Thursday, February 09, 2012




Chronic Wasting Disease

The Federal Chronic Wasting Disease (CWD) herd-certification program for farmed cervids operations has been in development since late 2003. A CWD final rule was published in the Federal Register in 2006 but was not implemented in response to several petitions. The CWD rule was amended in 2010 following the publication of proposed changes. The amended rule will set minimum standards for interstate movement and establish the Federal CWD Herd Certification Program (HCP).

The Federal CWD HCP for farmed cervids is intended to be a cooperative State-Federal-industry program. The CWD program goals are to control CWD in farmed cervid herds and to encourage State and Tribal wildlife agencies to conduct CWD surveillance in wild cervids.

The number of farmed cervids tested for CWD has increased steadily since FY 2003 from approximately 12,000 animals tested to nearly 20,000 in FY 2010. From FY 1997 through FY 2010, CWD was identified in 37 farmed elk herds and 13 farmed white-tailed deer herds in 11 States (Table 3.2). Three new farmed cervid herds were found to have animals diagnosed as positive for CWD in 2010.

Table 3.2: Number of farmed cervid herds with animals positive for CWD by State,

FY 1997–FY 2010

State FY 1997–2010 FY 2010 ( FY 1997–2010)

Colorado 18 18

Kansas 1 1

Michigan 1 1

Minnesota 4 4

Missouri 1 1

Montana 1 1

Nebraska 5 5

New York 2 2

Oklahoma 1 1

South Dakota 7 7

Wisconsin 9 9

Total 49 1 50

Of the 50 CWD-positive herds identified as of September 30, 2010, 6 elk herds (all in Colorado) remained under State quarantine. One White-tailed deer herd in Missouri was identified as CWD positive in February 2010 and remained under State quarantine through 2010 pending depopulation.

Since 2002, most States have been participating in CWD surveillance in free-ranging deer, elk, and more recently, moose. By September 30, 2010, 13 States had reported detecting CWD in wild cervids (Colorado, Illinois, Kansas, Nebraska, North Dakota, New Mexico, New York, South Dakota, Utah, Virginia, West Virginia, Wisconsin, and Wyoming). From the 2002 through the 2010 hunting seasons, an approximate total of 773,400 hunter-harvested and targeted wild cervids were tested with an average of 95,600 samples each season (Figure 3.4). Wildlife surveillance strategies have also evolved over the years from broad active surveillance of hunter-harvested animals to targeted and weighted surveillance of wild cervids considered to be at greater risk of CWD (based on our knowledge and understanding of CWD transmission in those populations).

Figure 3.4: Surveillance testing of hunter-killed and targeted wildlife for CWD

U.S. Wild Cervid CWD Surveillance
(Reported to VS through 03/26/2010)

Friday, February 03, 2012

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

Saturday, February 04, 2012

Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

Thursday, February 09, 2012

Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al


Summary of Chronic Wasting Disease Workshop in Edmonton on Feb. 9-10, 2011

and Alberta’s CWD Update as of March 23, 2011

By Blair Rippin and Dr. Margo Pybus


Jurisdictional Summaries

! Dr. Michael Miller, Colorado Division of Wildlife

- CWD known in Colorado in captive cervids since 1967 and in wild cervids since early 1980s but intensive study done only since 2001.

- no evidence of occurrence in other domestic ruminants nor other wild mammals.

- prevalence high in many local mule deer populations.

- patterns of infections influenced by time since introduction, herd demographics, movement and congregation patterns, land use, soil characteristics, and management strategies.

- attempts to control or contain CWD deemed ineffective and abandoned, partly because of lack of public support.

- surveillance through directing hunt pressure and testing hunter kills continues.

Dr. Michael Samuel, Department of Forest and Wildlife Ecology, University of Wisconsin

- CWD identified in Wisconsin wild cervids in 2002 (white-tailed deer) but it’s estimated that it may have been there for 2 or 3 decades.

