Follow Ups | Post Followup | Back to Discussion Board | VegSource
See spam or
inappropriate posts?
Please let us know.

From: TSS ()
Subject: Re: Wyoming Feedgrounds Double as CWD Time Bomb
Date: November 4, 2005 at 9:32 am PST

In Reply to: Wyoming Feedgrounds Double as CWD Time Bomb posted by TSS on November 3, 2005 at 7:02 pm:

Chronic wasting disease moves west
Casper Star Tribune November 3, 2005

LANDER -- State and now tribal game managers have detected three new cases of chronic wasting disease, a fatal brain disease that can affect all members of Wyoming’s deer family. The new locations north and west of Thermopolis. The disease had not previously been detected in this area. “We’re always concerned when we have a geographic expansion of this disease,” said Terry Cleveland, director of the Wyoming Game and Fish Department.

Well, duh , how about closing down your 23 elk winter feedlots in Wyoming -- another year or two and this disease is really going to explode out of the feedlots into Yellowstone and Grant Tetons Natl Parks.

The Ten Biggest Lies in CWD:

1- "CWD occurs naturally at a low background level in wild animals." [All CWD to date -- including zoo and game farm -- traces back to the original scrapie sheep-to-deer transmission at CDOW Foothills Research Station in 1967. No natural prion disease has ever been found in any animal species anywhere in the world, outside of human.]

2- "CWD does not transmit to human, so hunters are not at risk." [Too soon to say, TSEs can have 50 year incubations. No test -- no one knows how to distinguish CWD in human from sporadic CJDs. Epidemiology has poor power. Preclinical cases can propagate without species barrier via blood and tissue donation. Same was said about mad cow disease, wrongly as it turned out.]

3- "I've hunted for years in the CWD hot zone, eaten brain sausage, and I feel great, therefore it must be ok." [Needs no comment, too stupid, yet 2 WY and 1 CO researcher have said this repeatedly to Denver Post.]

4- "The deer I shot tested negative, so no problem." [Preclinical animals may be *more* infectious than overtly sick animals because of higher prion abundance in more commonly eaten tissues. Game processors commonly pool 100 animals prior to a rendering run; there is no effective way to decontaminate equipment between batches. False negatives are quite common when only obex is used. Hunters commonly sever the spinal cord without wearing Biohazard Level III clothing.]

5- "Absence of evidence is evidence of absence" [Needs no comment, too stupid, yet most common spin put out to journalists by CDC, Colorado officials.]

6- "CWD is restricted to cervids; a species barrier prevents transmission to bears, wolves, wolverines, cougars, livestock etc." [If you don't look, you don't find: zero testing has been on predators and scavengers, other than preliminary cougar and raccoon work. Species barriers are initial inefficiencies, not absolute; second and later passages are highly efficient.]

7- "Trust me, I'm an expert." [Few officials have read or understood the 7028 published papers on prion disease. Few veterinarians and epidemiologists are trained in protein chemistry and molecular biology, the realm of prion disease.]

8- "You can test your way out of this disease." [Facilities like game farms become hopelessly contaminated; culling clinically ill animals is too late; live animal tests are difficult and not sufficiently sensitive.]

9- "CWD is self-limited to the Tri-State area because of natural selection." [Animals with CWD can reach reproductive age before dying; migrations cover huge areas; game farm trafficking is effectively unregulated; escapes, releases, entrapment of wild animals and rut breakin are common.]

10-- "There's scientific uncertainty about transmission mechanisms, so nothing can be done about CWD in the wild." [Containment facilities are notorious for high incidence of CWD; artifically high winter densities -- the govt runs 23 huge elk feedlots in Wyoming -- mimic game farms and research facilities. The Grand Teton feedlots could be closed and elk dispersed.]

Possible CWD Surprises (over next year or two):

-- A live animal blood test might be approved. If sufficiently sensitive (no false negatives, esp. animals early on in infection), animal roundups for testing might be presented as an option. However, concentration of animals in a confinement facility such as winter feedlot would only result in further spread of CWD prior to ability to cull and incinerate infected animals.

-- Transmission to cows or sheep on public (or private) lands might be documented. This would bring calls for eradication of deer and elk or restriction to national parks, rather than allotment retirement. So far, experimental transmission to cattle has been difficult. Back transmission to sheep has not been tested. There are many evolving strains of CWD as each species has a unique prion protein sequence. Species barriers can change dramatically upon passage to a new species such as moose.

-- Transmission to humans might be proven. This could cause a plunge in out-fof-state hunting tags which in Colorado account fo over half the Fish and Game budget. Right now, CWD has no distinctive signature (unlike florid plaques of mad cow disease) that separates it from sporadic CJD. It is all but impossible to prove epidemiologically as hunters are hard to track over long incubation periods and often have other exposures such as decades of eating mutton or beef or UK visits. Asymptomatic hunters could spread the disease widely into non-hunters through blood donations, corneal transplants, endoscopes, root canals, etc.

