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WYOMING MULE DEER BUCK HARVESTED NEAR LYSITE TESTS POSITIVE FOR CWD December 27, 2010
MULE DEER BUCK HARVESTED NEAR LYSITE TESTS POSITIVE FOR CWD
 
12/27/2010
 
CHEYENNE - A mule deer buck harvested  in hunt area 39 near Bull Mountain, about 23 miles north of Lysite, has tested positive for chronic wasting disease (CWD), a brain disease known to affect some deer, elk and moose. This is the first time that CWD has been detected in hunt area 39.
 
Personnel at the Wyoming Game and Fish Department Laboratory analyzed samples taken as part of the department's annual CWD survey and discovered positive results for the deer.
 
Hunt area 39 is bordered by endemic areas 164 and 37 that have had deer test positive for CWD in previous years.
 
After a review of available scientific data, the World Health Organization in December 1999 stated, "There is currently no evidence that CWD in cervidae (deer and elk) is transmitted to humans." In 2004, Dr. Ermias Belay of the Center for Disease Control said, "The lack of evidence of a link between CWD transmission and unusual cases of CJD, [Creutzfeldt-Jakob disease, a human prion disease] despite several epidemiological investigations, suggest that the risk, if any, of transmission of CWD to humans is low." Nonetheless to avoid risk, both organizations say parts or products from any animal that looks sick and/or tests positive for CWD should not be eaten.
 
For more information on chronic wasting disease visit the Chronic Wasting Disease Alliance website at www.cwd-info.org. (Contact: Al Langston (307) 777-4540) -WGFD-
 
 
Monday, December 13, 2010
 
WYOMING DEER AREA 119 ADDED TO CWD LIST
 
 
Friday, November 12, 2010
 
WHITE-TAILED BUCK HARVESTED NEAR MOORCROFT TESTS POSITIVE FOR CWD WYOMING
 
 
Wednesday, October 20, 2010
 
WYOMING ELK NEAR GLENDO TESTS POSITIVE FOR CWD 10/18/2010
 
 
Sunday, October 31, 2010
 
TWO DEER HARVESTED NEAR GREYBULL TEST POSITIVE FOR CWD WYOMING
 
 
Wednesday, November 25, 2009
 
CHRONIC WASTING DISEASE FOUND IN ELK AREA 35 NEAR BUFFALO
 
 
Wednesday, November 11, 2009
 
CHRONIC WASTING DISEASE DISCOVERED IN DEER HUNT AREA 42 WYOMING
 
 
Sunday, November 01, 2009
 
CWD confirmed in Johnson County Wyoming Sunday, November 1, 2009
 
 
Wednesday, October 14, 2009 Deer on western Bighorns has chronic wasting disease Shell Creek drainage Wyoming
 
 
Monday, December 22, 2008 CWD DETECTED IN ELK HUNT AREA 117 SOUTH OF SUNDANCE WYOMING http://chronic-wasting-disease.blogspot.com/2008/12/cwd-detected-in-elk-hunt-area-117-south.html
 
Saturday, October 18, 2008 WYOMING STAR VALLEY MOOSE TESTS POSITIVE FOR CWD
 
 
UPDATED DATA ON 2ND CWD STRAIN
 
Wednesday, September 08, 2010
 
CWD PRION CONGRESS SEPTEMBER 8-11 2010
 
 
There are now two documented strains of CWD, and science is showing that indeed CWD could transmit to humans via transmission studies ;
 
PPo3-7:
 
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.
 
PPo2-27:
 
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.
 
PPo2-7:
 
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
 
 
 
P35
 
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 8 - 11, 2010; Salzburg, Austria Volume 4, Issue 3 July/August/September 2010
 
 
Wednesday, December 29, 2010
 
CWD Update 99 December 13, 2010
 
 
TSS
 
 
 
Thursday, December 30, 2010
 
WYOMING MULE DEER BUCK HARVESTED NEAR LYSITE TESTS POSITIVE FOR CWD December 27, 2010
 
 
 
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I've wondered, since it

I've wondered, since it appears to be so wide spread, is it possible that CWD has always been there, but we just learned to classify it more in the last 20 years?

Much like with humans, we hear about certain diseases, autism for one, that's "on the rise".  Well, 25 years ago, would those kids have just been classified as "slow" or "mentally retarded"?  maybe now that we know what it is, we are classiifying it as such. 

It is scary, for sure, but how widespread has it been or is it now?  Something to ponder.

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