Thursday, June 09, 2011

Michigan NRC voted 4-3 to lift the baiting and feeding ban LP

The Natural Resources Commission has voted 4-3 to lift the baiting and feeding ban in the Lower Peninsula, except in DMU 487, AKA the TB Zone, where baiting and feeding will remain prohibited. Only 2 gallons may be scattered at any one time in a 10 foot by 10 foot square area, this limit applies to both baiting AND recreational feeding. Additional details will be posted as they become available. www.michigan.gov/nrc




FOR IMMEDIATE RELEASE

June 10, 2011

Contact: Mary Dettloff 517-335-3014

Natural Resources Commission Votes to Lift Deer Baiting Ban

The Michigan Natural Resources Commission on Thursday voted 4-3 to lift the current deer baiting and feeding ban in the state’s Lower Peninsula. The ban had been in place since 2008, when Chronic Wasting Disease (CWD) was detected in a deer at a private deer breeding facility in Kent County.

Baiting will still be prohibited in Deer Management Unit (DMU) 487, the six-county Bovine Tuberculosis zone in northeastern Lower Michigan. The counties where baiting will continue to be prohibited are Alcona, Alpena, Iosco, Montmorency, Oscoda and Presque Isle.

The NRC approved a proposal to allow baiting in limited quantities from Oct. 1 to Jan. 1. Hunters may place any type of bait, no more than two gallons at a time, across a 10-foot by 10-foot area per hunting location.

The NRC also reinstated recreational feeding of deer in the Lower Peninsula, with the exception of DMU 487. Property owners may place two gallons of bait on their property within 100 yards of their residence year-around.

The NRC also placed a three-year sunset on the regulations, which means it will reconsider the baiting issue again in 2014.

In 2008, the Department of Natural Resources announced it had detected the state’s first case of CWD in a three year-old female deer at a private deer breeding facility in Kent County. At the time, the Department followed protocol as outlined in the state’s emergency response plan for CWD and immediately banned baiting and feeding of white-tailed deer in the Lower Peninsula. The NRC then passed regulations making the ban permanent, but said it would reconsider the ban in three years, giving the DNR adequate time to perform disease testing and surveillance in the state for CWD.

In the three year period, the DNR tested thousands of white-tailed deer for CWD, but did not detect another case.

The NRC also directed the Department to work with the Legislature to strengthen the penalties for baiting violations. A potential bill sponsor has been identified who supports establishing an escalating scale of penalties for repeat offenders, which would include mandatory hunting license revocation.

If hunters do use bait, the DNR requests they not place bait repeatedly at the same point on the ground, and only place bait out when they are actively hunting. This may minimize the chance of direct and indirect exposure of deer to any unknown disease that may be present.

For more information about CWD, go to www.michigan.gov/emergingdiseases.

The Michigan Department of Natural Resources is committed to the conservation, protection, management, use and enjoyment of the state’s natural and cultural resources for current and future generations. For more information, go to www.michigan.gov/dnr.

###



http://www.michigan.gov/dnr/0,1607,7-153--257664--,00.html




o.k., so if it's 9 feet and 11 inches X 9 feet and 11 inches, then the congregation of animals will not matter. they will not spread disease.

BUT, if it's 10 feet, and 1 inch X 10 feet and 1 inch, then the animals will spread disease.

does anyone think these animals carry a ruler with them.

i know hunters dont', and if they did, it would not matter. the previous feed ban could not be enforced anyway.

gimmie a break. this was nothing more than another knee jerk reaction to try and make everyone happy, and in doing so, you will still spread disease. they may have well just allowed all open baiting by the truck load, because when you allow any baiting at all, you will draw deer and other critters to the piles, and they will then rely on them, they become dependent, and they will congregate over the area, night, after night, after night, day after day, and spread disease, and it does not matter if it's 1 gallon, 2 gallon, or a dump truck load, the animals will know it's there, and then depend on it. but money trumps all science, and that's why we are still in this prion TSE mess. hunters will be able to sit in their blinds again and have the animals walk up to them, so they can hit them in the head and kill them if they want too, instead of even using a gun. i see no hope here, and no hunter that uses bait. a big step backwards for Michigan, and anyone that cares about the cervid population and cwd risk factors there from.

what's going to happen if worse case scenario happens, and the cervid population does start to become extinct, instead of the opposite now ???

how will those baiters and feeders feel then???



what changed NRC minds on science $



you have just about every CWD TSE scientist, biologist, DNR in most states, saying science shows that baiting and feeding enhances the likelyhood of disease transmission and spread there from.

simply put, money and politics trumped science at Michigan NRC on baiting and CWD risk factors. or, what changed their minds $


please see ;


Why didn’t DNR recommend that baiting and feeding be limited to a small amount rather than banning it?

Even small amounts of bait and feed appear to present a disease risk. A study in Michigan found that more nose-to-nose contacts among deer occurred over 5 gallons of bait than over larger piles of bait. This was true whether bait was in piles, rows, or scattered. Even though you might think that only a couple deer would use a small amount of feed, this is not always true. For example, one Wisconsin resident recently reported observing 35 different deer regularly visit a 2 gallon feeding site near his house. A few deer may consume the feed, but others continue to inspect the site and lick up whatever remains.

Why such drastic actions?

There is too much at stake to risk CWD and other infectious disease introduction and establishment in deer populations across the state. Disease experts believe that baiting and feeding are responsible for TB sustaining itself in Michigan’s deer herd. No one wants to have to establish new CWD eradication zones around the state. Baiting and feeding are one of the risk factors that we can do something about.


http://www.dnr.state.wi.us/org/land/wildlife/HUNT/deer/baitfeedfaq.pdf





Thursday, June 09, 2011

Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission

http://chronic-wasting-disease.blogspot.com/2011/06/detection-of-cwd-prions-in-salivary.html



Wednesday, June 08, 2011

CWD Keep the ban on deer baiting in Michigan

http://chronic-wasting-disease.blogspot.com/2011/06/cwd-keep-ban-on-deer-baiting-in.html



February 14, 2003

Chronic Wasting Disease and the Science in support of the Ban on Baiting and Feeding Deer.

Timothy R. Van Deelen Ph.D. Wisconsin DNR Research

Summary

Reliable science provides support for a ban of baiting and feeding of white-tailed deer to reduce disease risks for Chronic Wasting Disease (CWD). Peer-reviewed research papers published in reputable scientific journals indicate the following: • CWD is transmitted laterally (live diseased deer infect other deer) • Deer can get CWD by ingesting something contaminated with the disease prion • CWD prions may be shed in feces and saliva • Disease course and symptoms indicate high potential for transmission where deer are concentrated • Evidence from captive situations indicates that deer can get CWD from highly contaminated environments. • Baiting and Feeding causes unnatural concentration of deer • Reduction of contact through a ban on baiting and feeding is likely very important to eradicating or containing a CWD outbreak. • Baiting and feeding continues to put Wisconsin’s deer herd at risk to other serious diseases In addition, experts in CWD, wildlife disease and deer nutrition support bans on baiting and feeding as part of a comprehensive strategy to prevent and/or manage CWD. Under a baiting and feeding ban, disease outbreaks are more likely to be smaller in scale and more apt to be contained or eliminated. With the long CWD incubation period and other factors that make discovery of a new outbreak difficult, an outbreak that is already widespread when detected because of baiting and feeding may not be able to be contained or eliminated. This document provides details and explicit links to the supporting science.