What species have gotten CWD already? Note CWD has already passaged to carnivore and primate:

CWD-Donor CWD-Recipient Method Year
sheep white-tail deer shared pen at Foothills 1967+
sheep black-tail deer shared pen at Foothills 1967+
sheep mule deer shared pen at Foothills 1967+
sheep rocky mtn elk shared pen at Foothills 1967+
sheep rocky mtn elk intracerebral injection 2004
cervid moose unknown Colorado wild 2005
mule deer cow intracerebral injection 2001
white-tail cow in vitro conversion 2000
white-tail sheep in vitro conversion 2000
mule deer goat intracerebral injection 2001
mule deer sheep intracerebral injection 2001
white-tail human in vitro conversion 2000
mule deer squirrel monkey intracerebral injection 2005
white-tail ferret intracerebral injection 1998
ferret hamster intracerebral injection 1998
elk humanized mice intracerebral injection 2005*
elk elkized mice intracerebral injection 2005
mule deer muleized mice intracerebral injection 2004

*first passage negative, second passage underway

Abstracts for published scientific articles on CWD: PubMed using "chronic wasting disease" as search term. Also you can sign up for automatic email alerts there.

Extensive history of CWD: use 'advanced search' google restricted to url, Some great eat-more-rotten-venison-today newspaper quotes from CO and WY game and fish staffers. An email/phone directory to about 200 scientists working in prion disease can be found at

Some recent abstracts

Vet Rec. 2003 Jul 26;153(4):121-3. [no abstract, unclear if raccoon, another Carnivora, became infected]
Experimental inoculation of scrapie and chronic wasting disease agents in raccoons (Procyon lotor).
Hamir AN, Miller JM, Cutlip RC, Stack MJ, Chaplin MJ, Jenny AL, Williams ES.
National Animal Disease Center, ARS, USDA, 2300 Dayton Avenue, PO Box 70, Ames, IA 50010, USA.

PLOS Biology 2005: "Unlike BSE, CWD is not thought to be transmitted through feed. But three species of cervids are naturally susceptible, and the question arises of how many other species might be in danger. To help answer that question, Michael Samuel and colleagues at the University of Wisconsin are staking out deer carcasses to see which scavengers come to feed. With flashlit photography, they've discovered “an amazing cast of characters,” including hawks, owls, crows, dogs, cats, coyotes, raccoons, skunks, mink, foxes, and opossums (Figure 2). Mammalian scavengers in the state's CWD-affected region will later be examined for disease."

J Vet Diagn Invest. 2004 Jul;16(4):316-21. [cwd looks just like scrapie, no surprise given inadvertent transmission at Foothills Research Station]
Transmission of sheep scrapie to elk (Cervus elaphus nelsoni) by intracerebral inoculation: final outcome of the experiment.
Hamir AN, Miller JM, Cutlip RC, Kunkle RA, Jenny AL, Stack MJ, Chaplin MJ, Richt JA.
National Animal Disease Center, ARS, USDA, Ames, IA 50010, USA.

This is a final report of an experimental transmission of sheep scrapie agent by intracerebral inoculation to Rocky Mountain elk (Cervus elaphus nelsoni). It documents results obtained in experimental (n = 6) and control (n = 2) elk. During the first 2 years postinoculation (PI), 3 animals died or were euthanized because of infection or injuries other than spongiform encephalopathy (SE). In years 3 and 4 PI, 3 other inoculated elk died after brief terminal neurological episodes. Necropsy of these animals revealed moderate weight loss but no other gross lesions. Microscopically, characteristic lesions of SE were seen throughout the brain and spinal cord, and the tissue was positive for proteinase K-resistant prion protein (PrPres) by immunohistochemistry (IHC) and by Western blot. Scrapie-associated fibrils (SAF) were observed by negative-stain electron microscopy in the brain of elk with neurologic signs. PrPres and SAF were not detected in the 3 inoculated elk necropsied during the first 2 years or in the 2 control animals. Retrospective analysis of the gene-encoding cervid PrP revealed a polymorphism at codon 132. The elk with SE were either homozygous (MM) or heterozygous (LM). These findings confirm that intracerebral inoculation of sheep scrapie agent results in SE with accumulations of PrPres in the central nervous system of elk. Based on morphologic and IHC findings, the experimentally induced SE cannot be distinguished from chronic wasting disease of elk with currently available diagnostic techniques.

