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

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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Tuesday, January 27, 2009

Chronic Wasting Disease found in a farmed elk from Olmsted County ST. PAUL, Minn.

FOR IMMEDIATE RELEASE: Monday, January 26, 2009

Contact: Malissa Fritz, BAH Communications Director, 651-201-6830

Chronic Wasting Disease found in a farmed elk from Olmsted County

Mandatory surveillance program leads to detection of positive elk; state initiates investigation

ST. PAUL, Minn. – The Minnesota Board of Animal Health today announced that a farmed elk from an Olmsted County herd tested positive for Chronic Wasting Disease (CWD). The brain stem and lymph nodes from a 7-year-old female elk were submitted to the U.S. Department of Agriculture’s National Veterinary Services Laboratory (NVSL) in Ames, Iowa, after the animal was slaughtered. NVSL confirmed the animal had CWD. The Board of Animal Health quarantined the herd on January 23, 2009. This quarantine means no cervidae (members of the deer and elk family) can move on or off the farm. Meanwhile, officials continue to investigate the source of the infection and whether other cervidae may have been exposed. In 2003, Minnesota implemented mandatory registration and CWD surveillance programs for farmed cervidae herds. When farmed cervidae over 16 months of age die or are slaughtered, herd owners must submit brain samples for CWD testing. CWD is a fatal brain and nervous system disease found in cervidae in certain parts of North America. The disease is caused by an abnormally shaped protein called a prion, which can damage brain and nerve tissue. Infected animals show progressive loss of body weight with accompanying behavioral changes. In later stages of the disease, infected animals become emaciated (thus “wasting” disease). Other signs include staggering, consuming large amounts of water, excessive urination, and drooling. According to state health officials and the federal Centers for Disease Control and Prevention, there is no evidence that CWD can be transmitted to humans. For more information on CWD and the BAH, visit their website at www.bah.state.mn.us.

http://www.bah.state.mn.us/bah/releases/nr2009-01-26.pdf


Saturday, January 24, 2009

Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report

http://bse-atypical.blogspot.com/2009/01/research-project-detection-of-tse.html


CWD UPDATE 2009

-------------------- BSE-L@LISTS.AEGEE.ORG --------------------

Research Project: Detection of Transmissible Spongiform Encephalopathy Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: Foodborne Contaminants Research

2008 Annual Report

1a.Objectives (from AD-416) We will develop highly sensitive diagnostic tests to detect transmissible spongiform encephalopathy (TSE) in livestock and wildlife animal species prior to the onset of clinical disease. We will also develop tests to confirm the presence or absence of TSE disease agents in ingredients of animal origin and decontaminated environments.

1b.Approach (from AD-416) The threat of BSE continues to affect export economics for US meat. Meanwhile scrapie continues to influence sheep profits and herd biosecurity, and CWD is spreading throughout North America. Thus U.S. animal industry stakeholders have identified detection of the TSE infectious agent (prions) as a priority biosecurity research issue essential for prevention of TSE diseases. We will build on our previous successes using mass spectrometry (MS) for high-sensitivity and specificity in detection of PrPsc as a marker for TSE infectivity in blood using a hamster scrapie model. We will also develop a novel PrP-null mouse strain and related myeloma cell culture system for production of monoclonal antibodies (MAb), which may be specific for PrPsc. We will then choose MS or MAb and validate our novel diagnostic for preclinical diagnosis of scrapie in sheep blood. Whereas MS and MAb methods rely on dissolved samples, contamination of agricultural products and environmental surfaces is associated with solid samples. So we will produce a cell culture based assay for TSE infectivity that is surface-adsorbed. After using the relatively convenient hamster model for early development, we will validate this technology for detection of scrapie in sheep brain on meat-and-bone meal and stainless steel. Replacing 5325-32000-007-00D (3/19/2008).

3.Progress Report At this point in the Project, in general, we are completing preliminary studies using our relatively convenient hamster and mouse models, and are starting to work with more agriculturally relevant sheep and deer tissues. We are finding the cervid tissues quite different from rodent tissues, in their requirements for sample workup (e.g., amount and quality of lipid and fiber) and in their expression of TSE infectivity and presence of markers. OSQR required us to establish a new collaboration with a reputable cell biologist, to assist with our cell-based scrapie assay. We now have a new MTA with Dr. Charles Weissmann (Scripps), under which we are sharing cell lines and laboratory protocols. We have completed one part of our speed congenics project to develop PrP-null (disease-resistant) mice for use in antibody generation. After conceiving a new procedure for immunogen enrichment, we performed experimental vaccination of these animals in our facilities. This project relates to NP103 Component 8: Prevention and control of transmissible spongiform encephalopathies. Problem statement 9A: Scrapie; 9B Chronic Wasting Disease (CWD); and 9C: Bovine Spongiform Encephalopathy (BSE).