- early eradication attempts deemed ineffective and abandoned 3 years ago

- present management aimed only at containment through directing hunt pressure, testing and monitoring.

- spread estimated to be 2 -3 miles per year.

- genetic research indicates some evidence of developing resistence but it is a very slow to occur and estimated to take in the order of 200 years to make a difference.

Dr. Trent Bollinger, University of Saskatchewan

- CWD brought in from the US in late 1980s via imported game farm animals and now found in three populations of wild cervids.

- over the past decade CWD became wide spread in the province and occurs in both deer species and wild elk.

- containment efforts by directing hunt pressure have been unsuccessful and there is fear that caribou may become infected.

- management currently focused on tracking movements of the disease.

- considerable concern that if CWD crosses the species barrier (i.e. to domestic stock and/or humans) there will be far reaching negative economic and social consequences.

- largely depending on research to result in effective management programs.

Dr. Greg Douglas, Chief Veterinary Officer, Saskatchewan Ministry of Agriculture

- game farms and hunt farms involving 54,000 cervids is currently worth $60 million annually to Saskatchewans economy.

- described the challenges in efforts (mainly involving surveillance and culling) to eradicate CWD from Saskatchewan game farms via mechanisms to improve traceability, inventory, and surveillance.

Dr. Stephane McLachlan and Misty Potts-Sanderson, University of Manitoba

- CWD not present in Manitoba to date but is approaching from eastern Saskatchewan

- First Nations very concerned about “corralling” or “penning” (game farming) wild animals.

- considerable concern expressed about the decline in environmental quality from industrial sources and its effect on wildlife, indicating that CWD may be a symptom of a much larger problem.

- considerable concern expressed about the lack of effective communication between scientific community and First Nations.

Impacts of CWD presence on society

Dr. Vic Adamowicz, Department of Rural Economy, University of Alberta

- presented results of questionnaires designed to investigate how CWD affects recreational hunting.

- further work will determine the effects of CWD presence on the province’s economy.

- found awareness of CWD varied among societal cohorts, particularly urban/rural differences.

- CWD presence resulted in greater change in hunting venue among urban as opposed to rural dwellers.

Helen Cote-Quewezance, Cote First Nations, Saskatchewan

- outlined the importance of healthy wildlife to First Nations people in the form of sustenance, health, and spirituality.

- very concerned that CWD will likely degrade that aspect of aboriginal life.

- is willing to share knowledge with scientific community but asked for a forum that includes an effective understanding of aboriginal culture.

Dr. Ellen Goddard, et al, Department of Rural Economy, University of Alberta

- Canadians in general currently have a very limited understanding of CWD, however, it is somewhat greater than that of Americans.

- concern that CWD constitutes a significant human health risk is very low in both countries (i.e. much lower ranking than concerns about BSE or other known meat borne pathogens).

- Canadians support efforts to eradicate CWD much more than Americans.

Research initiatives

Dr. Michael Coulthart, et al, Public Health Agency of Canada

- although not occurring to date, he estimates that report of just one probable case of human CWD could trigger a public health crisis in North America.

- epidemiological studies so far indicate the probability is very slight, however, prion agents and their transmission properties are highly mutable and adaptable and the possibility can not be ruled out.

- suggests those involved in human prion disease surveillance should consider the possibility of human CWD and develop a readiness to deal with it.

Dr. Margit Westphal, McLaughlin Centre for Population Health Risk Assessment, University of Ottawa

- CWD identified in captive research animals in 1967 has now spread to 18 US states and 2 Canadian provinces in farmed and free ranging cervids.

- complicating development of an effective plan to combat CWD are the facts that it has a very long latency period, extended environmental persistence, and it lacks a quick and sensitive diagnostic anti-mortem test.

- “Effective management of CWD requires the development and application of an integrated risk management framework based on sound principles of risk assessment and management, and the harmonization of regulation that align trans-border management efforts”.

