CWD Update 99
December 13, 2010
State and Provincial Updates
The following press release was issued on December 13, 2010 by the North Dakota Game & Fish Department
( http://gf.nd.gov/multimedia/news/2010/12/101204.html )
Another Deer from 3F2 Tests Positive for CWD
A mule deer taken in November during the deer gun season from unit 3F2 is the second deer in North Dakota to test positive for chronic wasting disease. The first was a mule deer taken during the hunting season in 2009, also from unit 3F2.
Dr. Dan Grove, North Dakota Game and Fish Department wildlife veterinarian, said a hunter shot a doe in western Grant County and submitted the head for testing as part of the hunter-harvested surveillance program.
"As a collaborative effort with South Dakota Game, Fish and Parks, and the Standing Rock Sioux Tribe Game and Fish Department, a total of 633 samples were collected from unit 3F2 this fall, and all but one tested negative for CWD," Grove said. "Although we hoped the one positive from 2009 was an isolated incident, it was not unexpected that another one surfaced."
The two deer testing positive for CWD were taken 10 miles from each other, which Grove said is not surprising because of the same general area.
"Hunter cooperation was tremendous," Grove said. "We can’t thank them enough, and we look forward to their continued support with this important issue in the future."
The hunter-harvested surveillance program annually collects samples taken from hunter-harvested deer in specific regions of the state. In addition to unit 3F2, samples during the 2010 deer gun season were collected from units in the eastern third of the state. The entire state has already been sampled twice.
"Michigan State University will be testing approximately 3,600 samples over the next several weeks from deer taken in the eastern third of the state," Grove said. "Those results should be available by spring."
In addition to hunter-harvested deer, the Game and Fish Department has a targeted surveillance program that is an ongoing, year-round effort that tests animals found dead or sick.
Since the department’s sampling efforts began in 2002, more than 16,000 deer, elk and moose have tested negative for CWD.
CWD affects the nervous system of members of the deer family and is always fatal. Scientists have found no evidence that CWD can be transmitted naturally to humans or livestock.
The following press release was issued on November 18, 2010 by the Wisconsin Department of Agriculture, Trade and Consumer Protection
( http://datcp.state.wi.us/press_release/result.jsp?prid=2574 )
CWD Tests Negative for Deer on Northwest Wisconsin Hunting Preserve
Contact: Donna Gilson
MADISON -- Final chronic wasting disease results are negative for a white-tailed deer on a northwestern Wisconsin hunting preserve, State Veterinarian Dr. Robert Ehlenfeldt announced today. This means the deer did not have CWD.
The National Veterinary Services Laboratories in Ames, Iowa, reported the test results late Tuesday. Ehlenfeldt released the quarantine that had been in place since Nov. 4 for the hunting preserve and an associated deer breeding farm.
NVSL pathologists ran tissue samples through what they described as "an exhaustive process using all diagnostic techniques available" and did not detect CWD.
The 3½-year-old buck was routinely tested after being killed by a hunter Oct. 18 in Bayfield County. Initial screening tests at the Wisconsin Veterinary Diagnostic Laboratory were reported positive on Nov. 4. Following standard procedure, WVDL sent the samples to the national laboratory for confirmation. Screening tests for any disease are deliberately over-sensitive, so they do sometimes yield false positives.
DATCP does not name owners or locations of CWD-suspect animals unless final test results are positive. However, the hunting preserve and farm in question has a long record of negative CWD results, with nearly 130 animals tested in the past five years. Animal health regulations in Wisconsin require that all farm-raised deer and elk 16 months and older, including those in hunting preserves, must be tested for CWD when they die or are killed. There is no live test for CWD.
To date, more than 27,600 farm-raised deer have been tested in Wisconsin. Of those, 97 were positive for CWD on eight farms and hunting preserves -- 82 on a single Portage County operation, where legal action delayed destruction of the herd for more than three years after the initial case was found. One of the infected animals was an elk, the rest have been white-tailed deer. All infected herds have been destroyed. There has not been a new case of CWD detected in a farm-raised animal for two years.
Rapid End-Point Quantitation of Prion Seeding Activity with Sensitivity Comparable to Bioassays
Jason M. Wilham, Christina D. Orrú, Richard A. Bessen, Ryuichiro Atarashi, Kazunori Sano, Brent Race, Kimberly D. Meade-White, Lara M. Taubner, Andrew Timmes, Byron Caughey.