4.Accomplishments 1. Proteinase K-free method for preparation of samples facilitates TSE blood assay.

The most widely used and regulatory approved methods for detection of Transmissible Spongiform Encephalopathy (TSE) contain a step in which the sample is subjected to digestion by a very strong enzyme, proteinase K, which degrades almost all proteins in the sample except for an Infectious isoform of the normal cellular prion protein, a prion (PrPsc). Although PrPsc has served well as a marker for brain disease, infectivity in the blood is mostly not proteinase K resistant. The proteinase K-free technique developed by ARS scientists in the Foodborne Contaminants Research Unit in Albany, CA will allow scientists to detect infectivity in blood. These efforts will lead to diagnostic tests that will save farmers and ranchers money and resources by allowing them to identify infected animals prior to purchase, sale or slaughter, and keep TSE-infected animals out of the US food supply. This accomplishment addresses NP103 Component 8: Prevention and Control of Transmissible Spongiform Encephalopathies; Problem Statement 9A: Scrapie; 9B: Chronic Wasting Disease (CWD); and 9C: Bovine Spongiform Encephalopathy (BSE).

2. Demonstrated conversion of a non-infectious normal cellular prion protein (PrP) into disease isoform in cell culture.

Although Transmissible Spongiform Encephalopathy (TSE) infectivity can be detected using animal models and mass spectroscopy, a cell culture system offers increased speed and throughput. ARS scientists in the Foodborne Contaminants Research Unit in Albany, CA developed conditions for growth and infection of existing cell cultures and cultures expressing transgenic PrP genes, observing conversion to the disease-associated PrPsc isoform. This method will be further developed to detect infectivity that is adsorbed onto surfaces, such as stainless steel and soil. These efforts will lead to diagnostic tests that will save farmers and ranchers money and resources by allowing them to identify infected areas and equipment before these areas or items can infect their animals. This accomplishment addresses NP103 Component 8: Prevention and Control of Transmissible Spongiform Encephalopathies; Problem Statement 9A: Scrapie; 9B: Chronic Wasting Disease (CWD); and 9C: Bovine Spongiform Encephalopathy (BSE).

5.Significant Activities that Support Special Target Populations None.

6.Technology Transfer Number of New Commercial Licenses Executed 1

Review Publications Bruederle, C.E., Hnasko, R.M., Kraemer, T., Garcia, R.A., Haas, M.J., Marmer, W.N., Carter, J.M. 2008. Prion infected Meat-and-Bone Meal is still infectious after biodiesel production. PLoS Pathogens. Available: http://dx.plos.org/10.1371/journal.pone.0002969

Onisko, B.C., Chen, N., Napoli, J. 2008. The Nuclear Transcription Factor RAR Associates with Neuronal RNA Granules and Suppresses Translation. Journal of Biological Chemistry. 283(30):20841-20847.

Sajnani, G., Pastrana, M.A., Dynin, I.A., Onisko, B.C., Requena, J.R. 2008. Insights on scrapie prion protein (prpsc) structure obtained by limited proteolysis and mass spectrometry. Journal of Molecular Biology. 382(2008):88-98.

http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=413072&showpars=true&fy=2008


FY2006: Tests for prion contamination in soil and water will be developed.

http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=405202&showpars=true&fy=2003


???

Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years Bjoern Seidel1#*, Achim Thomzig2#, Anne Buschmann3#, Martin H. Groschup3, Rainer Peters1, Michael Beekes2, Konstantin Terytze4

1 Fraunhofer Institute for Molecular Biology und Applied Ecology (IME), Schmallenberg, Germany, 2 P24 -Transmissible Spongiform Encephalopathies, Robert Koch-Institut, Berlin, Germany, 3 Institute for Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Insel Riems, Germany, 4 German Federal Environmental Agency (Umweltbundesamt, UBA), Dessau, Germany

Abstract The persistence of infectious biomolecules in soil constitutes a substantial challenge. This holds particularly true with respect to prions, the causative agents of transmissible spongiform encephalopathies (TSEs) such as scrapie, bovine spongiform encephalopathy (BSE), or chronic wasting disease (CWD). Various studies have indicated that prions are able to persist in soil for years without losing their pathogenic activity. Dissemination of prions into the environment can occur from several sources, e.g., infectious placenta or amniotic fluid of sheep. Furthermore, environmental contamination by saliva, excrements or non-sterilized agricultural organic fertilizer is conceivable. Natural transmission of scrapie in the field seems to occur via the alimentary tract in the majority of cases, and scrapie-free sheep flocks can become infected on pastures where outbreaks of scrapie had been observed before. These findings point to a sustained contagion in the environment, and notably the soil. By using outdoor lysimeters, we simulated a contamination of standard soil with hamster-adapted 263K scrapie prions, and analyzed the presence and biological activity of the soil-associated PrPSc and infectivity by Western blotting and hamster bioassay, respectively. Our results showed that 263K scrapie agent can persist in soil at least over 29 months. Strikingly, not only the contaminated soil itself retained high levels of infectivity, as evidenced by oral administration to Syrian hamsters, but also feeding of aqueous soil extracts was able to induce disease in the reporter animals. We could also demonstrate that PrPSc in soil, extracted after 21 months, provides a catalytically active seed in the protein misfolding cyclic amplification (PMCA) reaction. PMCA opens therefore a perspective for considerably improving the detectability of prions in soil samples from the field.