Judd Aikens et al, Centre for Protein Folding Diseases, University of Alberta

- have identified two prion protein gene variants in Alberta white-tailed deer that are linked to disease prolongation.

- implications could lead to possible development of resistence but would likely take a very long time.

Scott Adams and Scott Napper, University of Saskatchewan

- testing is currently underway to determine the effectiveness of a newly developed injectable CWD vaccine that has shown considerable promise.

- an effective vaccine could be used to prevent CWD in game farm animals but additional study would be required to determine an effective application method in the wild.

Conclusions drawn from the workshop presentations and discussions

CWD is a newly invasive and fatal neurodegenerative prion disease of cervids known in North America only since 1967 (45 years) and hosts have not had time to adapt. To date it is present in 18 US states and 2 Canadian provinces.

$ Attempts to eradicate CWD via intensive culling has generally proved to be ineffective except where infection is very recent. Evidence of recent timing of infection was shown in Alberta by lymph node positive but brain negative in tested specimens.

$ In wild cervids the two deer species are most commonly involved. Of those, mule deer are most heavily infected in western jurisdictions while in east-central states, where mule deer are absent, white-tails are the only host. Further, of the various cohorts, adult males are most commonly infected and regulations aimed at providing trophy antlers may be exacerbating efforts to control CWD prevalence and spread.

$ Culling by management agencies and/or by directing hunting pressure was shown to be ineffective in eradicating and even the in halting the spread of the disease.

$ Surveillance for prevalence and degree of spread via testing hunter-killed animals is currently the most common management method in practice. It has also been shown that public awareness, understanding, and attitudes are critical factors to consider when embarking on control activities.

$ Factors complicating the control or management of CWD are:

- CWD has a very long latency period.

- Currently the only tests for diagnosing CWD in living animals is to collect tonsil or rectal lymph biopsy tissues.

- Prions will bind with clay particles in soil and thus remain persistent in areas containing infected animals.

- Although there are some signs of developing immunity or resistence in hosts it will take very long time (i.e. > 200 years) to manifest itself.

-In infected foci, close relatedness appears to be a factor in increase prevalence, which could also result from mule deer being more gregarious and exhibiting clumping behavior, particularly during winter when CWD transmission is most likely to occur.

- Some mule deer are migratory, which further complicates CWD containment efforts.

$ CWD is slow to show population effects but with time it is predicted to result in significant reductions in density and distributions of ecologically, economically, socially important cervids in all jurisdictions with CWD infections.

Presently there are only speculative indications of CWD crossing species barrier but on the slim chance human CWD occurs, it is predicted there will be general public panic and adverse repercussions to recreational and First Nation’s use of cervids and subsequent negative effects on economies in several jurisdictions.

$ Social science is directing further effort into determining probable effects of CWD presence on public understanding, awareness, and attitudes toward control efforts and in turn how this may influence hunter behavior, food safety, and the economy.

Identified needs for future efforts to manage CWD


Chronic Wasting Disease (CWD) Surveillance Update: March 23, 2011

All heads of deer and elk received to date from the fall hunting seasons have been tested, although a few heads continue to dribble into the lab. Herein we provide the summary of the 2010 fall surveillance. However, the ongoing CWD Surveillance Program will continue to test heads whenever they are received throughout the year.

From September 1, 2010 to March 23, 2011 we tested 5062 heads (primarily deer heads) and detected nineteen (0.4%) new cases of CWD in wild deer in Alberta. Seventeen of the positive deer were mule deer: twelve males, five females The two remaining positive deer were white-tail males All positive deer were harvested by hunters and were in very good to excellent body condition.

All but one positive deer were adults. The remaining positive deer was a yearling in the early stages of infection.

Many of the infected deer were near previous known CWD cases, largely in the Battle River and Ribstone Creek drainages in the north and the Red Deer River drainage in the south.

A cluster of infected deer was found north and west of Dinosaur Provincial Park in WMU 152 – a significant extension of the disease westward along the Red Deer River.