http://www.dnr.state.wi.us/org/land/wildlife/Whealth/issues/Cwd/doc/cwdscsu.pdf




CWD, GAME FARMS, BAITING, AND POLITICS

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


http://chronic-wasting-disease.blogspot.com/2008/08/cwd-feeding-and-baiting-piles.html


Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

http://scrapie-usa.blogspot.com/2011/02/environmental-sources-of-scrapie-prions.html


Saturday, May 14, 2011

Modeling Routes of Chronic Wasting Disease Transmission: Environmental Prion Persistence Promotes Deer Population Decline and Extinction

http://chronic-wasting-disease.blogspot.com/2011/05/modeling-routes-of-chronic-wasting.html




Friday, February 25, 2011

Soil clay content underlies prion infection odds

http://chronic-wasting-disease.blogspot.com/2011/02/soil-clay-content-underlies-prion.html



Wednesday, October 14, 2009

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html



ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD ;


http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html


http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf





Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.


http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html


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


Wednesday, April 06, 2011

Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2011/04/presence-and-seeding-activity-of.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


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


Saturday, May 14, 2011

Modeling Routes of Chronic Wasting Disease Transmission: Environmental Prion Persistence Promotes Deer Population Decline and Extinction

http://chronic-wasting-disease.blogspot.com/2011/05/modeling-routes-of-chronic-wasting.html



Wednesday, June 01, 2011

Management of CWD in Canada: Past Practices, Current Conditions, Current Science, Future Risks and Options

http://chronic-wasting-disease.blogspot.com/2011/06/management-of-cwd-in-canada-past.html




terry

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Wednesday, June 08, 2011

CWD Keep the ban on deer baiting in Michigan

Online commentary: Keep the ban on deer baiting

4:37 PM, Jun. 7, 2011

The state Natural Resources Commission is expected to vote this week on rescinding its ban on baiting. But to allow baiting for deer again would be a reckless decision, and a sign of the commission caving to a clamorous minority.

Currently, 28 states prohibit the use of bait while hunting deer. Eight other states place heavy restrictions on this practice.

In 2008, Michigan banned the use of hunting deer over bait throughout the entire Lower Peninsula, after the discovery of a deer with chronic wasting disease at a game ranch in Kent County. This action was taken according to a comprehensive 2002 plan created to respond to such an outbreak. It is reinforced by the fact that most wildlife experts believe that unnatural concentrations of food products (bait) could serve as vectors in the transmission of this and other diseases.

In spite of these regulations, the "baiting ban" has been largely ignored by legions of hunters who have callously ignored the risks associated with this 100% fatal disease.

The NRC has reached out to experts in order to guide them in the process of crafting policy -- with science being the only rudder -- as it should. That practice was solidified with Proposal G, the 1996 ballot proposal that put game management in the hands of the commission with a requirement for science-based decision-making. To date:

• Not one of our scientists has stated that they favor baiting.

• Very few of our scientists have come out as even being neutral on baiting.

• Virtually all of our scientists and all of our experts have been resolute in voice. They are whispering a single word in to the NRC's ear: Danger!

For the NRC to ignore them is to say, in essence, that our own scientists, whom we pay for this counsel, are wrong. To ignore them is to render Proposal G as somewhat meaningless.

For the record, I have no hidden anti-baiting agenda. Prior to the ban, I regularly placed carrots and sugar beets on my hunting property, and I still have two 55-gallon spin feeders, which now have become a vibrant retirement community for about 4 zillion hornets.

My better angels tell me that the NRC understands the terrible threat associated with CWD. And, while we do not have all the answers, our only response must be to err on the side of caution. No cases of CWD have emerged in Michigan during the past three years, but the disease has been discovered a mere 100 miles from Michigan's borders in McHenry County, Illinois.

The bottom line is this: The risk is too great, and the resource is too precious.

The NRC seems to believe that this decision will affect only the 6% of the population who happen to be hunters. That is folly. These matters touch all citizens who love and respect the abundant resources within our state. The commission should not be responding to a minority so entrenched in a practice that it is willing to risk the resource.

Maintaining the ban on baiting will not be a popular decision for the NRC, but it is the right decision. And, while new cases of CWD may ultimately emerge, 100 years from now citizens will be able to look back at the right decision that the NRC took this year and say; "At least they did their part."

Bill Audette of Lake Orion is an avid outdoor enthusiast and owner of Orion Automotive, LLC, a marketing and financial products consulting agency.

http://www.freep.com/article/20110608/OPINION05/106070452/Online-commentary-Keep-ban-deer-baiting?odyssey=mod%7Cnewswell%7Ctext%7CFRONTPAGE%7Cp



NRC proposes lifting ban on deer baiting and feeding in Lower Peninsula

By Steve Griffin for the Daily News | Posted: Sunday, May 15, 2011 7:00 am

http://www.ourmidland.com/sports/article_b13a6779-69c3-54aa-84cf-d1fa30e8547b.html



D. Baiting and Feeding of Deer in the Lower Peninsula Wildlife Conservation Order Amendment No. 10 of 2011............................24-30

http://www.michigan.gov/documents/dnr/agnJune11_354207_7.pdf




WITH more and more science showing the environmental exposure and infection there from via CWD shedding etc, and of course the environmental risk factors of TB, in my opinion, to legalize any sort of baiting again, in my opinion is absurd. but i suppose those recreational hunters that need the bait to have their kill walk right up on them, i suppose there voices may be louder, and their pocket books bigger, and they may win out. if so, a tough loss for Michigan, and another step backwards. ...


kind regards,

terry


CWD, GAME FARMS, BAITING, AND POLITICS

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


http://chronic-wasting-disease.blogspot.com/2008/08/cwd-feeding-and-baiting-piles.html


Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

http://scrapie-usa.blogspot.com/2011/02/environmental-sources-of-scrapie-prions.html


Saturday, May 14, 2011

Modeling Routes of Chronic Wasting Disease Transmission: Environmental Prion Persistence Promotes Deer Population Decline and Extinction

http://chronic-wasting-disease.blogspot.com/2011/05/modeling-routes-of-chronic-wasting.html


Monday, February 14, 2011

THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER


NO, NO, NOT NO, BUT HELL NO !


Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html


Friday, February 25, 2011

Soil clay content underlies prion infection odds

http://chronic-wasting-disease.blogspot.com/2011/02/soil-clay-content-underlies-prion.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, February 22, 2010

Aerosol and Nasal Transmission of Chronic Wasting Disease in Cervidized Mice

http://chronic-wasting-disease.blogspot.com/2010/02/aerosol-and-nasal-transmission-of.html


AS THE CROW FLIES, SO DOES CWD



Sunday, November 01, 2009

American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases

http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html


Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2009/07/deer-carcass-decomposition-and.html


Sunday, December 06, 2009

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer

http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html


THEN YOU have water that has been contaminated from a CWD-endemic area ;


Wednesday, October 14, 2009

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html


ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD ;


http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html


http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf



Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.


http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html


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


Wednesday, April 06, 2011

Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2011/04/presence-and-seeding-activity-of.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



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



Saturday, May 14, 2011

Modeling Routes of Chronic Wasting Disease Transmission: Environmental Prion Persistence Promotes Deer Population Decline and Extinction

http://chronic-wasting-disease.blogspot.com/2011/05/modeling-routes-of-chronic-wasting.html



Wednesday, June 01, 2011

Management of CWD in Canada: Past Practices, Current Conditions, Current Science, Future Risks and Options

http://chronic-wasting-disease.blogspot.com/2011/06/management-of-cwd-in-canada-past.html



Tuesday, May 31, 2011

Chronic Wasting Disease DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011

http://chronic-wasting-disease.blogspot.com/2011/05/chronic-wasting-disease-doi.html



Friday, May 13,

2011 EFSA Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/efsa-joint-scientific-opinion-on-any.html



Topics in Current Chemistry, 2011, 1-28, DOI: 10.1007/128_2011_161

Atypical Prion Diseases in Humans and Animals

Michael A. Tranulis, Sylvie L. Benestad, Thierry Baron and Hans Kretzschmar

Abstract

Although prion diseases, such as Creutzfeldt–Jakob disease (CJD) in humans and scrapie in sheep, have long been recognized, our understanding of their epidemiology and pathogenesis is still in its early stages. Progress is hampered by the lengthy incubation periods and the lack of effective ways of monitoring and characterizing these agents. Protease-resistant conformers of the prion protein (PrP), known as the “scrapie form” (PrPSc), are used as disease markers, and for taxonomic purposes, in correlation with clinical, pathological, and genetic data. In humans, prion diseases can arise sporadically (sCJD) or genetically (gCJD and others), caused by mutations in the PrP-gene (PRNP), or as a foodborne infection, with the agent of bovine spongiform encephalopathy (BSE) causing variant CJD (vCJD). Person-to-person spread of human prion disease has only been known to occur following cannibalism (kuru disease in Papua New Guinea) or through medical or surgical treatment (iatrogenic CJD, iCJD). In contrast, scrapie in small ruminants and chronic wasting disease (CWD) in cervids behave as infectious diseases within these species. Recently, however, so-called atypical forms of prion diseases have been discovered in sheep (atypical/Nor98 scrapie) and in cattle, BSE-H and BSE-L. These maladies resemble sporadic or genetic human prion diseases and might be their animal equivalents. This hypothesis also raises the significant public health question of possible epidemiological links between these diseases and their counterparts in humans.

Keywords Animal - Atypical - Atypical/Nor98 scrapie - BSE-H - BSE-L - Human - Prion disease - Prion strain - Prion type

http://resources.metapress.com/pdf-preview.axd?code=f433r34h34ugg617&size=largest



MUCH MORE HERE ;


Monday, May 23, 2011

Atypical Prion Diseases in Humans and Animals 2011

Top Curr Chem (2011)

DOI: 10.1007/128_2011_161

# Springer-Verlag Berlin Heidelberg 2011

http://bse-atypical.blogspot.com/2011/05/atypical-prion-diseases-in-humans-and.html



Saturday, March 5, 2011




MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA



http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html




Tuesday, April 26, 2011



sporadic CJD RISING Text and figures of the latest annual report of the NCJDRSU covering the period 1990-2009 (published 11th March 2011)



http://creutzfeldt-jakob-disease.blogspot.com/2011/04/sporadic-cjd-rising-text-and-figures-of.html







TSS

Labels: , , ,

Wednesday, April 06, 2011

Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease

Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease

Abstract Introduction Results Discussion Materials and Methods Acknowledgments Author Contributions References Martin L. Daus1, Johanna Breyer2, Katja Wagenfuehr1, Wiebke M. Wemheuer2, Achim Thomzig1, Walter J. Schulz-Schaeffer2, Michael Beekes1*

1 P24 - Transmissible Spongiform Encephalopathies, Robert Koch-Institut, Berlin, Germany, 2 Prion and Dementia Research Unit, Department of Neuropathology, University Medical Center Göttingen, Göttingen, Germany

Chronic wasting disease (CWD) is a contagious, rapidly spreading transmissible spongiform encephalopathy (TSE), or prion disease, occurring in cervids such as white tailed-deer (WTD), mule deer or elk in North America. Despite efficient horizontal transmission of CWD among cervids natural transmission of the disease to other species has not yet been observed. Here, we report for the first time a direct biochemical demonstration of pathological prion protein PrPTSE and of PrPTSE-associated seeding activity, the static and dynamic biochemical markers for biological prion infectivity, respectively, in skeletal muscles of CWD-infected cervids, i. e. WTD for which no clinical signs of CWD had been recognized. The presence of PrPTSE was detected by Western- and postfixed frozen tissue blotting, while the seeding activity of PrPTSE was revealed by protein misfolding cyclic amplification (PMCA). Semi-quantitative Western blotting indicated that the concentration of PrPTSE in skeletal muscles of CWD-infected WTD was approximately 2000-10000 -fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE was located in muscle-associated nerve fascicles but not, in detectable amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.

snip...

Discussion

In the wake of the BSE epidemic, variant Creutzfeldt-Jakob disease has emerged as a previously unknown prion disease of humans. This has shown that significant risks for public health may potentially emanate from the presence of animal prions in human foodstuffs. When assessing such risks in the context of CWD, key factors that need to be considered are i) the distribution of CWD prions in infected animals and ii) the potential transmissibility of such prions to humans.

PMCA-based in vitro studies have indicated a rather high transmission barrier for CWD to macaques as well as to transgenic mice expressing the human prion protein, as no conversion of cellular prion proteins into PrPres could be induced by seeding PMCA reactions with CWD-infected brain tissue [22]. Consistent with these findings, transgenic mice overexpressing human prion protein with methionine or valine at polymorphic residue 129 were resistant to infection with CWD prions from mule deer [23]. Furthermore, recent in vivo studies revealed a robust barrier for the transmission of CWD to macaques which, again, is suggestive of a rather low risk for CWD transmission to humans [24]. However, squirrel monkeys could be infected with CWD [24], and increasing evidence points to the existence of different CWD isolates [25], [26]. Thus, it remains to be further clarified whether CWD may be caused by multiple prion strains with distinct transmission properties.

It has been shown previously that skeletal muscle tissue from CWD infected mule deer may contain prion infectivity [18]. Also, Western blot- and immunohistochemical analyses of heart muscles from CWD-infected Rocky mountain elk and white-tailed deer revealed the presence of pathological prion protein in cardiac myocytes. PrPTSE was found in the left ventricle of the heart at a 10- to 100- fold lower concentration as compared to the brain, but not in skeletal muscle [27].

Here we report the direct detection of pathological prion protein PrPTSE and of PrPTSE-associated seeding activity in skeletal muscles from cervids, i. e. WTD for which no clinical signs of prion disease had been recognized, using Western blotting, tissue blotting and PMCA as analytical techniques. Kurt et al. [22] recently reported that normal brain homogenate (NBH) from Syrian hamsters effectively supports the amplification of PrPres from CWD seeds in serial PMCA. Building on similar findings previously made in our laboratory (not shown) we also used hamster NBH as substrate for our PMCA analyses. We found that PrPres generated by PMCA after seeding with CWD- or 263K scrapie agents did not exhibit significant differences in the glycosylation- or electrophoretic migration patterns (not shown). As a safeguard to PMCA specificity safety measures aimed at preventing inadvertent cross-contamination with both prions from cervids or hamsters were implemented. Specifically, we sealed our PMCA reaction tubes with parafilm and paraffin wax, performed all pipetting steps exclusively with plugged single-use pipette tips, and changed gloves each time before handling a new PMCA sample. With these safety measures in place unseeded controls in which PMCA was performed with normal hamster brain homogenate only did not produce any unspecific PrPres staining in our experimental setup.

