Tuesday, January 25, 2011

Minnesota, National Veterinary Services Laboratory in Ames, Iowa, has confirmed CWD case near Pine Island

Minnesota, National Veterinary Services Laboratory in Ames, Iowa, has confirmed CWD case near Pine Island



Managing Chronic Wasting Disease The National Veterinary Services Laboratory in Ames, Iowa, has confirmed that a deer harvested by a hunter in November 2010 near Pine Island in southeastern Minnesota had Chronic Wasting Disease (CWD), which is fatal to deer, elk and moose but not known to affect humans or cattle. The diagnosis, which was confirmed Jan. 25, marks the first time CWD has been found in Minnesota's wild deer herd.

The disease is a serious concern, not only because of the obvious harmful effects on cervid health, but also due to the negative impacts to landowners, hunters and businesses.

The DNR has been actively on the lookout for CWD since 2002, when the disease was first found in a domestic elk farm in central Minnesota. The agency has been conducting surveillance for the disease because an important management strategy is early detection.

Since 2002, the DNR has tested more than 32,000 hunter-harvested or road-killed deer, 60 elk and and 90 moose as part of its early CWD detection strategy. Until now, laboratory analysis had never found a wild deer "presumed positive" for CWD.

http://www.dnr.state.mn.us/mammals/deer/cwd/index.html



MINNESOTA HIGHLY SUSPECT CWD POSITIVE WILD DEER FOUND NEAR PINE ISLAND

Managing Chronic Wasting Disease

A preliminary screening test strongly indicates that a deer harvested by a hunter in November 2010 near Pine Island in southeast Minnesota had Chronic Wasting Disease (CWD), which is fatal to deer, elk and moose but not known to affect human health. If the National Veterinary Services Laboratory in Ames, Iowa, confirms the University of Minnesota's preliminary diagnosis this marks the first time CWD has been found in Minnesota's wild deer herd.

The disease is a serious concern, not only because of the obvious harmful effects on cervid health, but also due to the negative impacts to landowners, hunters and businesses.

The DNR has been actively on the lookout for CWD since 2002, when the disease was first found in a domestic elk farm in central Minnesota. The agency has been conducting surveillance for the disease because an important management strategy is early detection.

Since 2002, the DNR has tested more than 32,000 hunter-harvested or road-killed deer, 60 elk and and 90 moose as part of its early CWD detection strategy. Until now, laboratory analysis had never found a wild deer "presumed positive" for CWD.

snip...

The Minnesota Department of Natural Resources has learned that an adult female deer harvested during the 2010 hunting season will likely be diagnosed with Chronic Wasting Disease (CWD), a brain and nervous system disorder found in deer, elk and moose. This is disappointing news but the DNR is well prepared to address it.

The discovery occurred last week during laboratory analysis of more than 500 samples (lymph nodes) taken from hunter-harvested deer taken within a 20-mile radius of Pine Island in southeastern Minnesota. Initial screening of all samples has been completed and this is the only suspect. The DNR collects and evaluates lymph nodes because CWD can be detected through microscopic analysis.

Official confirmation of the disease requires further analysis by the National Veterinary Services Laboratory (NVSL) in Ames, Iowa. The following information answers many common questions.

What is the practical implication of this finding? If the preliminary finding is confirmed by NVSL, this will mark the first time CWD has been found in wild deer in Minnesota. Though the disease has been detected in Minnesota on four previous occasions since 2002, all of the instances involved ?captive cervids,? meaning domestic deer or elk confined to a fenced-in commercial operation.

How did the disease enter Minnesota's wild deer herd? At this point, no one knows. In fact, we may never know. What is known is that the 'presumed positive' deer was harvested about three miles southwest of a former domestic elk farm near Pine Island. The farm's elk herd was depopulated after a seven-year-old female elk tested positive for CWD in January 2008. Three additional elk were found to be infected with CWD during the depopulation effort. The closest wild deer with CWD in Wisconsin is 150 miles from the location this CWD-suspect deer was harvested in Minnesota.

What other states have CWD? CWD is found in wild deer, elk or moose in 13 other states and two Canadian provinces, including the Midwestern states of Wisconsin, Illinois, North Dakota and South Dakota. For specifics, visit the CWD Alliance Website.

What has DNR done to manage CWD? The DNR has done much to prevent CWD from entering Minnesota's wild deer herd. For many years the agency has worked closely with the Minnesota Board of Animal Health (the regulators of domestic deer and elk farms) on policies, procedures, and statutes to protect wild deer from coming into contact with commercially-raised elk and deer. The agency has also worked with the state Legislature to create animal transportation laws that minimize the risk of CWD from entering the state. For example, whole deer, elk, caribou or moose carcasses from other states or provinces may not be brought into Minnesota from areas known to have CWD in the wild.

The DNR has been actively on the lookout for CWD since 2002 when the disease was first found in a domestic elk farm in central Minnesota. The agency has been actively looking for the disease because an important management strategy is early detection. Since 2002, the DNR has tested more than 32,000 hunter-harvested or road-killed deer, 60 elk and and 90 moose in the name of early CWD detection. Until now, laboratory analysis had never found a wild deer "presumed positive" for CWD.

Was DNR specifically looking for CWD in the Pine Island area? Yes. It is a logical place to look because it's an area where CWD was recently discovered. The DNR collected 515 deer lymph node samples during the past deer season. This followed the collection of 934 deer from the same area in 2009. All of these deer were taken within a 25-mile radius of Pine Island. The DNR obtained these samples from hunters who voluntarily allowed DNR staff, University of Minnesota veterinary students and other experts to extract the lymph nodes at deer registration stations. In 2008, the DNR tested the lymph nodes of 500 hunter-harvested deer along the Wisconsin border from Houston County to St. Croix State Park. In 2009, the agency tested a total of 2,685 deer taken in southeastern Minnesota.