Of particular significance, the positive yearling mule deer buck was the first case of CWD found in the North Saskatchewan River valley in Alberta. This is strong evidence of recent expansion of the disease into or within the valley.

As anticipated, additional infected deer were found in CFB Wainwright in association with the Battle River valley.

The 19 new hunter-kill cases are in addition to the road-kill case found in February 2010, thus the annual total for 2010 is 20 cases.

Ongoing NEGATIVE test results were posted to AlbertaRelm and made available to individual hunters. To date, approximately 50% of the test results have been read by the hunter.

Ongoing POSITIVE test results were provided by phone directly to the hunter who harvested the infected deer.

As in previous years, hunters who harvest a CWD-infected deer were given the options of

! keeping the meat

! turning in the meat and receiving a replacement licence for this year (if the season was still open where the infected deer was harvested)

! turning in the meat and receiving a replacement licence for next year for the same species and location as the infected deer

The total number of CWD cases detected in wild deer in Alberta since September 2005 is 94.

As part of the ongoing provincial surveillance program, we also are testing a random sample of emaciated cervids associated with severe winter conditions occurring in various parts of Alberta

To learn more about CWD in Alberta, visit:

Attention Hunters!

If you have frozen deer heads that you would like to submit to the ongoing CWD
surveillance program, please drop them off at any Fish and Wildlife office during
regular office hours. For more details, visit:

CWD Map and Statistics



snip...see full text ;

now, a few things to ponder about those said double fences that will supposedly stop those deer from escaping.

what about water that drains from any of these game farms. surrounding water tables etc., are the double fences going to stop the water from becoming contaminated? where does it drain? who's drinking it?

Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area


Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author-

Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.


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.

snip...end...full text at ;

what about rodents there from? 4 American rodents are susceptible to CWD to date. are those double fences going to stop these rodents from escaping these game farms once becoming exposed to CWD?

Chronic Wasting Disease Susceptibility of Four North American Rodents

Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email:

We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.

please see ;

Oral.29: Susceptibility of Domestic Cats to CWD Infection

Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author; Email:

Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature. Prion

Avian Scavengers as Vectors of Prion Disease—
Mechanisms for the spread of CWD in North American
deer and other cervids are not completely understood.
NWRC researchers hypothesize that avian
scavengers may play a role in translocating CWD in
the wild, potentially encountering CWD-infected
carcasses, consuming infected tissue, and transporting
it over long distances before depositing feces. In
a recent study, researchers inoculated 100 mice with
fecal extracts obtained from American crows (Corvus
brachyrhynchos) that were force-fed material infected
with mouse scrapie (PrPSc). These mice showed
severe neurological dysfunction 196 to 231 days post
inoculation and tested positive for PrPSc. These results
demonstrate that a common, migratory North American
scavenger can pass infective prions in feces and,
therefore, could play a role in the geographic spread
of CWD in the environment.

Distribution and Epizootiology of CWD in
Nebraska Deer—Western Nebraska is considered
part of the core endemic area of CWD, yet little is
known about prevalence rates or the factors affecting
the distribution of CWD in this area. NWRC
researchers used data on the occurrence of CWD
collected from 2000 to 2007 throughout Nebraska
to calculate prevalence rates and investigate
the role that key spatial, temporal, demographic,
and environmental factors have on the distribution
of this disease. Researchers conducted analyses
at two spatial scales, including the Panhandle
region of western Nebraska and Statewide.
Results show that the dynamics of CWD were
similar between the different spatial scales. CWD
was more prevalent in mule deer (Odocoileus
hemionus) than in white-tailed deer (Odocoileus
virginianus), in male deer than in female deer, and
in adult deer than in fawns. Overall prevalence has
increased from 0.3 to 1.4 percent in the Panhandle
and from 0.2 to 0.5 percent Statewide. The sex of
the animal and the interaction of latitude and longitude
had the most influence when predicting CWD
occurrence in Nebraska at both spatial scales. Age,
year collected, and soil texture were also predictors.
These results concur with studies conducted
in other areas of the CWD core endemic area, suggesting
that CWD dynamics are governed by similar
processes throughout the disease’s range.