Our findings were obtained by an alternative methodology to bioassays in animals (i. e. combined biochemical detection of PrPTSE and its proteinaceous seeding activity) but are consistent with the observations reported by Angers et al. [18]. They may also provide an explanation for the negative findings by Jewell et al. [27] in skeletal muscle, since our Western blot results indicate a substantially lower concentration of PrPTSE in such tissue than reported for heart muscle.

Yet, it has to be noted that our assessments of PrPTSE levels in skeletal muscles were based on findings in presumably pre- or subclinically infected animals. Therefore, the concentration of PrPTSE in skeletal muscles of WTD with clinically manifest CWD may possibly exceed our estimate which refers to clinically inconspicuous animals that are more likely to enter the human food chain. Our tissue blot findings in skeletal muscles from CWD-infected WTD would be consistent with an anterograde spread of CWD prions via motor nerve fibres to muscle tissue (figure 4A). Similar neural spreading pathways of muscle infection were previously found in hamsters orally challenged with scrapie [28] and suggested by the detection of PrPTSE in muscle fibres and muscle-associated nerve fascicles of clinically-ill non-human primates challenged with BSE prions [29]. Whether the absence of detectable PrPTSE in myofibers observed in our study is a specific feature of CWD in WTD, or was due to a pre- or subclinical stage of infection in the examined animals, remains to be established. In any case, our observations support previous findings suggesting the precautionary prevention of muscle tissue from CWD-infected WTD in the human diet, and highlight the need to comprehensively elucidate of whether CWD may be transmissible to humans. While the understanding of TSEs in cervids has made substantial progress during the past few years, the assessment and management of risks possibly emanating from prions in skeletal muscles of CWD-infected cervids requires further research.

Citation: Daus ML, Breyer J, Wagenfuehr K, Wemheuer WM, Thomzig A, et al. (2011) Presence and Seeding Activity of Pathological Prion Protein (PrPTSE) in Skeletal Muscles of White-Tailed Deer Infected with Chronic Wasting Disease. PLoS ONE 6(4): e18345. doi:10.1371/journal.pone.0018345

Editor: Jason Bartz, Creighton University, United States of America

Received: December 17, 2010; Accepted: March 1, 2011; Published: April 1, 2011

Copyright: © 2011 Daus et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The study was sponsored by the Alberta Prion Research Institute (APRI, www.prioninstitute.ca), and the study was carried out within the APRI-sponsored research project “Comprehensive risk assessment of Chronic Wasting Disease (CWD) transmission to humans using non-human primates”. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

* E-mail: BeekesM@rki.de

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0018345


Thank you Professor Beekes et al, and again to PLos for open access !


This is another important study showing risk factors that should be taken seriously for human health via CWD, and risk factors there from iatrogenically i.e. via friendly fire or the pass it forward mode of human and animal Transmissible Spongiform Encephalopathy. in my opinion, we have floundered too long. IN 2001 i brought this up to the O.I.E., and they said they too were concerned, but yet a decade later, they too are still floundering, thus, humans and animals are still being exposed, and more and more science shows that CWD can transmit to humans. ...

kind regards, terry


Sent: Saturday, April 02, 2011 11:02 AM

Subject: [BSE-L] CWD Canada, 19 new cases

Current as of: 2011-02-29

Date confirmed Location Animal type infected January

January 19 Saskatchewan Deer January

January 4 Saskatchewan Deer

http://inspection.gc.ca/english/anima/disemala/rep/2011cwdmdce.shtml


CWD spreading in USA too ;

CWD Canada, 19 new cases 2011

TEN KANSAS DEER CONFIRMED POSITIVE IN CWD TESTS

CWD IN NEBRASKA IS INCREASING WITH 51 POSITIVE CAS...

South Dakota finds 25 more cases of Chronic Wastin...

Soil clay content underlies prion infection odds

Chronic wasting disease spreads farther west in Al...

THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPAR...

Chronic Wasting Disease Found In A White-Tailed De...

CWD ILLINOIS UPDATE FEBRUARY 2011

CWD Minnesota deer feeding ban covering Dodge, Goo...

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



CANADA CJD UPDATE 2011


CJD Deaths Reported by CJDSS1, 1994-20112 As of January 31, 2011

3. Final classification of 49 cases from 2009, 2010, 2011 is pending.

snip...

http://www.phac-aspc.gc.ca/hcai-iamss/cjd-mcj/cjdss-ssmcj/pdf/stats_0111-eng.pdf


USA 2011

USA

National Prion Disease Pathology Surveillance Center

Cases Examined1

(November 1, 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 87 51 43 7 1 0

1999 121 73 65 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 13

2005 344 194 157 36 1 0

2006 383 197 166 29 0 24

2007 377 214 187 27 0 0

2008 394 231 205 25 0 0

2009 425 258 215 43 0 0

2010 333 213 158 33 0 0

TOTAL 38315 22656 1907 328 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 18 cases in which the diagnosis is pending, and 18 inconclusive cases;

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.

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


Please notice where sporadic CJD cases in 1996 went from 28 cases, to 215 cases in 2009, the highest recorded year to date. sporadic CJD is on a steady rise, and has been since 1996.

I also urge you to again notice these disturbing factors in lines 5 and 6 ;

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

6 Includes 23 (22 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.


========end=====tss=====2011


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



Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html




THE steady rise of sporadic CJD cases in Canada AND USA, with many unusual cases of ''PENDING CLASSIFICATIONS" which have been pending now FOR 3 YEARS ???



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 Soto5,* + Author Affiliations

1 University of Texas Medical School at Houston, United States; 2 University of Kentucky, United States; 3 Case Western Reserve University, United States; 4 University of Chicago, United States; 5 University of Texas Medical School, United States * Corresponding author; email: claudio.soto@uth.tmc.edu

Received October 28, 2010. Accepted January 4, 2011. Copyright © 2011, The American Society for Biochemistry and Molecular Biology

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


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. ...end


PLEASE SEE FULL TEXT ;

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 Soto5,* + Author Affiliations

1 University of Texas Medical School at Houston, United States; 2 University of Kentucky, United States; 3 Case Western Reserve University, United States; 4 University of Chicago, United States; 5 University of Texas Medical School, United States * Corresponding author; email: claudio.soto@uth.tmc.edu

Received October 28, 2010. Accepted January 4, 2011. Copyright © 2011, The American Society for Biochemistry and Molecular Biology eneration

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


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


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


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.

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


and why do we not want to do TSE transmission studies on chimpanzees $


snip...

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

snip...

R. BRADLEY

http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf



Prions in Skeletal Muscles of Deer with Chronic Wasting Disease

Rachel C. Angers1,*, Shawn R. Browning1,*?, Tanya S. Seward2, Christina J. Sigurdson4,?, Michael W. Miller5, Edward A. Hoover4 and Glenn C. Telling1,2,3,§ + Author Affiliations

Abstract

The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.