PLoS Pathogens 6(12): e1001217. doi:10.1371/journal.ppat.1001217.
A major problem for the effective diagnosis and management of prion diseases is the lack of rapid high-throughput assays to measure low levels of prions. Such measurements have typically required prolonged bioassays in animals. Highly sensitive, but generally non-quantitative, prion detection methods have been developed based on prions' ability to seed the conversion of normally soluble protease-sensitive forms of prion protein to protease-resistant and/or amyloid fibrillar forms. Here we describe an approach for estimating the relative amount of prions using a new prion seeding assay called real-time quaking induced conversion assay (RT-QuIC). The underlying reaction blends aspects of the previously described quaking-induced conversion (QuIC) and amyloid seeding assay (ASA) methods and involves prion-seeded conversion of the alpha helix-rich form of bacterially expressed recombinant PrPC to a beta sheet-rich amyloid fibrillar form. The RT-QuIC is as sensitive as the animal bioassay, but can be accomplished in 2 days or less. Analogous to end-point dilution animal bioassays, this approach involves testing of serial dilutions of samples and statistically estimating the seeding dose (SD) giving positive responses in 50% of replicate reactions (SD50). Brain tissue from 263K scrapie-affected hamsters gave SD50 values of 1011-1012/g, making the RT-QuIC similar in sensitivity to end-point dilution bioassays. Analysis of bioassay-positive nasal lavages from hamsters affected with transmissible mink encephalopathy gave SD50 values of 103.5–105.7/ml, showing that nasal cavities release substantial prion infectivity that can be rapidly detected. Cerebral spinal fluid from 263K scrapie-affected hamsters contained prion SD50 values of 102.0–102.9/ml. RT-QuIC assay also discriminated deer chronic wasting disease and sheep scrapie brain samples from normal control samples. In principle, end-point dilution quantitation can be applied to many types of prion and amyloid seeding assays. End point dilution RT-QuIC provides a sensitive, rapid, quantitative, and high throughput assay of prion seeding activity.
The Interaction of Ruminant PrPSc with Soils Is Influenced by Prion Source and Soil Type
Ben C. Maddison, Jonathan P. Owen, Keith Bishop, George Shaw, Helen C. Rees, and Kevin C. Gouch.
Environmental Science and Technology 2010, 44, 8503–8508.
The persistence of prions within the environment is implicated in the horizontal transmission of ovine scrapie and cervid chronic wasting disease. Description of the interaction of prion strains derived from their natural hosts with a range of soil types is imperative in understanding how prions persist in the environment and, therefore, the characteristics of prion transmission. Here, we demonstrate that all detectable ovine scrapie and bovine BSE PrPSc bind to a range of soil types within 24 h. This highly efficient binding of prions to soils is characterized by truncation of desorbed PrPSc in a soil dependent manner, with clay-rich soils resulting in N-terminal truncation of the PrPSc and sand-rich soils yielding full length PrPSc species. PrPSc did not migrate through soil columns during incubation for up to 18 months, and for all combinations of soil and prion types, a decrease in recoverable PrPSc was seen over time. Persistence of PrPSc within soil and their interaction with soil particles of distinct sizes was dictated by both the soil type and the source of the prion, with ovine scrapie being apparently more persistent in some soils than cattle BSE. These data indicate that natural ruminant prion strains are stable in the soil environment for at least 18 months and that PrPSc-soil interaction is dictated by both the soil properties and the strain/host species of PrPSc.
Minor Oral Lesions Facilitate Transmission of Chronic Wasting Disease
Nathaniel D. Denkers, Glenn C. Telling, and Edward A. Hoover.
Journal of Virology doi:10.1128/JVI.01655-10 (published online ahead of print on 17 November 2010).
