Tuesday, February 28, 2012

newly developed injectable CWD vaccine, live rectal mucosa testing and Deer Game Farms Update

newly developed injectable CWD vaccine, live rectal mucosa testing and Deer Game Farms Update



- testing is currently underway to determine the effectiveness of a newly developed injectable CWD vaccine that has shown considerable promise.


- an effective vaccine could be used to prevent CWD in game farm animals but additional study would be required to determine an effective application method in the wild.




snip...see full text ;


http://joomla.wildlife.org/Alberta/images/Documents/Cons_committee/cwd%20update%202011.pdf




http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html





Development of an oral vaccine for Chronic Wasting Disease

Principal Investigator: Scott Napper, Vaccine and Infectious Disease Organization

Co-investigators: Andrew Potter, Vaccine and Infectious Disease Organization Philip Griebel, Vaccine and Infectious Disease Organization Neil Cashman, Brain Research Centre, University of British Columbia Suresh Tikoo, Vaccine and Infectious Disease Organization Nate Osgood, Computer Sciences, University of Saskatchewan Trent Bollinger, Western College of Veterinary Medicine, University of Saskatchewan Ted Leighton, Western College of Veterinary Medicine, University of Saskatchewan Cheryl Waldner, Western College of Veterinary Medicine, University of Saskatchewan Murray Woodbury, Western College of Veterinary Medicine, University of Saskatchewan

Project Description

Members of our team have been focused on a disease specific epitope (DSE) termed YYR which is specifically exposed on PrPSc. Through optimization of the length and presentation of this epitope, as well as strategies of formulation and delivery, we have developed a first generation prion vaccine. This vaccine was developed with a priority on farmed cervids and employed strategies compatible with parenteral injection, the traditional route of vaccine delivery. This vaccine induces high-titre, PrPSc-specific immune responses in a variety of species and significantly delays the onset of disease in experimentally challenged sheep. Having validated the DSE immunotherapy concept, we are positioned to develop a second generation vaccine based upon additional, newly discovered DSE’s as well as an oral route of delivery. Oral delivery is required for vaccination of wild animals and is the preferred route for farmed cervids. Oral delivery may also offer greater protection against oral routes of infection, which is central to CWD transmission. Funding by PrioNet will enable and accelerate development of this novel tool to control Chronic Wasting Disease.

(Open Call IV)

Last Updated: 10/21/2011 4:44:47 PM



http://www.prionetcanada.ca/detail.aspx?menu=7&dt=293742&app=125&cat1=735&tp=2&lk=d&searchtext=prion+vaccine&sc=





Title: Diagnosis of preclinical CWD in farmed white-tailed deer in Canada by the immunohistochemical examination of recto-anal mucosa- associated lymphoid tissue (RAMALT)

Authors

Balachandran, Aru - Thomsen, Bruce - Gidlewski, Thomas - Spraker, Terry - Mitchell, G - Soutyrine, Andrei - Harrington, Noel - Munger, Randy - SCHNEIDER, DAVID OROURKE, KATHERINE

Submitted to: Meeting Abstract Publication Type: Abstract Publication Acceptance Date: September 12, 2009 Publication Date: September 22, 2009 Repository URL:



http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/brochure-tse_workshop.pdf




Citation: Balachandran, A., Thomsen, B.V., Gidlewski, T., Spraker, T.R., Mitchell, G., Soutyrine, A., Harrington, N.P., Munger, R., Schneider, D.A., Orourke, K.I. 2009. Diagnosis of preclinical CWD in farmed white-tailed deer in Canada by the immunohistochemical examination of recto-anal mucosa- associated lymphoid tissue (RAMALT). NeuroPrion Workshop: New developments in TSEs of domestic and wild animals. pg.9