If CWD is confirmed, what will DNR do? DNR will implement its CWD response plan. The critical first step is to identify the number and current distribution of deer in the Pine Island area. This will be done using an aerial survey. Once DNR managers compile this data they will make plans to collect additional lymph nodes later this winter. Potential options for collecting these samples include a late winter deer hunting season, landowner shooting permits or sharp-shooting with permission of cooperating landowners. DNR will also implement a deer feeding ban in a CWD management zone surrounding the location of the positive animal, and restrict carcass movements out of the area.

Do you believe other deer in southeastern Minnesota have CWD?

A deer infected with CWD That's possible but it's premature to speculate. The only way to know if other deer have CWD is to continue doing surveillance. Collection of additional samples this winter will be done in a highly targeted way and only with permission of cooperating landowners.

If I harvested a deer from that area, should I be concerned about eating the venison? Based on the fact that only one deer has tested positive for CWD among more than 500 samples, the rate of occurrence is likely low. Still, people with venison in their freezer from this area should know the following:

The National Center for Disease Control (CDC) and the World Health Organization (WHO) have found no scientific evidence that CWD is transferrable from animals to humans; and The CDC advises against eating animals known to have CWD. So, people with venison in their freezer that was harvested from this area will need to make decisions based on the information above. The Minnesota Department of Health – not the DNR – provides guidance to citizens on food consumption issues.

What else can you tell me about CWD? CWD causes a characteristic spongy degeneration of the brains of infected animals resulting in emaciation, abnormal behavior, loss of bodily functions and death. CWD belongs to a group of diseases known as transmissible spongiform encephalopathies (TSEs). Though many observers try to compare CWD with "mad cow disease", the diseases are distinctly different.

What causes CWD? The disease agent is a prion, an abnormal form of cellular protein that is most commonly found in the central nervous system and in lymphoid tissue. The prion "infects" the host animal by promoting conversion of normal cellular protein to the abnormal form.

Where and how did CWD originate? The origin of CWD is unknown, and it may never be possible to definitively determine how or when CWD arose. It was first recognized as a syndrome in captive mule deer held in wildlife research facilities in Colorado in the late 1960s, but it was not identified as a TSE until the 1970s. Computer modeling suggests the disease may have been present in free-ranging populations of mule deer for more than 40 years.

How does CWD spread? It is not known exactly how CWD is transmitted. The infectious agent may be passed in feces, urine or saliva. Transmission is thought to be lateral (from animal to animal). Although maternal transmission (from mother to fetus) may occur, it appears to be relatively unimportant in maintaining epidemics.

Because CWD infectious agents are extremely resistant in the environment, transmission may be both direct and indirect. Concentrating deer and elk in captivity or by artificial feeding probably increases the likelihood of both direct and indirect transmission between individuals. Contaminated pastures appear to have served as sources of infection in some CWD epidemics. The apparent persistence of the infectious agents in contaminated environments represents a significant obstacle to eradication of CWD from either captive or free-ranging cervid populations.

The movement of live animals is one of the greatest risk factors in spreading the disease into new areas. Natural movements of wild deer and elk contribute to the spread of the disease, and human-aided transportation of both captive and wild animals greatly exacerbates this risk factor.

Why should Minnesotans be concerned about CWD? CWD poses serious problems for wildlife managers, and the implications for free-ranging deer, elk and moose are significant:

Ongoing surveillance programs are expensive and draw resources from other wildlife management needs; Impacts of CWD on population dynamics of deer and elk are presently unknown. Computer modeling suggests that CWD could substantially reduce infected cervid populations by lowering adult survival rates and destabilizing long-term population dynamics; Where it occurs, CWD may alter the management of wild deer and elk populations, and it has already begun to do so; and Ultimately, public and agency concerns and perceptions about human health risks associated with all TSE's may erode hunters' confidence and their willingness to hunt in areas where CWD occurs.


http://www.dnr.state.mn.us/mammals/deer/cwd/index.html



Friday, January 21, 2011

MINNESOTA HIGHLY SUSPECT CWD POSITIVE WILD DEER FOUND NEAR PINE ISLAND

http://chronic-wasting-disease.blogspot.com/2011/01/minnesota-highly-suspect-cwd-positive.html




Tuesday, January 25, 2011

Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions

Marcelo A. Barria1, Glenn C. Telling2, Pierluigi Gambetti3, 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 77030, 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.

Running Title: Conversion of human PrPC by cervid PrPSc

Keywords: Prion / transmissible spongiform encephalopathy / infectivity / misfolded prion protein / prion strains

* To whom correspondence should be addressed. University of Texas Houston Medical School, 6431 Fannin St, Houston, TX 77030. Tel 713-5007086; Fax 713-5000667; E-mail Claudio.Soto@uth.tmc.edu

Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded 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 conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of prion species barrier and indicate that the transmission barrier is a dynamic process that depend on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans, and that this ability depends on CWD strain adaptation.

snip...

Besides the importance of our results for public health in relation to the putative transmissibility of CWD to humans, our data also illustrate a very important and novel scientific concept related to the mechanism of prion transmission across species barriers. Today the view is that species barrier is mostly controlled by the degree of similarity on the sequence of the prion protein between the host and the infectious material (4). In our study we show that the strain and moreover the stabilization of the strain plays a major role in the inter-species transmission. In our system there is no change on the protein sequence, but yet strain adaptation results in a complete change on prion transmissibility with potentially dramatic consequences. Therefore, our findings lead to a new view of the species barrier that should not be seen as a static process, but rather a dynamic biological phenomenon that can change over time when prion strains mature and evolve. It remains to be investigated if other species barriers also change upon progressive strain adaptation of other prion forms (e.g. the sheep/human barrier).

Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man.


please see full text and more here ;


Tuesday, January 25, 2011


Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions


http://chronic-wasting-disease.blogspot.com/2011/01/generation-of-new-form-of-human-prpsc.html



http://chronic-wasting-disease.blogspot.com/



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

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Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions

Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions

Marcelo A. Barria1, Glenn C. Telling2, Pierluigi Gambetti3, 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 77030, 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.