Received for publication 21 November 2005. Accepted for publication 13 January 2006.

http://www.sciencemag.org/cgi/content/abstract/sci;311/5764/1117


Journal of Virology, September 2009, p. 9608-9610, Vol. 83, No. 18 0022-538X/09/$08.00+0 doi:10.1128/JVI.01127-09 Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Prion Infectivity in Fat of Deer with Chronic Wasting Disease

Brent Race,# Kimberly Meade-White,# Richard Race, and Bruce Chesebro* Rocky Mountain Laboratories, 903 South 4th Street, Hamilton, Montana 59840

Received 2 June 2009/ Accepted 24 June 2009

ABSTRACT Top ABSTRACT TEXT REFERENCES

Chronic wasting disease (CWD) is a neurodegenerative prion disease of cervids. Some animal prion diseases, such as bovine spongiform encephalopathy, can infect humans; however, human susceptibility to CWD is unknown. In ruminants, prion infectivity is found in central nervous system and lymphoid tissues, with smaller amounts in intestine and muscle. In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.

snip...

The highest risk of human contact with CWD might be through exposure to high-titer CNS tissue through accidental skin cuts or corneal contact at the time of harvest and butchering. However, the likelihood of a human consuming fat infected with a low titer of the CWD agent is much higher. It is impossible to remove all the fat present within muscle tissue, and fat consumption is inevitable when eating meat. Of additional concern is the fact that meat from an individual deer harvested by a hunter is typically consumed over multiple meals by the same group of people. These individuals would thus have multiple exposures to the CWD agent over time, which might increase the chance for transfer of infection.

In the Rocky Mountain region of North America, wild deer are subject to predation by wolves, coyotes, bears, and mountain lions. Although canines such as wolves and coyotes are not known to be susceptible to prion diseases, felines definitely are susceptible to BSE (9) and might also be infected by the CWD agent. Deer infected with the CWD agent are more likely to be killed by predators such as mountain lions (11). Peripheral tissues, including lymph nodes, muscle, and fat, which harbor prion infectivity are more accessible for consumption than CNS tissue, which has the highest level of infectivity late in disease. Therefore, infectivity in these peripheral tissues may be important in potential cross-species CWD transmissions in the wild.

The present finding of CWD infectivity in deer fat tissue raises the possibility that prion infectivity might also be found in fat tissue of other infected ruminants, such as sheep and cattle, whose fat and muscle tissues are more widely distributed in both the human and domestic-animal food chains. Although the infectivity in fat tissues is low compared to that in the CNS, there may be significant differences among species and between prion strains. Two fat samples from BSE agent-infected cattle were reported to be negative by bioassay in nontransgenic RIII mice (3, 6). However, RIII mice are 10,000-fold-less sensitive to BSE agent infection than transgenic mice expressing bovine PrP (4). It would be prudent to carry out additional infectivity assays on fat from BSE agent-infected cattle and scrapie agent-infected sheep using appropriate transgenic mice or homologous species to determine the risk from these sources.

http://jvi.asm.org/cgi/content/full/83/18/9608



THE LATEST DATA ON TISSUE INFECTIVITY

WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010

MAJOR CATEGORIES OF INFECTIVITY: TABLES IA, IB, IC

The assignment of tissues to high, low, and undetected infectivity categories is based exclusively upon observations of naturally occurring disease, or primary experimental infection by the oral route (in ruminants). The Tables do not include results from disease models using strains of TSE that have been adapted to experimental animals, because passaged strain phenotypes can differ significantly and unpredictably from those of naturally occurring disease. However, for tissues and fluids of exceptional public health interest, such as muscle, intestine, skin, secretions and excretions, experimental results have been indicated in footnotes.

Because the detection of misfolded prion protein (PrPTSE) broadly parallels infectivity titers in various tissues [Beekes et al 1996; Andreoletti et al 2004], PrPTSE testing results are presented in parallel with bioassay data.

Although a given tissue may be positive or negative in different varieties of TSE, the expert group considered a tissue to be potentially infectious even if a positive result occurred in only a single disease. The categorical assignment of tissues will almost certainly undergo further revision as new data accumulate from increasingly sensitive tests.

IA: High-infectivity tissues: CNS tissues that attain a high titer of infectivity in the later stages of all TSEs, and certain tissues that are anatomically associated with the CNS.

IB: Lower-infectivity tissues: peripheral tissues that have tested positive for infectivity and/or PrPTSE in at least one form of TSE.

IC: Tissues with no detectable infectivity: tissues that have been examined for infectivity and/or PrPTSE with negative results.

Data entries are shown as follows:

+ Presence of infectivity or PrPTSE

- Absence of detectable infectivity or PrPTSE

NT Not tested

NA Not applicable ?

Uncertain interpretation

( ) Limited or preliminary data

[ ] Infectivity or PrPTSE data based exclusively on bioassays in transgenic

(Tg)mice over-expressing the PrP-encoding gene or PrPTSE amplification methods.

A word of caution is offered about tissues in Table IB for which positive results are so far limited to either detection of PrPTSE using amplification techniques (PMCA), or infectivity bioassays in Tg mice that over-express PrP. The amounts of pathological protein or infectious agent detected by these exquisitely sensitive assays may well fall below the threshold of transmissibility for normal animals and humans. WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies 5

A good example is illustrated in the studies of urine and feces from deer infected with CWD: bioassays using normal deer as recipient subjects were negative; subsequent bioassays performed in Tg mice were positive. A similar discordance was observed for BSE muscle inoculated into cattle and Tgmice. Until more evidence is compiled showing that positive results in experimental PMCA and Tg mouse assays equate to a risk of transmitting disease under natural conditions, it cannot be assumed that such results imply the existence of a substantial risk to the health of animals or humans.

Considering the succession of updated Tables of the past few years, and the fact that inflammation has been shown to result in PrPTSE deposition in tissues that are not normally involved in TSE pathogenesis, it is evident that as testing continues, more tissues will find their way from Table IC into Table IB (but probably not from either Table IC or IB into Table IA). It is also evident that the data generated to date are far from complete, and that a great deal more work needs to be done if conclusions about the tissue distribution and significance of infectivity in a given TSE are to be based on direct measurements rather than by analogy to other forms of the disease.

Finally, it is critically important to understand that categories of infectivity are not the same as categories of risk, which require consideration not only of the level of infectivity in tissue, but also of the amount of tissue to which a person or animal is exposed, and the route by which infection is transmitted. For example, although the level of tissue infectivity is the most important factor in estimating the risk of transmission by instrument crosscontamination during surgical procedures (e.g., neurosurgery versus general surgery), it will be only one determinant of the risk of transmission by blood transfusions, in which a large amount of low-infectivity blood is administered intravenously, or the risk of transmission by foodstuffs that, irrespective of high or low infectivity, involve a comparatively inefficient oral route of infection.

snip...

Table IC: Tissues with no detected infectivity or PrPTSE

snip...

Musculo-skeletal tissues

Bone NT - NT - - NT NT NT NT NT

Tendon NT - NT - - NT NT NT NT NT

snip...

please see full text with tables here ;

WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies Updated 2010

also in the references at bottom i saw ;

12. A single positive marrow in multiple transmission attempts from cattle orally dosed with BSE-infected brain [Wells et al., 1999; Wells et al., 2005; Sohn et al., 2009].

http://www.who.int/bloodproducts/tablestissueinfectivity.pdf


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



Subject: Re: CWD AMERICA ???