Interpretive Summary: Diagnosis of prion disease [for example, scrapie in sheep and chronic wasting disease (CWD) in elk and deer] relies upon sensitive detection of disease-associated prion protein in the brain or tissues containing lymph follicles. Live animal testing for scrapie disease in sheep has included evaluation of biopsy samples of the tonsil, third eyelid and rectal mucosa. Similarly, diagnosis of CWD in live elk has been recently accomplished through biopsy of the rectal mucosa. This invited report to the annual NeuroPrion meeting summarizes the diagnostic performance (test sensitivity) of various tissue sampling sites that were collected after death. The report summarizes the findings from two different populations of captive white-tailed deer from Saskatchewan, Canada. The diagnostic performance of the rectal mucosa samples were similar but lower than that achieved in two other lymphoid tissues, but greater than that achieved in the brain. While these studies were conducted on tissues collected after death, the findings demonstrate the comparative potential for biopsy of the rectal mucosa in live deer not yet showing signs of disease. While many factors may influence test performance in other deer populations, these studies showed that false-negative diagnosis occurred most often in deer presumed to be in an early stage of disease and carrying a mutation in the prion protein gene (codon 96). Technical Abstract: This report summarizes the comparative diagnostic performance of postmortem rectoanal mucosa-associated lymphoid tissue (RAMALT) sampling in two white-tailed deer farms from Saskatchewan, Canada. The apparent prevalence of disease in these two farms was 21% and 31%. None of these deer were demonstrating signs consistent with CWD. The overall tissue-specific test sensitivities were ranked: RPLN>tonsil>RAMALT>obex. Test sensitivities in deer having at least one PRNP G96S allele were generally lower but similarly ranked. False negative RAMALT results were associated with early disease progression, as assessed by PrPCWD accumulation scores in the obex, and/or the PRNP G96S allele. The proportion of CWD-positive RAMALT follicles were generally lowest in deer early in disease progression and/or heterozygous at PRNP codon 96. And, as expected, variation in the proportion CWD-positive RAMALT follicles was inversely related to the total number of observable follicles per sample. These comparisons made on samples collected postmortem suggest general diagnostic evaluation of RAMALT samples in white-tailed deer would have intermediate test sensitivity as compared to evaluation of RPLN and obex. While many factors may influence actual test performance, early stage of disease progression and the PRNP G96S allele are two that were associated with lower test sensitivities.



http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=244240





Title: Sensitive detection of PrPCWD in rectoanal mucosa-associated lymphoid tissue from preclinical white-tailed deer

Authors

SCHNEIDER, DAVID OROURKE, KATHERINE Balachandran, Aru - Keane, Delwyn -

Submitted to: United States Animal Health Association Proceedings Publication Type: Abstract Publication Acceptance Date: October 11, 2009 Publication Date: October 11, 2009 Repository URL:

http://www.usaha.org/meetings/2009/2009_USAHA_Proceedings.pdf



new url ;

http://portals5.gomembers.com/Portals/6/Proceedings/2009_USAHA_Proceedings.pdf





Citation: Schneider, D.A., Orourke, K.I., Balachandran, A., Keane, D. 2009. Sensitive Detection of PrPCWD in Rectoanal Mucosa-Associated Lymphoid Tissue from Preclinical White-Tailed Deer. United States Animal Health Association Proceedings. pg.224-225.

Interpretive Summary: Diagnosis of prion disease [for example, scrapie in sheep and chronic wasting disease (CWD) in elk and deer] relies upon sensitive detection of disease-associated prion protein in the brain or tissues containing lymph follicles. Live animal testing for scrapie disease in sheep has included evaluation of biopsy samples of the tonsil, third eyelid and rectal mucosa. Similarly, diagnosis of CWD in live elk has been recently accomplished through biopsy of the rectal mucosa. This report summarizes the diagnostic performance (test sensitivity) of various tissue sampling sites that were collected after death. The report summarizes the findings from four different populations of white-tailed deer. Two of these populations were from Wisconsin and two from Saskatchewan, Canada; three were captive herds and one consisted of a sample of free-ranging deer. The diagnostic performance of the rectal mucosa samples were similar but lower than that achieved in two other lymphoid tissues, but greater than that achieved in the brain. While these studies were conducted on tissues collected after death, the findings demonstrate the comparative potential for biopsy of the rectal mucosa in live deer not yet showing signs of disease. While many factors may influence test performance in other deer populations, these studies showed that false-negative diagnosis occurred most often in deer presumed to be in an early stage of disease and carrying a mutation in the prion protein gene (codon 96). Technical Abstract: This report summarizes the comparative diagnostic performance of postmortem rectoanal mucosa-associated lymphoid tissue (RAMALT) sampling in four white-tailed deer test populations: from Wisconsin, a sample of free-ranging deer and a captive herd; and from Saskatchewan, Canada, two captive herds. The apparent prevalence of disease in these test populations ranged from 6-79%. None of these deer were demonstrating signs consistent with CWD. The overall tissue-specific test sensitivities were ranked: RPLN>tonsil>RAMALT>obex. Test sensitivities in captive herd deer having at least one PRNP G96S allele were generally lower but similarly ranked. False negative RAMALT results were associated with early disease progression, as assessed by PrPCWD accumulation scores in RPLN or obex, and/or the PRNP G96S allele. As determined in two of the captive herds, the proportion of CWD-positive RAMALT follicles were generally lowest in deer early in disease progression and/or heterozygous at PRNP codon 96. And, as expected, variation in the proportion CWD-positive RAMALT follicles was inversely related to the total number of observable follicles per sample. These comparisons made on samples collected postmortem suggest general diagnostic evaluation of RAMALT samples in white-tailed deer would have intermediate test sensitivity as compared to evaluation of RPLN and obex. While many factors may influence actual test performance, early stage of disease progression and the PRNP G96S allele are two that were associated with lower test sensitivities.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=244239