http://www.plosone.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0000435&representation=PDF


Prions Adhere to Soil Minerals and Remain Infectious Christopher J. Johnson1,2, Kristen E. Phillips3, Peter T. Schramm3, Debbie McKenzie2, Judd M. Aiken1,2, Joel A. Pedersen3,4*

1 Program in Cellular and Molecular Biology, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 2 Department of Animal Health and Biomedical Sciences, School of Veterinary Medicine, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 3 Molecular and Environmental Toxicology Center, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 4 Department of Soil Science, University of Wisconsin Madison, Madison, Wisconsin, United States of America

Abstract An unidentified environmental reservoir of infectivity contributes to the natural transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) in sheep, deer, and elk. Prion infectivity may enter soil environments via shedding from diseased animals and decomposition of infected carcasses. Burial of TSE-infected cattle, sheep, and deer as a means of disposal has resulted in unintentional introduction of prions into subsurface environments. We examined the potential for soil to serve as a TSE reservoir by studying the interaction of the disease-associated prion protein (PrPSc) with common soil minerals. In this study, we demonstrated substantial PrPSc adsorption to two clay minerals, quartz, and four whole soil samples. We quantified the PrPSc-binding capacities of each mineral. Furthermore, we observed that PrPSc desorbed from montmorillonite clay was cleaved at an N-terminal site and the interaction between PrPSc and Mte was strong, making desorption of the protein difficult. Despite cleavage and avid binding, PrPSc bound to Mte remained infectious. Results from our study suggest that PrPSc released into soil environments may be preserved in a bioavailable form, perpetuating prion disease epizootics and exposing other species to the infectious agent.

Synopsis Transmissible spongiform encephalopathies (TSEs) are a group of incurable diseases likely caused by a misfolded form of the prion protein (PrPSc). TSEs include scrapie in sheep, bovine spongiform encephalopathy ("mad cow" disease) in cattle, chronic wasting disease (CWD) in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and CWD are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity, because PrPSc likely enters soil environments through urinary or alimentary shedding and decomposition of infected animals. In this manuscript, the authors test the potential for soil to serve as a reservoir for PrPSc and TSE infectivity. They demonstrate that PrPSc binds to a variety of soil minerals and to whole soils. They also quantitate the levels of protein binding to three common soil minerals and show that the interaction of PrPSc with montmorillonite, a common clay mineral, is remarkably strong. PrPSc bound to Mte remained infectious to laboratory animals, suggesting that soil can serve as a reservoir of TSE infectivity.

http://www.plospathogens.org/article/info:doi%2F10.1371%2Fjournal.ppat.0020032


Direct Detection of Soil-Bound Prions Sacha Genovesi1, Liviana Leita2, Paolo Sequi3, Igino Andrighetto4, M. Catia Sorgato1,5, Alessandro Bertoli1*

1 Dipartimento di Chimica Biologica, Università di Padova, Padova, Italy, 2 Istituto Sperimentale per la Nutrizione delle Piante, Gorizia, Italy, 3 Istituto Sperimentale per la Nutrizione delle Piante, Roma, Italy, 4 Istituto Zooprofilattico Sperimentale delle Venezie, Legnaro, Italy, 5 CNR Istituto di Neuroscienze, Padova, Italy

Abstract Scrapie and chronic wasting disease are contagious prion diseases affecting sheep and cervids, respectively. Studies have indicated that horizontal transmission is important in sustaining these epidemics, and that environmental contamination plays an important role in this. In the perspective of detecting prions in soil samples from the field by more direct methods than animal-based bioassays, we have developed a novel immuno-based approach that visualises in situ the major component (PrPSc) of prions sorbed onto agricultural soil particles. Importantly, the protocol needs no extraction of the protein from soil. Using a cell-based assay of infectivity, we also report that samples of agricultural soil, or quartz sand, acquire prion infectivity after exposure to whole brain homogenates from prion-infected mice. Our data provide further support to the notion that prion-exposed soils retain infectivity, as recently determined in Syrian hamsters intracerebrally or orally challanged with contaminated soils. The cell approach of the potential infectivity of contaminated soil is faster and cheaper than classical animal-based bioassays. Although it suffers from limitations, e.g. it can currently test only a few mouse prion strains, the cell model can nevertheless be applied in its present form to understand how soil composition influences infectivity, and to test prion-inactivating procedures.

http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0001069


now, something i have pondered long about, with the atypical BSE in Texas and Alabama, where, as far as i know, those farms WERE NOT quarantined for 5 years due to an atypical TSE. HOWEVER, the farms of the atypical scrapie from where the mad sheep of mad river valley occurred, these farms were quarantined. ...

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

From: Terry S. Singeltary Sr.

To: Boyd.Rutherford@usda.gov

Sent: Sunday, February 25, 2007 12:35 PM

Subject: FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP

Greetings USDA,

I respectfully request the final results of the mouse bio-assays test that were to have supposedly began 2+ years late, 5 years ago, on the imported sheep from Belgium ?

WHAT happened to the test results and MOUSE BIO-ASSAYS of those imported sheep from Belgium that were confiscated and slaughtered from the Faillace's, what sort of TSE did these animals have ?

WERE they atypical scrapie, BSE, and or typical scrapie ?

HOW much longer will you refuse to give us this information ? and for what reason ?

WHY is it that the Farm of the Mad Sheep of Mad River Valley were quarantined for 5 years, but none of these farms from Texas and Alabama with Atypical TSE in the Bovine, they have not been quarantined for 5 years,why not, with the real risk of BSE to sheep, whom is to say this was not BSE ?

snip...

full text ;

http://foiamadsheepmadrivervalley.blogspot.com/2008/04/re-foia-of-declaration-of-extraordinary.html


Monday, September 1, 2008 RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [No. 00-072-1] September 1, 2008

Greetings again BSE-L members,

I had a pleasant surprise this past Saturday. I got an unexpected package from O.I.G. on my old F.O.I.A. request, of the final test results of the infamous mad sheep of mad river valley. IF you all remember, back on Thu, 24 Apr 2008 15:00:20 -0500 I wrote ;

snip...full text ;

http://foiamadsheepmadrivervalley.blogspot.com/2008/09/re-foia-of-declaration-of-extraordinary.html


http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=12;t=000469


http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=print_topic;f=12;t=000469


i remember a few years back ???

that a study showed the prion uptake in a tomato plant, not that this would surprise me ;

56. Members considered that there is no evidence that crops grown on the land which received composted excreta from BSE-challenged animals pose a TSE risk to humans or animals. One member suggested that, as some of these animals are orally challenged with high doses of BSE-infected materials, and the distribution of infectivity in the digestive system is not completely understood, it might be premature to conclude that there is no infective agent in the manure. Furthermore, an unpublished study had indicated low level absorption of PrP from soil by tomato plants although it should be noted that this study had not been repeated. Details of this work would be sent to the SEAC Secretary. Dr Matthews explained that most of the manure from animals challenged with high doses of BSE had already been composted and used for coppicing. Members agreed that the risks from disposal of residual manure from experimental animals would be much less than historic risks of on farm contamination from naturally infected animals at the height of the BSE epidemic.

http://www.seac.gov.uk/minutes/final91.pdf


disturbing to say the least. ...TSS

Tuesday, January 13, 2009

Antemortem detection of PrPCWD in preclinical, ranch-raised Rocky Mountain elk (Cervus elaphus nelsoni) by biopsy of the rectal mucosa Full Scientific Reports

http://chronic-wasting-disease.blogspot.com/2009/01/antemortem-detection-of-prpcwd-in.html


Saturday, January 10, 2009

Chronic Wasting Disease Investigation Update Michigan December 18, 2008

http://chronic-wasting-disease.blogspot.com/2009/01/chronic-wasting-disease-investigation.html


Sunday, September 07, 2008

CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA

http://chronic-wasting-disease.blogspot.com/2008/09/cwd-live-test-and-political-aspects-or.html


2008 CWD Laboratory Testing for Wild White-tailed Deer

http://www.michigan.gov/emergingdiseases/0,1607,7-186-25806-202922--,00.html


Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-to-tighten-taxidermy-rules-hunters.html



Monday, January 05, 2009

CWD, GAME FARMS, BAITING, AND POLITICS

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html


Thursday, December 25, 2008 Lions and Prions and Deer Demise

http://chronic-wasting-disease.blogspot.com/2008/12/lions-and-prions-and-deer-demise.html


Tuesday, January 06, 2009

CWD Update 93 December 29, 2008

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


Tuesday, September 09, 2008 CWD MICHIGAN UPDATE September 5, 2008

http://chronic-wasting-disease.blogspot.com/2008/09/cwd-michigan-update-september-5-2008.html


Monday, August 25, 2008 CWD FIRST DOCUMENTED IN MICHIGAN

http://chronic-wasting-disease.blogspot.com/2008/08/cwd-first-documented-in-michigan.html


TSS

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