Date: Fri, 12 Jul 2002 19:10:18 +0200

From: "INFORMATION DEPT" Organization: O.I.E

To: "Terry S. Singeltary Sr."

References: <3D2F0169.3@wt.net> <012901c229b2$ad43bb90$7f00000a@HPKB> <3D2F2358.5010700@wt.net>

I agree with you Dr Terry. The OIE, namely the International Animal Health Code Commission is working on making proposals to Member Countries to change the OIE lists so to avoid some the problems mentioned in you e-mail. This will take at least two years before adoption by the International Committee. For BSE, countries asked the OIE to post information on BSE on the OIE web site.

Personally, I am interested in Chronic Wasting Disease and I follow what is distributed through ProMed. Delegates of OIE Member Countries can propose diseases to be added to the list.

Kind regards.

Karim Ben Jebara

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

From: "Terry S. Singeltary Sr."

To: "INFORMATION DEPT"

Sent: Friday, July 12, 2002 8:43 PM

Subject: Re: CWD AMERICA ???

hello Dr. Jebara,

many thanks for your swift and kind reply.

if i am not mistaken, it was the same email address. it was 3 or 4 weeks ago i wrote, as it is, i don't save 'sent' emails anymore, unless very important.

my main concern (besides the fact that a potential TSE has been in the USA cattle for some time, but the APHIS do not test to find), is that the CWD could very well be transmitting to humans, and i just did not see to much posted about it on OIE site.

Coming back to your question, Chronic Wasting Disease is not an OIE

listed disease. Please see OIE disease lists at

http://www.oie.int/eng/maladies/en_classification.htm#ListeA).


why is this TSE (CWD) not listed and followed as with BSE ?

Article 1.1.3.2. 1. Countries shall make available to other countries, through the OIE, whatever information is necessary to minimise the spread of important animal diseases and to assist in achieving better worldwide control of these diseases.

http://www.oie.int/eng/normes/MCode/A_00005.htm


The USA CWD is an important animal disease.

why is it not followed?

The decision to add or delete a disease from the OIE lists, come

through proposals made by Member Countries and it has to be adopted by

the International Committee.

i _urgently_ suggest a proposal to the OIE to follow this disease very closely, and to propose _more_ testing in the USA for TSEs in the USA cattle...

kindest regards, terry



INFORMATION DEPT wrote:

Dear Sir,

This is the first time that I receive your e-mail. To whom have you written in the OIE or to which address?

Coming back to your question, Chronic Wasting Disease is not an OIE listed disease. Please see OIE disease lists at http://www.oie.int/eng/maladies/en_classification.htm#ListeA).

Countries should report to the OIE any disease even is not listed in the OIE's lists in some conditions (example: an exceptional epidemiological event). Please read Chapter 1.1.3 of the International animal health code to have more information on disease notification and epidemiological information agreed by OIE Member Countries at : http://www.oie.int/eng/normes/MCode/A_00005.htm


The decision to add or delete a disease from the OIE lists, come through proposals made by Member Countries and it has to be adopted by the International Committee.

Hope that I answered to your question.

Best regards.

Dr Karim Ben Jebara Head Animal Health Information Department OIE


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

From: "Terry S. Singeltary Sr."

To:

Sent: Friday, July 12, 2002 6:18 PM

Subject: CWD AMERICA ???

I WROTE TO OIE RECENTLY ASKING 'WHY OIE DOES NOT FOLLOW CWD IN AMERICA' ? with no reply ? i am still seeking an answer ?

many thanks, and kind regards, terry



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


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

Subject: OIE Scientific and Technical Review, Vol 11 (2) June 1992 Sub Acute Spongiform Encephalopathies in Animals (CWD???)

Date: Thu, 29 Jan 2004 14:49:03 -0600

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de

######## Bovine Spongiform Encephalopathy #########

Richard Kimberlin has obviously declined and suggested to OIE that Ray Bradley takes on the role of both author of the introductory chapter and coordinator...

http://www.bseinquiry.gov.uk/files/yb/1991/03/04002001.pdf




http://collections.europarchive.org/tna/20081106101342/http://www.bseinquiry.gov.uk/files/yb/1991/03/04002001.pdf



OIE Scientifoc and Technical Review, Vol 11 (2) June 1992 Sub Acute Spongiform Encephalopathies in Animals

91\02.20\1.1-1.2 20/02/91 Minute S C Hutchins I Crawford

snip...

a) I think it would be advisable to include scrapie, BSE and transmissible mink encephalopathy (hence the proposed title)...

snip...



http://www.bseinquiry.gov.uk/files/yb/1991/02/19004001.pdf


http://collections.europarchive.org/tna/20080103024333/http://www.bseinquiry.gov.uk/files/yb/1991/02/19004001.pdf




and i proposed to OIE years ago to include CWD. but with these new atypical case of TSE showing up in cattle and sheep, it will be interesting to see how the OIE handles the USA demands on weakening the BSE/TSE regs for exporting countries;

Date: Fri, 12 Jul 2002 16:11:42 -0700

Reply-To: B S E-l

Sender: Bovine Spongiform Encephalopathy

From: TSS Subject: CWD/USA -- CWD/OIE?

snip...

Greetings List Members,

speaking with someone at the OIE about my concerns with CWD and the non-testing for TSEs in USA cattle, i find it very sad that the OIE does not follow CWD related issues. BUT, they voice my same concerns and said changes are in the makings. sadly, the changes will take about 2 years?

snip...

''I agree with you Dr Terry. The OIE, namely the International Animal Health Code Commission is working on making proposals to Member Countries to change the OIE lists so to avoid some the problems mentioned in you e-mail. This will take at least two years before adoption by the International Committee.''

snip...

two years is a very long time, on an issue of such importance to both humans and animals...

kind regards, terry

snip...


PAGE 25 Transmission Studies Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculam (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in _all_ of these species with the shortest incubation period in the ferret...



http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf


http://collections.europarchive.org/tna/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf



Clearly, it is premature to draw firm conclusions about CWD passing naturally into humans, cattle and sheep, but the present results suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs.

snip...

http://www.emboj.org/current.shtml


and why do we not want to do TSE transmission studies on chimpanzees $


IN CONFIDENCE

TRANSMISSION TO CHIMPANZEES

snip...

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

snip...