Running Title: Conversion of human PrPC by cervid PrPSc

Keywords: Prion / transmissible spongiform encephalopathy / infectivity / misfolded prion protein / prion strains

* To whom correspondence should be addressed. University of Texas Houston Medical School, 6431 Fannin St, Houston, TX 77030. Tel 713-5007086; Fax 713-5000667; E-mail Claudio.Soto@uth.tmc.edu

Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded 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 conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of prion species barrier and indicate that the transmission barrier is a dynamic process that depend on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans, and that this ability depends on CWD strain adaptation.

snip...

Interestingly, when the Western blot profile of this newly generated form of human PrPSc (termed CWD-huPrPSc) was compared with known strains of human prions, it was clear that CWD-huPrPSc exhibited a different pattern (Fig. 4A). The electrophoretic migration of this protein after PK-digestion is similar to the type 1 strain of sCJD, but its glycosylation profile is clearly different, showing a highly predominant diglycosylated form (Fig. 4A and B). This result suggests that CWD hu-PrPSc corresponds to a new human prion strain. Interestingly, a detailed previous study from Gambetti’s group comparing the biochemical characteristics of PrPSc from cervids and humans showed that CWD PrPSc is similar to sCJDMM1 in terms of electrophoretic mobility (6). However, the misfolded protein associated with CWD is predominantly di-glycosylated, whereas PrPSc from type 1 sCJD is mostly monoglycosylated (6). Based on the fact that transmission of BSE prions to humans resulted in a new form of PrPSc very similar to the one in cattle (6;27), these authors predicted that if humans were infected by CWD it is likely that PrPSc would be of type 1 and with a predominance of the diglycosylated isoform (6). Our results agree with that prediction and suggest that the newly generated CWD-huPrPSc acquires the biochemical properties of the cervid infectious material (Fig. 4A and B). We and others have shown that PMCA replication of PrPSc obtained from experimental rodents, sheep, cervid and human samples faithfully maintains the prion strain characteristics (14;16;26;28-30). To further support the relevance of our results, we performed experiments in which human PrPC was attempted to be converted by either cattle BSE PrPSc or sheep scrapie PrPSc. Whereas the typical vCJD type of PrPSc was generated when human PrPC was converted by BSE PrPSc (Fig. 4C), no human PrPSc was generated under any condition when sheep scrapie PrPSc was used as inoculum (Fig. 4C). These results further validate our PMCA assay.

Discussion CWD is possibly the most worrisome prion zoonosis, because it affects free-ranging animals, making it very difficult to control its spread, and because it is highly efficiently transmitted (1;2). Indeed, in dense free-ranging cervid populations, CWD prevalence can reach as high as 30%, and among captive herds, the prevalence can climb to nearly 100%. The mechanisms and routes of transmission are currently unknown, but likely involve horizontal spread through exposure to prion infected secretions, excretions, or decomposed carcasses (1;2). Moreover, it is likely that CWD prions are progressively accumulating in the environment, since PrPSc binds tightly to soil and can maintain infectivity for a long time (31-33). Currently, it is unknown what proportion of natural CWD cases arises sporadically or comes from horizontal transmission among animals. Based on the available knowledge of the emergence, adaptation and stabilization of prion strains, it is likely that prions appear either spontaneously, through inter-species transmission or by genetic mutations. These “first generation” prions are unstable strains that begin a progressive and gradual process of adaptation that may take several passages and years or decades to complete. In addition natural strain stabilization may take considerable more time than the controlled adaptation done by intracerebral inoculation of brain homogenates in experimental animals. In natural cases, animals usually get infected by peripheral (most likely oral) exposure to small quantities of prions present in peripheral tissues or secretion fluids. Recent data indicates that in some cases the strain characteristics of natural prions in peripheral organs are different than those in the brain even in the same individuals (GCT, unpublished results; MAB and CS, unpublished data). In cervids, there are at least two different strains that can be differentiated by the incubation time and neuropathological characteristics produced when inoculated into transgenic mice expressing deer PrP (34). It is currently unknown the susceptibility of these two strains to human transmission.

Our findings demonstrate that cervid PrPSc, upon strain adaptation by serial passages in vitro or in cervid transgenic mice, is capable of converting human PrPC to produce PrPSc with unique biochemical properties, likely representing a new human prion strain. The newly generated CWD-huPrPSc material has been inoculated into transgenic mice expressing human PrP to study infectivity and disease phenotype and this data will be published elsewhere. We have safely ruled out that human PrPSc generated in these studies is not coming from spontaneous “de novo generation”, since under the conditions used, no spontaneous PK-resistant band was ever detected in brain homogenates of humans or transgenic mice expressing human PrPC, even after more than 20 serial rounds of PMCA (35). Furthermore, none of the many controls included in our experiments in which no PrPSc was added to the reaction, showed any PK-resistant PrP band.

Various studies aimed to analyze the transmission of CWD to transgenic mice expressing human PrP have consistently given negative results (9-11), indicating a strong species barrier. This conclusion is consistent with our many failed experiments to attempt converting human PrPC with natural CWD, even after pushing the PMCA conditions (see figure 1). We found successful conversion only after adaptation of the CWD prion strain by successive passages in vitro or in cervid transgenic mice. We are not aware that in any of the transgenic mice studies the inoculum used was a previously stabilized CWD strain. Although, it has been shown that strain stabilization in vitro by PMCA (17;26) and in vivo using experimental rodents (36) has similarities with the strain adaptation process occurring in natural hosts, we cannot rule out that the type of CWD strain adaptation that is required to produce strains transmissible to humans may take much longer time in cervids or not occur at all. An important experiment will be to study transmissibility to humanized transgenic mice of CWD passed experimentally in deer several times.