While chronic wasting disease (CWD) prion transmission, entry, and trafficking remains incompletely elucidated, natural exposure of the oral and/or nasal mucous membranes seems certain. Cervids commonly sustain minor lesions to oral mucous membranes that could have an impact on susceptibility to prion infection. To explore this potential co-factor, we studied cohorts of cervid PrP transgenic mice with or without superficial abrasions to the lingual mucosa, to determine whether minor oral mucosa lesions may enhance susceptibility to CWD infections. Results demonstrated that minor lingual abrasions substantially facilitate CWD transmission, a co-factor that may be significant in cervids and perhaps other species.
see full pdf file here ;
Thursday, November 25, 2010
Detection of the Abnormal Isoform of the Prion Protein Associated With Chronic Wasting Disease in the Optic Pathways of the Brain and Retina of Rocky Mountain Elk (Cervus elaphus nelsoni)
BMC Res Notes. 2010; 3: 314. Published online 2010 November 18. doi: 10.1186/1756-0500-3-314. PMCID: PMC2994889
Copyright ©2010 White et al; licensee BioMed Central Ltd.
Association analysis of PRNP gene region with chronic wasting disease in Rocky Mountain elk
Stephen N White,1,2,3 Terry R Spraker,4 James O Reynolds,1 and Katherine I O'Rourke1,2 1Animal Disease Research Unit, Agricultural Research Service, U.S. Department of Agriculture, Pullman, WA 99164, USA 2Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, WA 99164, USA 3Center for Integrated Biotechnology, Washington State University, Pullman, WA 99164, USA 4Colorado State University College of Veterinary Medicine & Biomedical Sciences, Fort Collins, CO 80526, USA Corresponding author. Stephen N White: email@example.com; Terry R Spraker: firstname.lastname@example.org; James O Reynolds: email@example.com; Katherine I O'Rourke: firstname.lastname@example.org Received June 22, 2010; Accepted November 18, 2010. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of cervids including white-tailed (Odocoileus virginianus) and mule deer (Odocoileus hemionus), Rocky Mountain elk (Cervus elaphus nelsoni), and moose (Alces alces). A leucine variant at position 132 (132L) in prion protein of Rocky Mountain elk confers a long incubation time with CWD, but not complete resistance. However, variants in regulatory regions outside the open reading frame of PRNP have been associated with varying degrees of susceptibility to prion disease in other species, and some variants have been observed in similar regions of Rocky Mountain elk PRNP. Thus, additional genetic variants might provide increased protection, either alone or in combination with 132L.
This study provided genomic sequence of all exons for PRNP of Rocky Mountain elk. Many functional sites in and around the PRNP gene region were sequenced, and this report approximately doubled (to 75) the number of known variants in this region. A haplotype-tagging approach was used to reduce the number of genetic variants required to survey this variation in the PRNP gene region of 559 Rocky Mountain elk. Eight haplotypes were observed with frequencies over 1.0%, and one haplotype was present at 71.2% frequency, reflecting limited genetic diversity in the PRNP gene region.
The presence of 132L cut odds of CWD by more than half (Odds Ratio = 0.43; P = 0.0031), which was similar to a previous report. However after accounting for 132L, no association with CWD was found for any additional variants in the PRNP region (P > 0.05).
As anticipated, these 75 total variants were found to be organized into a much smaller number of haplotypes. Out of 559 elk, only 19 haplotypes were observed 3 or more times in the sample set, and only 8 haplotypes were observed at 1.0% or greater allele frequency in the total sample, with only small variations once subdivided by captive or free-ranging state of the animals (Table 4). However, since the free-ranging animals were obtained from a smaller number of locations from only one state and since captive animals have had documented human-assisted gene flow, it is difficult to make any inferences about the genetic diversity of captive versus free-ranging animals from these data. Haplotype tagging enabled representation of all common underlying variants at r2 of 0.80 or greater using only 17 SNP markers, plus 5 derived genotypes composed of short multimarker haplotypes (Table 1). This represents a 77.3% reduction in variants that needed to be genotyped, which is comparable to other reports for haplotype tagging strategies in mammals [16,17]. Further, the haplotype tagging procedure required coverage of every variant in each of two animal groups, even though the variants observed in each group varied somewhat. This approach was a conservative way to ensure that all markers received coverage, but at the expense of possibly overestimating the number of markers required. The small number of haplotypes reflects relatively limited diversity in the PRNP gene region among Rocky Mountain elk , which is consistent with other reports of low genetic diversity using microsatellites in Rocky Mountain elk . However, the paucity of studies based on comparable marker types precludes conclusions regarding selective sweeps in the PRNP region as compared to the rest of the genome. Overall, this group of tagging markers provided representation of the genetic diversity in the PRNP gene region for measuring local linkage disequilibrium between gene regions and for association testing with CWD.