R. BRADLEY

http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf


http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf



http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf



same reason CJD/TSE is not reportable Nationally in the USA. same reason no CJD questionnaire exists in the USA that is issued to all victims and families of victims asking real questions pertaining to route and source of agent. no autopies for all demented of young AND OLD! same reason the USA is steadfast refusing to this day to rapid TSE test all cattle for human/animal consumption. the USA simply does not want to know$



hell, we should just retain it all, and just play like it has not happened for the next 40 years as well. hmm, something else to ponder ;


5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man


so, when/where is our first case transmission study of TSE on man going to be? i wish to witness this and have a few suggestions for our first human guinea-pigs ;-)


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


########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.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



FRIENDLY FIRE AND OR THE PASS IF FORWARD MODE OF TSE IATROGENIC


Monday, February 7, 2011

FDA's Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???

http://tseac.blogspot.com/2011/02/fdas-currently-recommended-policies-to.html


Thursday, August 12, 2010

USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010

http://creutzfeldt-jakob-disease.blogspot.com/2010/08/usa-blood-products-collected-from-donor.html


Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html


Tuesday, March 29, 2011

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY EXPOSURE SPREADING VIA HOSPITALS AND SURGICAL PROCEDURES AROUND THE GLOBE

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/transmissible-spongiform-encephalopathy.html


TSS

Labels: ,

Thursday, March 31, 2011

TEN KANSAS DEER CONFIRMED POSITIVE IN CWD TESTS

TEN KANSAS DEER CONFIRMED POSITIVE IN CWD TESTS

Number of confirmed cases same as last year PRATT— The number of positive cases of chronic wasting disease (CWD in Kansas appears to be stable for now. On March 2, the Kansas Department of Wildlife and Parks (KDWP) announced that 10 deer from northwestern Kansas had tested positive for chronic wasting disease, the same number as last year although two of those deer were found in counties farther east than any previous confirmations. These were animals taken by hunters in the 2010 hunting seasons.

Six confirmed cases of CWD deer were taken by hunters in Decatur County and one each from Graham, Norton, Sherman, and Smith counties. The Norton, Sherman, and Smith cases were firsts for those counties. The cases included nine white-tailed and one mule deer. This season’s testing results brings the total number of confirmed CWD cases in Kansas to 40 since testing began in 1996. In total, 2,503 animals were tested for CWD for the 2010 deer seasons. Although most testing is finished for the year, KDWP will continue testing some vehicle-killed and sick or suspect-looking deer, as well as deer taken with depredation permits, through July 31. If U.S. Department of Agriculture funding is available, and new surveillance period will begin Aug. 1.

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 and 10 tested positive in 2008, 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 (only two of the 40 positive animals showed symptoms) 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.

“It must be noted that many symptoms of CWD are indicative of other diseases,” says KDWP wildlife disease coordinator Shane Hesting. “Thus, a sick deer may or may not be infected with CWD. CWD is a serious deer disease but is still a rare disease in Kansas. There is no vaccine or other biological method that prevents the spread of CWD. However, there is no evidence that CWD poses a risk to humans or livestock in the natural environment.”

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/TEN-KANSAS-DEER-CONFIRMED-POSITIVE-IN-CWD-TESTS




Thursday, January 06, 2011


KANSAS FIRST CASE OF CHRONIC WASTING IN 2010 DEER SEASON CONFIRMED


http://chronic-wasting-disease.blogspot.com/2011/01/kansas-first-case-of-chronic-wasting-in.html





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

Labels: , ,

Wednesday, March 02, 2011

CWD IN NEBRASKA IS INCREASING WITH 51 POSITIVE CASES IN 2010

Fifty-One Deer Test Positive for CWD

March 1, 2011 News

LINCOLN, Neb. – Nebraska is experiencing an increase in the number of deer testing positive for chronic wasting disease (CWD), as well as a wider distribution, according to the Nebraska Game and Parks Commission. There were a record 51 positives in 2010.

CWD is a disease that can affect deer and elk and is always fatal to the affected animal. Humans have never been known to contract CWD.

There were 3,645 lymph node samples collected from deer harvested during the November firearm season. The 51 positives were the most in Nebraska in one year.

The counties with the highest number of positives were: Sioux, 11; Sheridan, 7; Dawes, 6; Garden, 6; Box Butte, 4; Scotts Bluff, 4; and Morrill, 3. There were two positives each in Banner and Hitchcock counties and one each in Hooker, Keith, Lincoln, Loup, Cherry, and Hall counties. The counties in which CWD was found for the first time are: Hitchcock, Hooker, Lincoln, and Loup.

No elk tested positive for CWD in 2010.

http://outdoornebraska.ne.gov/blogs/2011/03/fifty-one-deer-test-positive-cwd/




Can Humans Be Infected with CWD? There is currently no scientific evidence that CWD has or can spread to humans, either through contact with infected animals or by eating the meat of infected animals. The Centers for Disease Control and Prevention has conducted an exhaustive study of CWD and human risk and has stated: "The risk of infection with the CWD agent among hunters is extremely small, if it exists at all." However, as we are still learning about this disease, the Commission recommends that hunters take precautions to limit risks. First and foremost, do not harvest any animal that appears sick or is acting strange.

Note the animal's location and contact the Commission. Avoid cutting or puncturing the spinal cords or brains of animals taken in the areas where CWD occurs. Do not use household utensils to field dress or process your deer. Wear rubber or latex gloves when handling any harvested animal.

Can the Disease Spread to Other Animals, Such As Cattle? Again, there is no indication or scientific evidence that the disease can spread to species other than deer or elk, but research in this area continues. Studies have shown that cattle placed in close and confined proximity with infected deer and elk have not developed the disease after living with them for over seven years.

http://outdoornebraska.ne.gov/wildlife/guides/CWD/cwd.asp




http://outdoornebraska.ne.gov/blogs/




PLEASE NOTE CWD TO CATTLE TRANSMISSION, AND THE REAL RISK FACTORS OF CWD TO HUMANS ;


A kind greetings from Bacliff, Texas !

please use this information with how ever many grains of salt you wish, i don't care what you eat.

cutting out the high risk cns portions will not do away with all the risk, even if you don't cut yourselves by butcher. they have now found in CWD the prion TSE agent in muscle and fat tissue, now they say with smaller amounts of infectivity, but i personally believe in the accumaltion as a factor of risk as well. seems these prion strains as they mutate, the get more virulent. you accumulate enough of the prions and you become clinical. what the threshold from sub-clinical to clinical would be, would depend on the route, the source, titre of infectivity, and ones genetic make up, and whom you expose and or infect while being sub-clinically exposed via the medical and surgical arena's i.e. friendly fire, is a frightening thought now, and a real risk factor. for them to keep saying that there is no _known_ risk factor to humans, with the cjd surveillance system and diagnostic criteria, they would never know. you are correct about the officials being misinformed and misleading. that's why i post the science behind any reports they publish on CWD, hoping someone will read it. personally i think the deer and elk hunting industry were a pawn in a big game of chess. the king was the cattle industry. they have brain washed every one into believing scrapie will not transmit to man, when all science shows that it will. the deer and elk industry were sacrificed. USDA et al tried to cover up mad cow disease, because the evidence was already out (without using a human guinea pig, which i promote over primates i.e. death row inmates, that's another story though), so they just kept saying cwd would not transmit to humans. when the evidence was the same for BSE to humans as it was for CWD to humans, as with Scrapie, and they knew this in 2000, or earlier. the evidence was the same in that study i.e. raymand et al, no matter how low, or high the risk factor is, the risk was the same for BSE, Scrapie, and CWD to humans ;

Clearly, it is premature to draw firm conclusions about CWD passing naturally into humans, cattle and sheep, but the present results suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs.

http://www.nature.com/emboj/journal/v19/n17/full/7593259a.html




THEN, 11 years later you get this ;



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




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. ...end


PLEASE SEE FULL TEXT ;

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 Soto5,* + Author Affiliations

1 University of Texas Medical School at Houston, United States; 2 University of Kentucky, United States; 3 Case Western Reserve University, United States; 4 University of Chicago, United States; 5 University of Texas Medical School, United States * Corresponding author; email: claudio.soto@uth.tmc.edu

Received October 28, 2010. Accepted January 4, 2011. Copyright © 2011, The American Society for Biochemistry and Molecular Biology



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




then you had this data ;

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.