Besides the importance of our results for public health in relation to the putative transmissibility of CWD to humans, our data also illustrate a very important and novel scientific concept related to the mechanism of prion transmission across species barriers. Today the view is that species barrier is mostly controlled by the degree of similarity on the sequence of the prion protein between the host and the infectious material (4). In our study we show that the strain and moreover the stabilization of the strain plays a major role in the inter-species transmission. In our system there is no change on the protein sequence, but yet strain adaptation results in a complete change on prion transmissibility with potentially dramatic consequences. Therefore, our findings lead to a new view of the species barrier that should not be seen as a static process, but rather a dynamic biological phenomenon that can change over time when prion strains mature and evolve. It remains to be investigated if other species barriers also change upon progressive strain adaptation of other prion forms (e.g. the sheep/human barrier).

Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man.

Reference List

snip...

please see full text and many thanks to the Professor Soto and the other Authors of this study AND to The Journal Of Biological Chemistry for the free full text !!!



http://www.jbc.org/content/early/2011/01/04/jbc.M110.198465.long




PLEASE NOTE ;

there are now two documented strains of CWD, and science is showing that indeed CWD could transmit to humans via transmission studies ;

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.



http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf




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.





http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099





CJD9/10022

October 1994


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

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT


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. ...end




http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf




UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010




http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html





From: TSS (216-119-163-189.ipset45.wt.net)

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

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

From: "Belay, Ermias"

To:

Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

Sent: Monday, September 30, 2002 9:22 AM

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


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

From:

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

snip...


full text ;




http://chronic-wasting-disease.blogspot.com/2009/02/exotic-meats-usa-announces-urgent.html





FDA is not 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





http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html





see full text ;




http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html





Wednesday, December 29, 2010

CWD Update 99 December 13, 2010


http://chronic-wasting-disease.blogspot.com/2010/12/cwd-update-99-december-13-2010.html




http://chronic-wasting-disease.blogspot.com/




now, just what is in that deer feed? _ANIMAL PROTEIN_


Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES

Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-LTo: BSE-L

8420-20.5% Antler DeveloperFor Deer and Game in the wildGuaranteed Analysis Ingredients / Products Feeding Directions

snip...

_animal protein_

http://www.surefed.com/deer.htm

BODE'S GAME FEED SUPPLEMENT #400A RATION FOR DEERNET WEIGHT 50 POUNDS22.6 KG.

snip...

_animal protein_

http://www.bodefeed.com/prod7.htm

IngredientsGrain Products, Plant Protein Products, Processed Grain By-Products,Forage Products, Roughage Products 15%, Molasses Products,

__Animal Protein Products__,

Monocalcium Phosphate, Dicalcium Pyosphate, Salt,Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol(source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement,Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, CholineChloride, Folic Acid, Menadione Soduim Bisulfite Complex, PyridoxineHydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, ZincOxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, DriedSacchoromyces Berevisiae Fermentation Solubles, Cellulose gum,Artificial Flavors added.http://www.bodefeed.com/prod6.htm

===================================

MORE ANIMAL PROTEIN PRODUCTS FOR DEER

Bode's #1 Game PelletsA RATION FOR DEERF3153GUARANTEED ANALYSISCrude Protein (Min) 16%Crude Fat (Min) 2.0%Crude Fiber (Max) 19%Calcium (Ca) (Min) 1.25%Calcium (Ca) (Max) 1.75%Phosphorus (P) (Min) 1.0%Salt (Min) .30%Salt (Max) .70%IngredientsGrain Products, Plant Protein Products, Processed Grain By-Products,Forage Products, Roughage Products, 15% Molasses Products,

__Animal Protein Products__,

Monocalcium Phosphate, Dicalcium Phosphate, Salt,Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol(source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement,Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, CholineChloride, Folic Acid, Menadione Sodium Bisulfite Complex, PyridoxineHydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, ZincOxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, DriedSaccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum,Artificial Flavors added.FEEDING DIRECTIONSFeed as Creep Feed with Normal Diet

http://www.bodefeed.com/prod8.htm

INGREDIENTS

Grain Products, Roughage Products (not more than 35%), Processed GrainBy-Products, Plant Protein Products, Forage Products,

__Animal Protein Products__,

L-Lysine, Calcium Carbonate, Salt, Monocalcium/DicalciumPhosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, BasicCopper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite,Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide,Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin ASupplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, CalciumLignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium BisulfiteComplex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid,Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate

DIRECTIONS FOR USE

Deer Builder Pellets is designed to be fed to deer under rangeconditions or deer that require higher levels of protein. Feed to deerduring gestation, fawning, lactation, antler growth and pre-rut, allphases which require a higher level of nutrition. Provide adequateamounts of good quality roughage and fresh water at all times.

http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html

===================================================

DEPARTMENT OF HEALTH & HUMAN SERVICESPUBLIC HEALTH SERVICEFOOD AND DRUG ADMINISTRATIONApril 9, 2001 WARNING LETTER01-PHI-12CERTIFIED MAILRETURN RECEIPT REQUESTED

Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145

PHILADELPHIA DISTRICT

Tel: 215-597-4390

Dear Mr. Raymond:Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23,2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattleor other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.

In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal.Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.The above is not intended to be an all-inclusive list of deviations fromthe regulations. As a manufacturer of materials intended for animalfeed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance withthe law. We have enclosed a copy of FDA's Small Entity Compliance Guideto assist you with complying with the regulation... blah, blah, blah...

http://www.fda.gov/foi/warning_letters/g1115d.pdf

==================================

snip...end...full text ;


2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 1 Terry S. Singeltary Sr. Vol #: 1



http://www.fda.gov/ohrms/dockets/dailys/03/Jun03/060903/060903.htm




2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 7 Terry S. Singeltary Sr. Vol #: 1

2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

EMC 7 Terry S. Singeltary Sr. Vol #: 1



http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm




01N-0423 Substances Prohibited from use in animal food/Feed Ruminant

APE 5 National Renderers Association, Inc. Vol#: 2

APE 6 Animal Protein Producers Industry Vol#: 2

APE 7 Darling International Inc. Vol#: 2

EMC 1 Terry S. Singeltary Sr. Vol#: 3



http://www.fda.gov/ohrms/dockets/dailys/01/Oct01/101501/101501.htm




above urls dead, go here ;




http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html




Friday, January 7, 2011

MEAT AND BONE MEAL AND MINERAL FEED ADDITIVES MAY INCREASE THE RISK OF ORAL PRION DISEASE TRANSMISSION

Journal of Toxicology and Environmental Health, Part A, 74:161–166, 2011 Copyright © Taylor & Francis Group, LLC ISSN: 1528-7394 print / 1087-2620 online DOI: 10.1080/15287394.2011.529066



http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/meat-and-bone-meal-and-mineral-feed.html