J Gen Virol. 2005 Aug;86(Pt 8):2127-34. [explores possible natural occurence of genetic resistance due to prion gene polymorphisms]
Low frequency of PrP genotype 225SF among free-ranging mule deer (Odocoileus hemionus) with chronic wasting disease.
Jewell JE, Conner MM, Wolfe LL, Miller MW, Williams ES.
Department of Veterinary Sciences, University of Wyoming, Wyoming State Veterinary Laboratory, Laramie, WY.

The prion protein (PrP) gene was characterized in 1482 free-ranging mule deer (Odocoileus hemionus) from Wyoming and Colorado. Using DNA sequences from 363 deer, dimorphisms at codons 20 (aspartate/glycine) and 225 [serine (S)/phenylalanine (F)] were found; silent changes occurred at codons 131 (tyrosine) and 247 (isoleucine). The remaining samples were surveyed for codon 225 genotype and all were characterized for chronic wasting disease (CWD) infection status. A total of 112 deer with the genotype 225SF or FF were found, of which one was CWD-positive; 1370 were 225SS, with 289 positive for CWD. Among CWD-negative deer, the frequency of 225SF/FF genotypes was 9.3 % but among CWD-positive deer it was only 0.3 %. For all samples combined, CWD status was not independent of codon 225 genotype (P<0.0001). The odds that a deer of the 225SS genotype was CWD-infected were 30 times greater (95 % confidence intervals=4-213) than for a 225SF deer. The proportion of 225SF animals in sampled subpopulations varied from 0 to 18 %; the CWD prevalence varied from 0 to 25 %. However, no relationship was observed between genotype frequency and CWD prevalence in different areas. The PrP sequences of experimentally infected mule deer were analysed from pre-existing projects and 10 animals were found with 225SF genotypes, all of which were positive for CWD. Data available from some of these animals suggest that the 225SF genotype could be associated with longer incubation periods in CWD infection compared with the 225SS genotype.

J Vet Diagn Invest. 2003 Jul;15(4):320-3. [O'Rourke monoclonal antibody can be used in highly inconvenient live test using tonsil biopsy]
Abundant PrP(CWD) in tonsil from mule deer with preclinical chronic wasting disease.
O'Rourke KI, Zhuang D, Lyda A, Gomez G, Williams ES, Tuo W, Miller MW.
Agricultural Research Service, U.S. Department of Agriculture Pullman, WA 99164, USA.

A monoclonal antibody dot-blot assay was used to evaluate detergent lysates of tonsil tissue from mule deer to detect PrP(CWD), the marker for the cervid transmissible spongiform encephalopathy chronic wasting disease (CWD). Samples of formalin-fixed brain and tonsil tissues from mule deer were examined for PrP(CWD) using immunohistochemistry (IHC) with Mab F99/97.6.1, the gold standard for diagnosis of preclinical CWD. The contralateral tonsil from each of the 143 deer was prepared for confirmatory IHC and as a 10% (wt/vol) detergent lysate without purification or enrichment steps for monoclonal antibody dot-blot assay. PrP(CWD) was detected by dot-blot assay in 49 of 50 samples considered positive by IHC. Forty-eight of the positive samples were evaluated with a quantitative dot-blot assay calibrated with recombinant PrP. Tonsillar PrP(CWD) concentrations ranged from 34 to 1,188 ng per 0.5 mg starting wet weight of tissue. The abundant PrP(CWD) in mule deer tonsil will facilitate development and validation of high-throughput screening tests for CWD in large populations of free-ranging deer.

J Vet Diagn Invest. 2003 May;15(3):274-7 [no transmission observed yet deer-to-cattle in the field]
Survey of cattle in northeast Colorado for evidence of chronic wasting disease: geographical and high-risk targeted sample.
Gould DH, Voss JL, Miller MW, Bachand AM, Cummings BA, Frank AA.
Department of Pathology, Veterinary Medicine and Biomedical Sciences, Colorado State University, Ft. Collins, CO.

A geographically targeted survey of potentially high-risk, adult cattle in chronic wasting disease (CWD)-endemic areas in Colorado was initiated to assess the possibility of the spread of CWD from deer to cattle under natural conditions. Surveyed cattle were sympatric with free-roaming deer in geographically defined areas where CWD occurs and where CWD prevalence has been estimated. To qualify for inclusion in the survey, cattle had to be at least 4 years old and had to have spent a minimum of 4 years in surveyed areas. Brains from culled cattle were examined microscopically and immunohistochemically for tissue alterations indicative of a transmissible spongiform encephalopathy (TSE). Two hundred sixty-two brains were suitable for evaluation and were found to lack changes indicative of a TSE infection. Prion deposition was not demonstrable using a method involving formic acid and proteinase-K treatment before application of monoclonal antibody to bovine prion protein (F99/97.6.1). Some incidental neuropathologic changes unrelated to those of TSEs were detected. Findings from this study suggest that large-scale spread of CWD from deer to cattle under natural range conditions in CWD-endemic areas of northeast Colorado is unlikely.