Project Contact: Kurt VerCauteren


Sunday, November 01, 2009

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease

Monday, February 14, 2011



Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

Wednesday, October 14, 2009

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


Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

at least that’s my opinion. my intentions are NOT, and never has been to split up the hunters. it’s just been to inform them of the rest of the science. I cannot stress enough, it’s not just about you, and what you consume as hunters. I don’t care what you eat. but once you expose yourself to the TSE Prion via CWD infected deer and or elk, and then go have medical procedures done, surgical, dental, donate blood, tissue, etc., then you expose everybody with the TSE Prion disease. then it becomes everybody’s business. ...

kind regards, terry

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

Subject: Tracking spongiform encephalopathies in North America LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003

Date: Tue, 29 Jul 2003 17:35:30 –0500

From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy


Volume 3, Number 8 01 August 2003


Tracking spongiform encephalopathies in North America

Xavier Bosch

My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.

Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.


> he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. <

actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article.

Full Text

Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734.

2 January 2000

British Medical Journal

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

15 November 1999

British Medical Journal

vCJD in the USA * BSE in U.S.

Singeltary submission to PLOS ;

No competing interests declared.

see full text ;

Tuesday, November 08, 2011

Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011 Original Paper

Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.

Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***

14th ICID International Scientific Exchange Brochure -

Final Abstract Number: ISE.114

Session: International Scientific Exchange

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009

T. Singeltary

Bacliff, TX, USA


An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.


12 years independent research of available data


I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.


I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.


CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011

3. Final classification of 49 cases from 2009, 2010, 2011 is pending.


USA 2011


National Prion Disease Pathology Surveillance Center

Cases Examined1
(November 1, 2010)

Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

1996 & earlier 51 33 28 5 0 0

1997 114 68 59 9 0 0

1998 87 51 43 7 1 0

1999 121 73 65 8 0 0

2000 146 103 89 14 0 0

2001 209 119 109 10 0 0

2002 248 149 125 22 2 0

2003 274 176 137 39 0 0

2004 325 186 164 21 0 13

2005 344 194 157 36 1 0

2006 383 197 166 29 0 24

2007 377 214 187 27 0 0

2008 394 231 205 25 0 0

2009 425 258 215 43 0 0

2010 333 213 158 33 0 0

TOTAL 38315 22656 1907 328 4 3

1 Listed based on the year of death or, if not available, on year of referral;

2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;

3 Disease acquired in the United Kingdom;

4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;

5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.

I also urge you to again notice these disturbing factors in lines 5 and 6 ;

5 Includes 18 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.


Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)

(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)

THE steady rise of sporadic CJD cases in Canada AND USA, with many unusual cases of ''PENDING CLASSIFICATIONS" which have been pending now FOR 3 YEARS. HOW long can this cover-up continue $$$

The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.


Saturday, March 5, 2011


Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167


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.

NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

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 ;

From: TSS (


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

From: "Belay, Ermias"


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-----


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

To:;; ebb8@CDC.GOV


Sunday, November 10, 2002 6:26 PM




an oxymoron or what ???

To date, ongoing investigations by state and federal public health officials have shown no causal relationship between CWD and human health problems, for more information see CWD and Potential Transmission to Humans .

Monday, November 14, 2011

WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

Wednesday, November 16, 2011

Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

Sunday, November 13, 2011


PLEASE SEE THE LETTER THE British Deer Farmers Association October 1994


October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,


Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.


The Akron, Ohio-based CJD Foundation said the Center for Disease Control revised that number in October of 2004 to about one in 9,000 CJD cases per year in the population group age 55 and older.


if not, why not...

Friday, November 30, 2007





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