Wednesday, January 19, 2011

EFSA BIOHAZ Scientific Opinion on the revision of the quantitative risk assessment (QRA) of the BSE risk posed by processed animal proteins (PAPs)

EFSA Journal 2011;9(1):1947


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-biohaz-scientific-opinion-on.html




>>> Animals injected with iatrogenic Creutzfeldt-Jakob disease MM1 and genetic Creutzfeldt-Jakob disease MM1 linked to the E200K mutation showed the same phenotypic features as those infected with sporadic Creutzfeldt-Jakob disease MM1 prions, whereas kuru most closely resembled the sporadic Creutzfeldt-Jakob disease VV2 or MV2 prion signature and neuropathology.... <<<




http://www.jbc.org/cgi/content/abstract/M704597200v1?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=Cross-sequence+transmission+of+sporadic+Creutzfeldt-Jakob+disease+creates+a+new+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT




UPDATED DATA ON 2ND CWD STRAIN

snip... please see full text ;

Tuesday, January 18, 2011

Agent strain variation in human prion disease: insights from a molecular and pathological review of the National Institutes of Health series of experimentally transmitted disease


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/agent-strain-variation-in-human-prion.html



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


http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/molecular-typing-of-protease-resistant.html



Wednesday, January 19, 2011

EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/efsa-and-ecdc-review-scientific.html



Friday, January 21, 2011

Strain-Specific Barriers against Bovine Prions in Hamsters


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/strain-specific-barriers-against-bovine.html



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


http://transmissiblespongiformencephalopathy.blogspot.com/2010/12/oie-global-conference-on-wildlife.html



doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003.

Volume 3, Issue 8, August 2003, Page 463

"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 ...

............................



http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/fulltext



http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf



see full text ;

Tuesday, November 02, 2010

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992


http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html



USA

5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

2010

PLEASE NOTE REFERENCE LINES 5. AND 6.

Monday, August 9, 2010

National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 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 88 52 44 7 1 0

1999 120 72 64 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 1(3)

2005 344 194 157 36 1 0

2006 383 197 166 29 0 2(4)

2007 377 214 187 27 0 0

2008 394 231 204 25 0 0

2009 425 259 216 43 0 0

2010 204 124 85 20 0 0

TOTAL 3702(5) 2177(6) 1834 315 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 16 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.


http://www.cjdsurveillance.com/pdf/case-table.pdf



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)


http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html



Monday, August 9, 2010

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?


http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html



Wednesday, January 5, 2011

ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011

Prions

David W. Colby1,* and Stanley B. Prusiner1,2


http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html



Thursday, December 23, 2010

Alimentary prion infections: Touch-down in the intestine, Alzheimer, Parkinson disease and TSE mad cow diseases $ The Center for Consumer Freedom


http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html



strictly NOT private and confidential $$$

Saturday, January 22, 2011

Alzheimer's, Prion, and Neurological disease, and the misdiagnosis there of, a review 2011


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/alzheimers-prion-and-neurological.html



DID EVERYONE FILL OUT THEIR CJD QUESIONNAIRE FROM THE CDC AND OR THE CJD FOUNDATION ???

Friday, November 30, 2007

CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION


http://cjdquestionnaire.blogspot.com/



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

Labels:

Friday, January 21, 2011

MINNESOTA HIGHLY SUSPECT CWD POSITIVE WILD DEER FOUND NEAR PINE ISLAND

MINNESOTA HIGHLY SUSPECT CWD POSITIVE WILD DEER FOUND NEAR PINE ISLAND



Managing Chronic Wasting Disease


A preliminary screening test strongly indicates that a deer harvested by a hunter in November 2010 near Pine Island in southeast Minnesota had Chronic Wasting Disease (CWD), which is fatal to deer, elk and moose but not known to affect human health. If the National Veterinary Services Laboratory in Ames, Iowa, confirms the University of Minnesota's preliminary diagnosis this marks the first time CWD has been found in Minnesota's wild deer herd.

The disease is a serious concern, not only because of the obvious harmful effects on cervid health, but also due to the negative impacts to landowners, hunters and businesses.

The DNR has been actively on the lookout for CWD since 2002, when the disease was first found in a domestic elk farm in central Minnesota. The agency has been conducting surveillance for the disease because an important management strategy is early detection.

Since 2002, the DNR has tested more than 32,000 hunter-harvested or road-killed deer, 60 elk and and 90 moose as part of its early CWD detection strategy. Until now, laboratory analysis had never found a wild deer "presumed positive" for CWD.


snip...



The Minnesota Department of Natural Resources has learned that an adult female deer harvested during the 2010 hunting season will likely be diagnosed with Chronic Wasting Disease (CWD), a brain and nervous system disorder found in deer, elk and moose. This is disappointing news but the DNR is well prepared to address it.

The discovery occurred last week during laboratory analysis of more than 500 samples (lymph nodes) taken from hunter-harvested deer taken within a 20-mile radius of Pine Island in southeastern Minnesota. Initial screening of all samples has been completed and this is the only suspect. The DNR collects and evaluates lymph nodes because CWD can be detected through microscopic analysis.

Official confirmation of the disease requires further analysis by the National Veterinary Services Laboratory (NVSL) in Ames, Iowa. The following information answers many common questions.

What is the practical implication of this finding? If the preliminary finding is confirmed by NVSL, this will mark the first time CWD has been found in wild deer in Minnesota. Though the disease has been detected in Minnesota on four previous occasions since 2002, all of the instances involved ?captive cervids,? meaning domestic deer or elk confined to a fenced-in commercial operation.