These markers were used to investigate whether additional markers could improve the resistance provided by the previously described 132L variant (O'Rourke et al 1999). The 132L variant was underrepresented among CWD cases (P = 0.0031), occurring in cases less than half as often as the predominant genotype 132 MM (OR = 0.43, 95%CI: 0.25-0.75). However, after accounting for 132L no other variants showed significant association with CWD even on a nominal basis (P > 0.05), before any correction for multiple testing. The statistical tests specifically included comparison of CWD frequency among carriers of two haplotypes (2 and 7) that harbor L132, but no significant differences were observed (P = 0.99). Furthermore, all genotypes with any appreciable frequency showed CWD positive animals, suggesting that there is no complete resistance to CWD on the basis of common PRNP genotypes in these elk. While we are not aware of any epidemiological evidence to suggest that truly CWD resistant elk exist, future research could examine the possibility that complete genetic resistance to CWD does exist in Rocky Mountain elk, either because of a very low frequency PRNP allele or because of the influence of other genes.
see full text ;
Although atypical scrapie is not yet ruled out, it is important to realize this is a type of scrapie that thus far has only tended to appear as a sporadic condition in older animals. Currently it has not been shown to follow the same genetic tendencies for propagation as the usual scrapie.
However, the atypical phenotypic appearance has been shown to be preserved on experimental passage.
Atypical scrapie was first identified in Norwegian sheep in 1998 and has subsequently been identified in many countries, as Australia may join that list. It is likely that this case will be sent to the UK for definitive conformation.
[Ref: M Simmons, T Konold, L Thurston, et al. BMC Veterinary Research 2010, 6:14 [provisional abstract available at]
"Background ----------- "Retrospective studies have identified cases predating the initial identification of this form of scrapie, and epidemiological studies have indicated that it does not conform to the behaviour of an infectious disease, giving rise to the hypothesis that it represents spontaneous disease. However, atypical scrapie isolates have been shown to be infectious experimentally, through intracerebral inoculation in transgenic mice and sheep. [Many of the neurological diseases can be transmitted by intracerebral inoculation, which causes this moderator to approach intracerebral studies as a tool for study, but not necessarily as a direct indication of transmissibility of natural diseases. - Mod.TG]
"The 1st successful challenge of a sheep with 'field' atypical scrapie from an homologous donor sheep was reported in 2007.
"Results -------- "This study demonstrates that atypical scrapie has distinct clinical, pathological, and biochemical characteristics which are maintained on transmission and sub-passage, and which are distinct from other strains of transmissible spongiform encephalopathies in the same host genotype.
"Conclusions ------------ Atypical scrapie is consistently transmissible within AHQ homozygous sheep, and the disease phenotype is preserved on sub-passage."
Lastly, this moderator wishes to thank Terry Singletary for some of his behind the scenes work of providing citations and references for this posting. - Mod.TG]
Sunday, December 12, 2010
EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010
Thursday, November 18, 2010
Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep
Wednesday, November 17, 2010
CWD Update 98 November 10, 2010
Saturday, December 18, 2010
OIE Global Conference on Wildlife Animal Health and Biodiversity - Preparing for the Future (TSE AND PRIONS) Paris (France), 23-25 February 2011
Thursday, December 23, 2010
Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002–2009 Volume 17, Number 1–January 2011
There are now two documented strains of CWD, and science is showing that indeed CWD could transmit to humans via transmission studies ;
Prion Transmission from Cervids to Humans is Strain-dependent
Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA
Key words: CWD, strain, human transmission
Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.
Acknowledgement Supported by NINDS NS052319 and NIA AG14359.
Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions
Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA
Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.
Biochemical and Biophysical Characterization of Different CWD Isolates
Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany
Key words: CWD, strains, FT-IR, AFM
Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD
Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5
The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.
Wednesday, November 17, 2010
CWD Update 98 November 10, 2010
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
PRION 2010 Meeting Report International Prion Congress: From agent to disease; September 8â€“11, 2010; Salzburg, Austria Volume 4, Issue 3 July/August/September 2010
THIS FDA recall for CWD positive product in commerce, was NOT done for the welfare of the dead CWD postive elk. ...TSS
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
RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
PRODUCT a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;
b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;
c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;
d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;
e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;
f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9; CODE Elk Meats with production dates of December 29, 30, and 31
Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009. Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing.
Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD).
VOLUME OF PRODUCT IN COMMERCE Unknown
DISTRIBUTION NV, CA, TX, CO, NY, UT, FL, OK
Sunday, April 12, 2009
CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains
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"
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Sent: Sunday, September 29, 2002 10:15 AM
To: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
full text ;
see full text ;
Tuesday, February 09, 2010
Chronic Wasting Disease: Surveillance Update North America: February 2010
>>> In addition, we documented horizontal transmission of CWD from inoculated mice and to un-inoculated cohabitant cage-mates. <<<
yep, but the SECOND passage was especially a doozy, and remember, oral transmission will take much longer than intracerebral route, and we now have two documented strains of cwd i.e. the regular strain of cwd (whatever the hell that means), and the Wisconsin strain, with probably more in the pipeline. NOW, THE MILLION DOLLAR QUESTION, WAS THE WISCONSIN CWD STRAIN INCLUDED IN THE ORAL TRANSMISSION STUDY ?
also, cwd has been transmitted to deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi).
considering scrapie, over 20 regular strains, with the atypical NOR-98, TWO documented TME strains i.e. hyper and drowsy, c-BSE, h-BSE, l-BSE, all in North America, all of which have been rendered and fed to animals for human and animal food..............terry
Title: Experimental Second Passage of Chronic Wasting Disease (Cwd(mule Deer)) Agent to Cattle
Hamir, Amirali Kunkle, Robert Miller, Janice - ARS RETIRED Greenlee, Justin Richt, Juergen
Submitted to: Journal of Comparative Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 25, 2005 Publication Date: January 1, 2006 Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006. Experimental second passage of chronic wasting disease (CWD(mule deer)) agent to cattle. Journal of Comparative Pathology. 134(1):63-69.
Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB. Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.
PLUS, oral transmission between cervids, either infected carcases AND ESPECIALLY FEED THAT HAS ANIMAL PROTEIN, PLEASE SEE ;
PRODUCT Custom deer feed made for a Wisconsin farm. The product was in bags holding about 40 pounds each. Recall # V-122-4. CODE 1-30-04 on the product invoice and mixing record. RECALLING FIRM/MANUFACTURER Crivitz Feed Mill, Crivitz, WI, by telephone on February 20, 2004. Wisconsin State initiated recall is complete. REASON The recalled deer feed contained steamed bone meal which is prohibited material in feed for ruminants.
VOLUME OF PRODUCT IN COMMERCE 515 pounds.
END OF ENFORCEMENT REPORT FOR APRIL 7, 2004
Experimental oral transmission of chronic wasting disease to red deer (Cervus elaphus elaphus): Early detection and late stage distribution of protease-resistant prion protein
Aru Balachandran, Noel P. Harrington, James Algire, Andrei Soutyrine, Terry R. Spraker, Martin Jeffrey, Lorenzo González, Katherine I. O’Rourke
Abstract — Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure. Studies of host range susceptibility to oral infection, particularly of those species found in habitats where CWD currently exists are imperative. This report describes the experimental transmission of CWD to red deer following oral inoculation with infectious CWD material of elk origin. At 18 to 20 months post-inoculation, mild to moderate neurological signs and weight loss were observed and animals were euthanized and tested using 3 conventional immunological assays. The data indicate that red deer are susceptible to oral challenge and that tissues currently used for CWD diagnosis show strong abnormal prion (PrPCWD) accumulation. Widespread peripheral PrPCWD deposition involves lymphoreticular tissues, endocrine tissues, and cardiac muscle and suggests a potential source of prion infectivity, a means of horizontal transmission and carrier state.
Can Vet J 2010;51:169–178
Journal of General Virology (1999), 80, 2757-2764. © 1999 Society for General Microbiology
Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1
Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5
Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail email@example.com
Abstract TOP Abstract Introduction Methods Results Discussion References
Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.
Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure.
Thursday, December 25, 2008
Lions and Prions and Deer Demise
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: firstname.lastname@example.org
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.
Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007
Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: email@example.com
The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.