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




and why do we not want to do TSE transmission studies on chimpanzees $


snip...

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

snip...

R. BRADLEY

http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf




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




Title: Experimental Second Passage of Chronic Wasting Disease (Cwd(mule Deer)) Agent to Cattle

Authors

Hamir, Amirali Kunkle, Robert Miller, Janice - ARS RETIRED Greenlee, Justin Richt, Juergen

Submitted to: Journal of Comparative Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 25, 2005 Publication Date: January 1, 2006 Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006. Experimental second passage of chronic wasting disease (CWD(mule deer)) agent to cattle. Journal of Comparative Pathology. 134(1):63-69.

Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB. Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=178318




PLUS, oral transmission between cervids, either infected carcases AND ESPECIALLY FEED THAT HAS ANIMAL PROTEIN, PLEASE SEE ;

PRODUCT Custom deer feed made for a Wisconsin farm. The product was in bags holding about 40 pounds each. Recall # V-122-4. CODE 1-30-04 on the product invoice and mixing record. RECALLING FIRM/MANUFACTURER Crivitz Feed Mill, Crivitz, WI, by telephone on February 20, 2004. Wisconsin State initiated recall is complete. REASON The recalled deer feed contained steamed bone meal which is prohibited material in feed for ruminants.

VOLUME OF PRODUCT IN COMMERCE 515 pounds.

DISTRIBUTION WI.

END OF ENFORCEMENT REPORT FOR APRIL 7, 2004

###

http://www.fda.gov/bbs/topics/enforce/2004/ENF00842.html




Experimental oral transmission of chronic wasting disease to red deer (Cervus elaphus elaphus): Early detection and late stage distribution of protease-resistant prion protein

Aru Balachandran, Noel P. Harrington, James Algire, Andrei Soutyrine, Terry R. Spraker, Martin Jeffrey, Lorenzo González, Katherine I. O’Rourke

Abstract — Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure. Studies of host range susceptibility to oral infection, particularly of those species found in habitats where CWD currently exists are imperative. This report describes the experimental transmission of CWD to red deer following oral inoculation with infectious CWD material of elk origin. At 18 to 20 months post-inoculation, mild to moderate neurological signs and weight loss were observed and animals were euthanized and tested using 3 conventional immunological assays. The data indicate that red deer are susceptible to oral challenge and that tissues currently used for CWD diagnosis show strong abnormal prion (PrPCWD) accumulation. Widespread peripheral PrPCWD deposition involves lymphoreticular tissues, endocrine tissues, and cardiac muscle and suggests a potential source of prion infectivity, a means of horizontal transmission and carrier state.

Can Vet J 2010;51:169–178

http://canadianveterinarians.net/publications-journal-issue-abstracts.aspx




Journal of General Virology (1999), 80, 2757-2764. © 1999 Society for General Microbiology

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Other Agents

Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail ehoover@lamar.colostate.edu

Abstract TOP Abstract Introduction Methods Results Discussion References

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.

http://vir.sgmjournals.org/cgi/content/full/80/10/2757




Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure.

http://canadianveterinarians.net/publications-journal-issue-abstracts.aspx




Chronic Wasting Disease Susceptibility of Four North American Rodents

Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu

We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.


Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007

Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: rmaddox@cdc.gov

The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf



NOW FOR RISK FACTORS FOR CWD TRANSMISSION TO CATTLE ;


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

From: David Colby

To: flounder9@verizon.net

Cc: stanley@XXXXXXXX

Sent: Tuesday, March 01, 2011 8:25 AM

Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

Dear Terry Singeltary,

Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter.

Warm Regards, David Colby

--

David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware

PLEASE SEE FULL TEXT ;

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://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html




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

CWD to cattle figures CORRECTION

Greetings,

I believe the statement and quote below is incorrect ;

"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."

Please see ;

Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089




" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "


shouldn't this be corrected, 86% is NOT a low rate. ...


kindest regards,

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



Thank you!

Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.

http://cshperspectives.cshlp.org/letters/submit




please see full text of my submission here ;

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




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




Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

http://scrapie-usa.blogspot.com/2011/02/environmental-sources-of-scrapie-prions.html




Monday, February 14, 2011

THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER

NO, NO, NOT NO, BUT HELL NO !

Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html




Wednesday, February 04, 2009

Nebraska reports 22 cases of CWD in deer

http://chronic-wasting-disease.blogspot.com/2009/02/nebraska-reports-22-cases-of-cwd-in.html





Sunday, October 04, 2009

CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009

http://chronic-wasting-disease.blogspot.com/2009/10/cwd-new-mexico-spreading-south-to-texas.html




Monday, February 28, 2011

South Dakota finds 25 more cases of Chronic Wasting Disease

Latest Chronic Wasting Disease Testing Results

http://chronic-wasting-disease.blogspot.com/2011/02/south-dakota-finds-25-more-cases-of.html




Friday, February 25, 2011

Soil clay content underlies prion infection odds

http://chronic-wasting-disease.blogspot.com/2011/02/soil-clay-content-underlies-prion.html




Tuesday, February 22, 2011

Chronic wasting disease spreads farther west in Alberta

http://chronic-wasting-disease.blogspot.com/2011/02/chronic-wasting-disease-spreads-farther.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




Thursday, February 10, 2011

CWD ILLINOIS UPDATE FEBRUARY 2011 Locations of CWD-Positive Deer - Updated 2/07/2011

http://chronic-wasting-disease.blogspot.com/2011/02/cwd-illinois-update-february-2011.html




Thursday, February 10, 2011

Chronic Wasting Disease Found In A White-Tailed Deer In Maryland

http://chronic-wasting-disease.blogspot.com/2011/02/chronic-wasting-disease-found-in-white.html




Wednesday, February 09, 2011

CWD Minnesota deer feeding ban covering Dodge, Goodhue, Olmsted, and Wabasha counties will become effective Feb. 14, 2011

http://chronic-wasting-disease.blogspot.com/2011/02/cwd-minnesota-deer-feeding-ban-covering.html




Tuesday, January 25, 2011

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

http://chronic-wasting-disease.blogspot.com/2011/01/minnesota-national-veterinary-services.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




CWD, GAME FARMS, BAITING, AND POLITICS



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



http://chronic-wasting-disease.blogspot.com/2008/08/cwd-feeding-and-baiting-piles.html



Monday, February 22, 2010

Aerosol and Nasal Transmission of Chronic Wasting Disease in Cervidized Mice

http://chronic-wasting-disease.blogspot.com/2010/02/aerosol-and-nasal-transmission-of.html




AS THE CROW FLIES, SO DOES CWD

Sunday, November 01, 2009



American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases



http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html




Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2009/07/deer-carcass-decomposition-and.html



Sunday, December 06, 2009

Detection of Sub-Clinical CWD Infection in Conventional Test-Negative Deer Long after Oral Exposure to Urine and Feces from CWD+ Deer

http://chronic-wasting-disease.blogspot.com/2009/12/detection-of-sub-clinical-cwd-infection.html




THEN YOU have water that has been contaminated from a CWD-endemic area ;


Wednesday, October 14, 2009

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html




ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD ;


http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html




http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.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





layperson


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

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