How did the disease enter Minnesota's wild deer herd? At this point, no one knows. In fact, we may never know. What is known is that the 'presumed positive' deer was harvested about three miles southwest of a former domestic elk farm near Pine Island. The farm's elk herd was depopulated after a seven-year-old female elk tested positive for CWD in January 2008. Three additional elk were found to be infected with CWD during the depopulation effort. The closest wild deer with CWD in Wisconsin is 150 miles from the location this CWD-suspect deer was harvested in Minnesota.

What other states have CWD? CWD is found in wild deer, elk or moose in 13 other states and two Canadian provinces, including the Midwestern states of Wisconsin, Illinois, North Dakota and South Dakota. For specifics, visit the CWD Alliance Website.

What has DNR done to manage CWD? The DNR has done much to prevent CWD from entering Minnesota's wild deer herd. For many years the agency has worked closely with the Minnesota Board of Animal Health (the regulators of domestic deer and elk farms) on policies, procedures, and statutes to protect wild deer from coming into contact with commercially-raised elk and deer. The agency has also worked with the state Legislature to create animal transportation laws that minimize the risk of CWD from entering the state. For example, whole deer, elk, caribou or moose carcasses from other states or provinces may not be brought into Minnesota from areas known to have CWD in the wild.

The DNR has been actively on the lookout for CWD since 2002 when the disease was first found in a domestic elk farm in central Minnesota. The agency has been actively looking for the disease because an important management strategy is early detection. Since 2002, the DNR has tested more than 32,000 hunter-harvested or road-killed deer, 60 elk and and 90 moose in the name of early CWD detection. Until now, laboratory analysis had never found a wild deer "presumed positive" for CWD.

Was DNR specifically looking for CWD in the Pine Island area? Yes. It is a logical place to look because it's an area where CWD was recently discovered. The DNR collected 515 deer lymph node samples during the past deer season. This followed the collection of 934 deer from the same area in 2009. All of these deer were taken within a 25-mile radius of Pine Island. The DNR obtained these samples from hunters who voluntarily allowed DNR staff, University of Minnesota veterinary students and other experts to extract the lymph nodes at deer registration stations. In 2008, the DNR tested the lymph nodes of 500 hunter-harvested deer along the Wisconsin border from Houston County to St. Croix State Park. In 2009, the agency tested a total of 2,685 deer taken in southeastern Minnesota.

If CWD is confirmed, what will DNR do? DNR will implement its CWD response plan. The critical first step is to identify the number and current distribution of deer in the Pine Island area. This will be done using an aerial survey. Once DNR managers compile this data they will make plans to collect additional lymph nodes later this winter. Potential options for collecting these samples include a late winter deer hunting season, landowner shooting permits or sharp-shooting with permission of cooperating landowners. DNR will also implement a deer feeding ban in a CWD management zone surrounding the location of the positive animal, and restrict carcass movements out of the area.

Do you believe other deer in southeastern Minnesota have CWD?

A deer infected with CWD That's possible but it's premature to speculate. The only way to know if other deer have CWD is to continue doing surveillance. Collection of additional samples this winter will be done in a highly targeted way and only with permission of cooperating landowners.

If I harvested a deer from that area, should I be concerned about eating the venison? Based on the fact that only one deer has tested positive for CWD among more than 500 samples, the rate of occurrence is likely low. Still, people with venison in their freezer from this area should know the following:

The National Center for Disease Control (CDC) and the World Health Organization (WHO) have found no scientific evidence that CWD is transferrable from animals to humans; and The CDC advises against eating animals known to have CWD. So, people with venison in their freezer that was harvested from this area will need to make decisions based on the information above. The Minnesota Department of Health – not the DNR – provides guidance to citizens on food consumption issues.

What else can you tell me about CWD? CWD causes a characteristic spongy degeneration of the brains of infected animals resulting in emaciation, abnormal behavior, loss of bodily functions and death. CWD belongs to a group of diseases known as transmissible spongiform encephalopathies (TSEs). Though many observers try to compare CWD with "mad cow disease", the diseases are distinctly different.

What causes CWD? The disease agent is a prion, an abnormal form of cellular protein that is most commonly found in the central nervous system and in lymphoid tissue. The prion "infects" the host animal by promoting conversion of normal cellular protein to the abnormal form.

Where and how did CWD originate? The origin of CWD is unknown, and it may never be possible to definitively determine how or when CWD arose. It was first recognized as a syndrome in captive mule deer held in wildlife research facilities in Colorado in the late 1960s, but it was not identified as a TSE until the 1970s. Computer modeling suggests the disease may have been present in free-ranging populations of mule deer for more than 40 years.

How does CWD spread? It is not known exactly how CWD is transmitted. The infectious agent may be passed in feces, urine or saliva. Transmission is thought to be lateral (from animal to animal). Although maternal transmission (from mother to fetus) may occur, it appears to be relatively unimportant in maintaining epidemics.

Because CWD infectious agents are extremely resistant in the environment, transmission may be both direct and indirect. Concentrating deer and elk in captivity or by artificial feeding probably increases the likelihood of both direct and indirect transmission between individuals. Contaminated pastures appear to have served as sources of infection in some CWD epidemics. The apparent persistence of the infectious agents in contaminated environments represents a significant obstacle to eradication of CWD from either captive or free-ranging cervid populations.

The movement of live animals is one of the greatest risk factors in spreading the disease into new areas. Natural movements of wild deer and elk contribute to the spread of the disease, and human-aided transportation of both captive and wild animals greatly exacerbates this risk factor.

Why should Minnesotans be concerned about CWD? CWD poses serious problems for wildlife managers, and the implications for free-ranging deer, elk and moose are significant:

Ongoing surveillance programs are expensive and draw resources from other wildlife management needs; Impacts of CWD on population dynamics of deer and elk are presently unknown. Computer modeling suggests that CWD could substantially reduce infected cervid populations by lowering adult survival rates and destabilizing long-term population dynamics; Where it occurs, CWD may alter the management of wild deer and elk populations, and it has already begun to do so; and Ultimately, public and agency concerns and perceptions about human health risks associated with all TSE's may erode hunters' confidence and their willingness to hunt in areas where CWD occurs.


http://www.dnr.state.mn.us/mammals/deer/cwd/index.html




PLEASE NOTE ;


there are now two documented strains of CWD, and science is showing that indeed CWD could transmit to humans via transmission studies ;




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.

http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf



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.


http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099




UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010


http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html





From: TSS (216-119-163-189.ipset45.wt.net)

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

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

From: "Belay, Ermias"

To:

Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

Sent: Monday, September 30, 2002 9:22 AM

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

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

From:

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

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2009/02/exotic-meats-usa-announces-urgent.html



FDA is not 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

http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html



see full text ;

http://chronic-wasting-disease.blogspot.com/2009/04/cwd-update-infection-studies-in-two.html




Wednesday, December 29, 2010

CWD Update 99 December 13, 2010

http://chronic-wasting-disease.blogspot.com/2010/12/cwd-update-99-december-13-2010.html




http://chronic-wasting-disease.blogspot.com/





TSS

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Monday, January 17, 2011

Ten Additional Deer Test Positive for Chronic Wasting Disease in West Virginia

Earl Ray Tomblin, Governor Frank Jezioro, Director

News Release: January 14, 2011

Hoy Murphy, Public Information Officer (304) 558-2003 ext. 365 hoy.r.murphy@wv.gov Contact: Paul Johansen, Wildlife Resources Section 304-558-2771 dnr.wildlife@wv.gov


Ten Additional Deer Test Positive for Chronic Wasting Disease in West Virginia


SOUTH CHARLESTON, W.Va. – Preliminary test results indicate the Chronic Wasting Disease (CWD) agent was present in 10 hunter-harvested deer collected during the 2010 deer firearms hunting season.

“As part of our agency’s ongoing CWD monitoring effort, samples were collected from 1,056 hunter-harvested deer brought to game checking stations in Hampshire County and one station near the southern Hampshire County line in Hardy County,” said Frank Jezioro, Director of the West Virginia Division of Natural Resources (DNR).

The 10 CWD-positive deer included two 2.5 year-old does, two 1.5 year-old bucks, five 2.5 year-old bucks, and one 3.5 year-old buck. Nine of the latest positive deer were harvested within the borders of Hampshire County. However, one was harvested in Hardy County near the border with Hampshire County. The area in West Virginia from which CWD has been detected continues to expand, as evident with the latest CWD positive deer from northern Hardy County. The number of infected deer detected in West Virginia in 2010 now totals 22, two less than the number of infected deer detected in 2009.

CWD has now been detected in 83 deer in Hampshire County and one deer in Hardy County for a total of 84 CWD-positive deer in West Virginia. The DNR will continue to update management actions designed to control the spread of this disease, prevent further introduction of the disease, and possibly eliminate the disease from the state as information from deer testing within West Virginia is gathered and scientists across the country provide more information on how to combat CWD in white-tailed deer.

“The detection of the positive CWD deer in Hardy County is discouraging,” said Jezioro. “As we strive to meet this wildlife disease challenge and implement appropriate management strategies, the continued support and involvement of landowners and hunters will be essential.”

An expansion of the current ban on supplemental feeding and baiting of deer in Hampshire County is being considered with the occurrence of this CWD-positive deer in Hardy County. Current research indicates that supplemental feeding and baiting of deer increases the chance of disease transmission far above the normal clustering of deer on natural and agricultural feeding areas. The DNR remains committed to keeping the public informed and involved in wildlife disease management actions.

**DNR**

http://www.wvdnr.gov/2011news/11news003.shtm


Tuesday, June 29, 2010

W.Va. DNR Reports Results from Spring 2010 CWD Surveillance Efforts In Hampshire County; CWD Containment Area Expanded

http://chronic-wasting-disease.blogspot.com/2010/06/wva-dnr-reports-results-from-spring.html


Friday, January 15, 2010

Sixteen Additional Deer Test Positive for Chronic Wasting Disease In Hampshire County, West Virginia

http://chronic-wasting-disease.blogspot.com/2010/01/sixteen-additional-deer-test-positive.html


Friday, May 29, 2009

Seven Deer Test Positive for Chronic Wasting Disease During 2009 Spring Collections in Hampshire County, West Virginia

http://chronic-wasting-disease.blogspot.com/2009/05/seven-deer-test-positive-for-chronic.html


West Virginia:

The following was excerpted from a press release issued by the West Virginia DNR on December 22, 2008:

Five Additional Deer Test Positive for Chronic Wasting Disease in Hampshire County, West Virginia

Preliminary test results indicate the Chronic Wasting Disease (CWD) agent was present in five hunter-harvested deer collected in Hampshire County during the 2008 deer firearms hunting season.

“As part of our agency’s ongoing and intensive CWD monitoring effort, samples were collected from 1,355 hunter-harvested deer brought to game checking stations in Hampshire County and one station near the southern Hampshire County line in Hardy County,” noted Frank Jezioro, director for the West Virginia Division of Natural Resources (DNR).

The five CWD positive deer included one 4.5 year-old doe, two 2.5 year-old bucks, one 4.5 yearold buck and one 1.5 year-old buck. All five of the latest positive deer were harvested within the Hampshire County CWD Containment Area (i.e., that portion of Hampshire County located North of U.S. Route 50). However, the CWD agent previously has been detected outside the containment area but still within Hampshire County. The area in Hampshire County appears to continue to expand as one of the most recent infected deer was approximately five miles northeast of any previous known infected deer location.

CWD has now been detected in a total of 37 deer in Hampshire County (i.e., two road-killed deer - one in 2005 and one in 2008, four deer collected by the DNR in 2005, five deer collected by the DNR in 2006, one hunter-harvest deer taken during the 2006 deer season, three deer collected by the DNR in 2007, six hunter-harvested deer taken during the 2007 deer season, 11 deer collected by the DNR in 2008, and five hunter-harvested deer taken during the 2008 deer season). The DNR will continue to update management actions designed to control the spread of this disease, prevent further introduction of the disease, and possibly eliminate the disease from the state as information from deer testing within West Virginia is gathered and scientists across the country provide more information on how to combat CWD in white-tailed deer.