J Gen Virol. 2004 May;85(Pt 5):1339-46.
Polymorphisms in the prion precursor functional gene but not the pseudogene are associated with susceptibility to chronic wasting disease in white-tailed deer.
O'Rourke KI, Spraker TR, Hamburg LK, Besser TE, Brayton KA, Knowles DP.
US Department of Agriculture, Agricultural Research Service Pullman, WA 99164, USA.

Chronic wasting disease (CWD) status and PrP genotypes were determined for a group of 133 wild white-tailed deer in a 780 acre enclosure in western Nebraska, USA. Approximately half of the deer tested showed evidence of PrPd in the brainstem or lymphoid tissues. Four PRNP alleles encoding amino acid substitutions were identified, with substitutions at residues 95 (Q-->H), 96 (G-->S) or 116 (A-->G), each with serine (S) at residue 138. In addition, a processed pseudogene with two alleles encoding five or six copies of the octapeptide repeat was identified in 26 % of the deer. Both alleles encoded asparagine (N) at residue 138. The functional gene alleles sorted into five major diploid genotypes and four rare genotypes. Although all five major diploid genotypes were found in deer with CWD, unaffected deer were less likely to have the allele QGAS and more likely to have QSAS compared with CWD-affected deer. Late-stage disease (PrPd in brainstem) was noted in deer less than 1 year of age, although no single genotype was associated with this rapid neuroinvasion. Early-stage disease (PrPd distribution limited to the lymphoid system) was observed in deer estimated to be more than 5 years old, suggesting that they were infected as adults or that the incubation time might be extremely long in some individuals. The pseudogene was found in deer of all major PRNP genotypes and was not correlated with CWD status. The large number of susceptible genotypes and the possibility of adult-to-adult transmission suggest that much of the white-tailed deer population may be at risk for disease following exposure to CWD, despite the association of specific genotypes with CWD noted here.

Nature. 2003 Sep 4;425(6953):35-6. [incidence of cwd in confined herds becomes astronomic]
Prion disease: horizontal prion transmission in mule deer.
Miller MW, Williams ES.
Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, Colorado 80526, USA.

Epidemics of contagious prion diseases can be perpetuated by horizontal (animal to animal) and maternal (dam to offspring, before or after birth) transmission, but the relative importance of each mechanism is unclear. Here we compare the incidence of chronic wasting disease (CWD) in captive mule deer (Odocoileus hemionus) that is attributable to horizontal or maternal transmission. We find that horizontal transmission is remarkably efficient, producing a high incidence of disease (89%) in a cohort of deer in which maternal transmission was improbable. Our results indicate that horizontal transmission is likely to be important in sustaining CWD epidemics.

Vet Rec. 2004 Sep 4;155(10):295-302. [obex testing alone seriously understates actual cwd incidence]
Variable patterns of distribution of PrP(CWD) in the obex and cranial lymphoid tissues of Rocky Mountain elk (Cervus elaphus nelsoni) with subclinical chronic wasting disease.
Spraker TR, Balachandran A, Zhuang D, O'Rourke KI.
Colorado State University, Fort Collins, CO, USA.

Sections of medulla oblongata, taken at the level of the obex, palatine tonsil and medial retropharyngeal lymph node from 10,269 captive Rocky Mountain elk (Cervus elaphus nelsoni), were examined by immunohistochemical staining with monoclonal antibody for the prion protein associated with the transmissible spongiform encephalopathy of cervids, chronic wasting disease (PrP(CWD)). The protein was detected in 226 of them. On the basis of the anatomical location of the deposits in the brainstem of 183 elk, four distinct patterns of distribution of PrP(CWD) within the parasympathetic region of the dorsal motor nucleus of the vagus nerve and the adjacent nuclei were observed. Mild gross lesions of chronic wasting disease (serous atrophy of fat) were observed in only three elk, all with spongiform degeneration; the other elk were considered to be in the preclinical stage of the disease. In contrast with the relatively predictable distribution of prion protein (PrP) in the brain and cranial nodes of sheep and mule deer, the distribution of PrP(CWD) in the brain and nodes of the elk was more variable and unrelated to their PrP genotype. One hundred and fifty-five of the 226 positive elk had deposits of PrP(CWD) in the brainstem and lymphoid tissues, 43 had deposits only in the lymphoid tissue and 28 had deposits only in the brainstem. ...snip...end


Follow Ups:

Post a Followup

E-mail: (optional)


Optional Link URL:
Link Title:
Optional Image URL: