Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.





The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.



Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production


Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.



Detection of protease-resistant cervid prion protein in water from a CWD-endemic area


The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.



A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing


Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE


In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.





*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***


Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3



Longitudinal Detection of Prion Shedding in Saliva and Urine by CWD-Infected Deer by RT-QuIC


Davin M. Henderson1, Nathaniel D. Denkers1, Clare E. Hoover1, Nina Garbino1, Candace K. Mathiason1 and Edward A. Hoover1# + Author Affiliations


1Prion Research Center, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523 ABSTRACT Chronic Wasting Disease (CWD) is an emergent, rapidly spreading prion disease of cervids. Shedding of infectious prions in saliva and urine is thought to be an important factor in CWD transmission. To help elucidate this issue, we applied an in vitro amplification assay to determine the onset, duration, and magnitude of prion shedding in longitudinally collected saliva and urine samples from CWD-exposed white-tailed deer. We detected prion shedding as early as 3 months after CWD exposure and sustained shedding throughout the disease course. We estimated that a 50% lethal dose (LD50) for cervidized transgenic mice would be contained in 1 ml of infected deer saliva or 10 ml or urine. Given the average course of infection and daily production of these body fluids, an infected deer would shed thousands of prion infectious dosesover the course of CWD infection. The direct and indirect environmental impact of this magnitude of prion shedding for cervid and non-cervid species is surely significant.


Importance: Chronic wasting disease (CWD) is an emerging and uniformly fatal prion disease affecting free ranging deer and elk and now recognized in 22 United States and 2 C anadian Provinces. It is unique among prion diseases in that it is transmitted naturally though wild populations. A major hypothesis for CWD's florid spread is that prions are shed in excreta and transmitted via direct or indirect environmental contact. Here we use a rapid in vitro assay to show that infectious doses of CWD prions are in fact shed throughout the multi-year disease course in deer. This finding is an important advance in assessing the risks posed by shed CWD prions to animals as well as humans.




↵#To whom correspondence should be addressed: Edward A. Hoover, Prion Research Center, Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, Colorado, US Email: edward.hoover@colostate.edu



98 | Veterinary Record | January 24, 2015




Scrapie: a particularly persistent pathogen


Cristina Acín


Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’


From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).


Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.


Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.


The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).


In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.


Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).


In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.


The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).


Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).


So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?


What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.






98 | Veterinary Record | January 24, 2015



Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination


Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C. Maddison, BSc, PhD3 + Author Affiliations


1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and chronic wasting disease of deer/elk are contagious prion diseases where environmental reservoirs are directly implicated in the transmission of disease. In this study, the effectiveness of recommended scrapie farm decontamination regimens was evaluated by a sheep bioassay using buildings naturally contaminated with scrapie. Pens within a farm building were treated with either 20,000 parts per million free chorine solution for one hour or were treated with the same but were followed by painting and full re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue. All animals became infected over an 18-month period, even in the pen that had been subject to the most stringent decontamination process. These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.






Thorough pressure washing of a pen had no effect on the amount of bioavailable scrapie infectivity (pen B). The routine removal of prions from surfaces within a laboratory setting is treatment for a minimum of one hour with 20,000 ppm free chlorine, a method originally based on the use of brain macerates from infected rodents to evaluate the effectiveness of decontamination (Kimberlin and others 1983). Further studies have also investigated the effectiveness of hypochlorite disinfection of metal surfaces to simulate the decontamination of surgical devices within a hospital setting. Such treatments with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous treatment of the pen surfaces did not effectively remove the levels of scrapie infectivity over that of the control pens, indicating that this method of decontamination is not effective within a farm setting. This may be due to the high level of biological matrix that is present upon surfaces within the farm environment, which may reduce the amount of free chlorine available to inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had also became scrapie positive within nine months, with all animals in this pen being RAMALT positive by 18 months of age. Pen D was no further away from the control pen (pen A) than any of the other pens within this barn. Localised hot spots of infectivity may be present within scrapie-contaminated environments, but it is unlikely that pen D area had an amount of scrapie contamination that was significantly different than the other areas within this building. Similarly, there were no differences in how the biosecurity of pen D was maintained, or how this pen was ventilated compared with the other pens. This observation, perhaps, indicates the slower kinetics of disease uptake within this pen and is consistent with a more thorough prion removal and recontamination. These observations may also account for the presence of inadvertent scrapie cases within other studies, where despite stringent biosecurity, control animals have become scrapie positive during challenge studies using barns that also housed scrapie-affected animals (Ryder and others 2009). The bioassay data indicate that the exposure of the sheep to a farm environment after decontamination efforts thought to be effective in removing scrapie is sufficient for the animals to become infected with scrapie. The main exposure routes within this scenario are likely to be via the oral route, during feeding and drinking, and respiratory and conjunctival routes. It has been demonstrated that scrapie infectivity can be efficiently transmitted via the nasal route in sheep (Hamir and others 2008), as is the case for CWD in both murine models and in white-tailed deer (Denkers and others 2010, 2013). Recently, it has also been demonstrated that CWD prions presented as dust when bound to the soil mineral montmorillonite can be infectious via the nasal route (Nichols and others 2013). When considering pens C and D, the actual source of the infectious agent in the pens is not known, it is possible that biologically relevant levels of prion survive on surfaces during the decontamination regimen (pen C). With the use of galvanising and painting (pen D) covering and sealing the surface of the pen, it is possible that scrapie material recontaminated the pens by the movement of infectious prions contained within dusts originating from other parts of the barn that were not decontaminated or from other areas of the farm.


Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity. This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.


The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.


Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014



Monday, November 3, 2014


Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination





Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie


Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK


Key words: scrapie, evironmental persistence, sPMCA


Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.



Friday, December 14, 2012


DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012




In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.


Animals considered at high risk for CWD include:


1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and


2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.


Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.


The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.


Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.


There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.




36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.




The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).




In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.




In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.




Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.





Friday, December 14, 2012


DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012



I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...




In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.


***However, this recommendation is guidance and not a requirement by law.




31 Jan 2015 at 20:14 GMT


*** Ruminant feed ban for cervids in the United States? ***


Singeltary et al


31 Jan 2015 at 20:14 GMT




Article Citation: (2015)




Journal of Wildlife Diseases In-Press. doi: http://dx.doi.org/10.7589/2014-12-284


Ahead of Print




Chris Geremia1,6,7 Jennifer A. Hoeting2, Lisa L. Wolfe3, Nathan L. Galloway4, Michael F. Antolin4, Terry R. Spraker5, Michael W. Miller3, and N. Thompson Hobbs1


1 Natural Resource Ecology Laboratory, Graduate Degree Program in Ecology, Colorado State University, Fort Collins, Colorado, 80523-1499, USA


2 Department of Statistics, Colorado State University, Fort Collins, Colorado 80523, USA


3 Colorado Division of Parks and Wildlife, Wildlife Health Program, 4330 Laporte Avenue, Fort Collins, Colorado 80521, USA


4 Department of Biology, Colorado State University, Fort Collins, Colorado 80523-1878, USA


5 Colorado State University Diagnostics Laboratory, Colorado State University, Fort Collins, Colorado 80523, USA


Key words: Bayesian, capture–mark–recapture, chronic wasting disease, mule deer, prion, test sensitivity




Biopsy of rectal-mucosa associated lymphoid tissue provides a useful, but imperfect, live-animal test for chronic wasting disease (CWD) in mule deer (Odocoileus hemionus). It is difficult and expensive to complete these tests on free-ranging animals, and wildlife health managers will benefit from methods that can accommodate test results of varying quality. To this end, we developed a hierarchical Bayesian model to estimate the probability that an individual is infected based on test results. Our model was estimated with the use of data on 210 adult female mule deer repeatedly tested during 2010−2014. The ability to identify infected individuals correctly declined with age and may have been influenced by repeated biopsy. Fewer isolated lymphoid follicles (where PrPCWD accumulates) were obtained in biopsies of older deer and the proportion of follicles showing PrPCWD was reduced. A deer’s genotype in the prion gene (PRNP) also influenced detection. At least five follicles were needed in a biopsy to assure a 95% accurate test in PRNP genotype 225SS deer.


Received: December 15, 2014; Accepted: April 23, 2015


6 Current address: Yellowstone Center for Resources, P.O. Box 168, Yellowstone National Park, Mammoth Hot Springs, Wyoming 82190, USA


7 Corresponding author (email: chris_geremia@nps.gov)




Friday, January 30, 2015


*** Scrapie: a particularly persistent pathogen ***



Wednesday, August 05, 2015


*** Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed cases to date ***


Just got off the phone with Christy Clevenger of Ohio


Ohio Department of Agriculture March 2012 – Present (3 years 6 months)Reynoldsburg, Ohio CWD program


Ms. Clevenger confirmed, to date, from the Yoder debacle, 1 confirmed case of CWD from the Hunting Preserve, 2 confirmed cases from the Breeding Farm, and 16 confirmed cases of CWD from the Breeder Depopulation, with a total to date of 19 cases of CWD in Ohio...





Saturday, July 18, 2015


CHARLES "SAM" JAMES, Columbia, Missouri, was charged in a one-count federal indictment for violations of the Lacey Act involved the sale of white-tailed deer transported in violation of Missouri and Florida law



Tuesday, November 27, 2012


Pennsylvania ‘Pink 23’ Adams County exposed CWD Escaped Deer shot, but where are the other escapees ?



Saturday, June 29, 2013





Louisiana Deer Quarantine



Tuesday, August 11, 2015


Wisconsin doing what it does best, procrastinating about CWD yet again thanks to Governor Walker





‘’I see no evidence whatsoever here for a genetic link. The numbers are statistically insignificant and co-housing in contaminated facilities would strongly predispose to this outcome.’’


‘’if the father did have a bad amino acid variant allele, it would be diluted to heterozygozity with a normal gene in the half the four descendants since the father never would have survived to breeding age with two bad copies. sort of like met/val at position 129 in humans with greatly lengthened incubation times if prnp is propagating at all. Mutations such as repeat expansion leading to positive dominant infection have not been documented in cervids.’’


On 09 08 15, at 9:09 AM, Terry S. Singeltary Sr. wrote: ‘’


cwd Texas and then there were 4?


genetic link ?


He said 42 deer have been killed and tested since July 28, and three additional positives were the result.


***He added that all four deer confirmed to have the disease were males from the same father, which leads him to believe the problem is genetic.









on my mothers grave, when I wrote up the ‘have you been thunderstruck’ about super ovulation, and what if? I had no clue about all this. hell, I had it in draft for a month. then a week or so later, bam.


it’s been like this all along Obi-Wan Kenobi.


every shooting pen owner in Texas are praying this familial cwd is the going thing now.


no link to sperm.


no link to super ovulation.


they sell those sperm straws like the meth heads and crack heads sell meth and crack.


genetic link with four deer in the same herd, same father ?


familial ?


sperm ?


super ovulation ?


what say ye master ?




Friday, August 07, 2015


Texas CWD Captive, and then there were 4 ?



Thursday, August 06, 2015





Tuesday, July 21, 2015


Texas CWD Medina County Herd Investigation Update July 16, 2015


• 66 Texas sites, 2 Mexico sites




Monday, August 10, 2015


*** Scientific Opinion on a request for a review of a scientific publication concerning the zoonotic potential of ovine scrapie prions



Thursday, July 24, 2014


*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations



Wednesday, July 15, 2015


*** Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?



Wednesday, July 29, 2015


Further characterisation of transmissible spongiform encephalopathy phenotypes after inoculation of cattle with two temporally separated sources of sheep scrapie from Great Britain



Wednesday, July 29, 2015


Porcine Prion Protein Amyloid or mad pig disease PSE



Monday, August 10, 2015


Detection and Quantification of beta-Amyloid, Pyroglutamyl A beta, and Tau in Aged Canines



Friday, August 7, 2015


Transgenic Mouse Bioassay: Evidence That Rabbits Are Susceptible to a Variety of Prion Isolates



Thursday, July 30, 2015


SCRAPIE USDA APHIS June 2015 Monthly Report



Tuesday, June 23, 2015


Report on the monitoring and testing of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in the EU in 2013 Final version 18 May 2015



Saturday, March 21, 2015


*** Canada and United States Creutzfeldt Jakob TSE Prion Disease Incidence Rates Increasing





Sunday, November 23, 2014


*** Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European ***


the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.



Sunday, December 14, 2014


*** ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report ***



Thursday, July 30, 2015


Professor Lacey believes sporadic CJD itself originates from a cattle infection number of cattle farmers falling victim to Creutzfeld-Jakob Disease is much too high to be mere chance




Tuesday, August 4, 2015


*** FDA U.S. Measures to Protect Against BSE aka MAD COW DISEASE ***




Thursday, July 30, 2015


*** Prion Disease Induces Alzheimer Disease-Like Neuropathologic Changes




Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease


Received July 24, 2014; Accepted September 16, 2014; Published November 3, 2014




*** Singeltary comment ;





Terry S. Singeltary Sr.


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