The entire press release can be viewed at:

http://www.wvdnr.gov/2008news/08news202.shtm.


SEE REPORT HERE ;

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-update-93-december-29-2008.html


Thursday, May 08, 2008

Eleven Deer Test Positive for Chronic Wasting Disease During Spring Collections in Hampshire County, West Virginia

http://chronic-wasting-disease.blogspot.com/2008/05/eleven-deer-test-positive-for-chronic.html


West Virginia:

The following press release (shortened for inclusion on this update) was issued by the West Virginia Department of Natural Resources on December 17, 2007: Five Additional Deer Test Positive for Chronic Wasting Disease in Hampshire County, West Virginia. Preliminary test results have detected the Chronic Wasting Disease (CWD) agent in five hunter-harvested deer collected in Hampshire County during the 2007 deer firearms hunting season. “As part of our agency’s ongoing and intensive CWD surveillance effort, samples were collected from 1,285 hunter-harvested deer brought to game checking stations in Hampshire County,” noted Frank Jezioro, Director for the West Virginia Division of Natural Resources (DNR). The five CWD positive deer included one 2.5 year-old doe, two 2.5 year-old bucks, one 3.5 year-old buck, and one 4.5 year-old buck. Four of the five deer were harvested within the Hampshire County CWD Containment Area (i.e., that portion of Hampshire County located North of U.S. Route 50). The fifth deer was also harvested in Hampshire County, but it was killed outside the CWD Containment Area near Yellow Springs, West Virginia. CWD has now been detected in a total of 19 deer in Hampshire County (i.e., one road-killed deer confirmed in 2005, four deer collected by the DNR in 2005, five deer collected by the DNR in 2006, one hunter-harvest deer taken during the 2006 deer season, three deer collected by the DNR in 2007 and five hunter-harvested deer taken during the 2007 deer season). Operating within guidelines established by its CWD – Incident Response Plan, the DNR has taken the steps necessary to implement appropriate management actions designed to control the spread of this disease, prevent further introduction of the disease, and possibly eliminate the disease from the state. Full text of the press release is at:

http://www.wvdnr.gov/2007news/07news174.shtm


West Virginia DNR CWD information is available at:

http://www.wvdnr.gov


FULL REPORT ;

http://chronic-wasting-disease.blogspot.com/2008/01/cwd-update-89-january-4-2008.html


Monday, December 17, 2007

Five Additional Deer Test Positive for Chronic Wasting Disease In Hampshire County, West Virginia

http://chronic-wasting-disease.blogspot.com/2007/12/five-additional-deer-test-positive-for.html


UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html


TSS

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Thursday, January 06, 2011

KANSAS FIRST CASE OF CHRONIC WASTING IN 2010 DEER SEASON CONFIRMED

FIRST CASE OF CHRONIC WASTING IN 2010 DEER SEASON CONFIRMED


White-tailed deer taken in Decatur County Nov. 7; complete results due in springPRATT — The Kansas Department of Wildlife and Parks (KDWP) has announced the first confirmed case of chronic wasting disease (CWD) found in a deer taken during a 2010 deer season. The animal was the only one of 90 tested by KDWP as of Dec. 8 to show a “presumptive positive” result. Samples of deer tissue taken by KDWP are sent to the K-State Diagnostic Veterinary Lab in Manhattan for preliminary testing. If the K-State lab determines the sample is a presumptive positive, the sample is then sent to the National Veterinary Services Lab in Ames, Iowa, for confirmation.


This deer was a 3 ½-year-old male taken in Decatur County by an archery hunter on Nov. 7. Because samples from the January whitetail antlerless only seasons have yet to be collected, complete results of testing won’t be available until March. Last year, 2,738 animals were tested for CWD, including 17 elk, 289 mule deer, and 2,428 white-tailed deer, and four unknown species. Of those samples, 15 were confirmed positive.
Annual testing is part of ongoing effort by KDWP to monitor the prevalence and spread of CWD. The fatal disease was first detected in a wild deer taken in Cheyenne County in 2005. Three infected deer were taken in Decatur County in 2007, 10 tested positive in 2008, and 15 in 2009, all in northwest Kansas.


CWD is a member of the group of diseases called transmissible spongiform encephalopathies (TSEs). Other diseases in this group include scrapie in sheep and goats, bovine spongiform encephalopathy (BSE or Mad Cow Disease) in cattle, and Cruetzfeldt-Jacob disease in people. CWD is a progressive, fatal disease that results in small holes developing in the brain, giving it a sponge-like appearance under the microscope. An animal may carry the disease without outward indication but in the later stages, signs may include behavioral changes such as decreased interactions with other animals, listlessness, lowering of the head, weight loss, repetitive walking in set patterns, and a lack of response to humans. Anyone who discovers a sick or suspect deer should contact the nearest KDWP office.


There is no vaccine or other biological method that prevents the spread of CWD. However, there is no evidence that CWD in the natural environment poses a risk to humans or livestock. Still, precautions should be taken. Hunters are advised not to eat meat from animals known to be infected, and common sense precautions are advised when field dressing and processing meat from animals taken in areas where CWD is found.


More information on CWD can be found on KDWP’s website, www.kdwp.state.ks.us or at the Chronic Wasting Disease Alliance website, www.cwd-info.org-30


http://www.kdwp.state.ks.us/news/Hunting/FIRST-CASE-OF-CHRONIC-WASTING-IN-2010-DEER-SEASON-CONFIRMED



Thursday, January 21, 2010

Kansas has more CWD cases


http://chronic-wasting-disease.blogspot.com/2010/01/kansas-has-more-cwd-cases.html



http://chronic-wasting-disease.blogspot.com/



TSS

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