Title: Validation of Use of Rectoanal Mucosa-Associated Lymphoid Tissue for Immunohistochemical Diagnosis of Chronic Wasting Disease in White-Tailed Deer (Odocoileus virginianus)

Authors

Keane, D - UNIV OF WISCONSIN Barr, D - UNIV OF WISCONSIN Osborn, R - WISC DEPT OF NAT RESOURCE Langenberg, J - WISC DEPT OF NAT RESOURCE OROURKE, KATHERINE SCHNEIDER, DAVID Bochsler, P - UNIV OF WISCONSIN

Submitted to: Journal of Veterinary Diagnostic Investigation Publication Type: Peer Reviewed Journal Publication Acceptance Date: February 20, 2009 Publication Date: May 1, 2009 Repository URL:

http://jcm.asm.org/cgi/reprint/47/5/1412?maxtoshow=&hits=10&RESULTFORMAT=&searchid=1&FIRSTINDEX=0&volume=47&firstpage=1412&resourcetype=HWCIT



Citation: Keane, D., Barr, D., Osborn, R., Langenberg, J., Orourke, K.I., Schneider, D.A., Bochsler, P. 2009. Validation of Use of Rectoanal Mucosa-Associated Lymphoid Tissue for Immunohistochemical Diagnosis of Chronic Wasting Disease in White-Tailed Deer (Odocoileus virginianus). Journal of Veterinary Diagnostic Investigation. 47(5):1412-1417.

Interpretive Summary: The prion diseases are a group of fatal brain disorders of sheep, goats, cattle, deer and elk. An abnormally folded protein accumulates in some lymphoid tissues of sheep early in disease. Biopsy sampling of lymphoid tissue, including tissue in the rectum, is a suitable live animal test in sheep. Adaptation of that test for use in deer exposed to the cervid prion disease Chronic Wasting Disease has been proposed. In this paper, the investigators compared the results of testing rectal tissue with test results on brain and the lymphoid tissues currently used for early diagnosis of the disease. Deer from a captive farm with a high prevalence of disease and wild deer with a low prevalence of disease were included in the study. Nearly eighty percent of the deer with abnormal prions in lymphoid tissue or brain had detectable abnormal prion proteins in the rectal lymphoid tissues. Although lymphoid tissues of the head remain the tissue of choice for early diagnosis of the disease in deer, the use of rectal lymphoid tissue is a suitable adjunct, particularly for live-screening farmed deer at risk for chronic wasting disease. Technical Abstract: The transmissible spongiform encephalopathies are a family of fatal neurodegenerative diseases characterized by accumulation of abnormal prion proteins in the brain. The abnormal prion protein is the major constituent of the infectious agent and is a reliable marker for disease. The occurrence of a zoonotic prion disease in cattle has resulted in efforts to eradicate or control all prion diseases in domestic livestock, including scrapie of sheep and chronic wasting disease CWD of deer and elk. Antemortem testing of sheep, deer and elk is based on the finding that abnormal prion proteins accumulate in some lymphoid tissues months or years before being detectable in brain. Biopsy of tonsil is a suitable test for live deer but requires general anesthesia. Biopsy sampling of the recto-anal mucosal associated lymphoid tissue (RAMALT) has been suggested as an alternative site for antemortem testing in sheep. In this study, postmortem sampling of RAMALT tissue from deer was performed to estimate the diagnostic sensitivity and specificity of the test. Samples were assayed by monoclonal antibody based immunohistochemistry and the results of RAMALT testing were compared with testing of brain, tonsil and retropharyngeal lymph node, the currently preferred tissue for early diagnosis. Sensitivity of the test was 80% in a sample of 76 white tailed deer from a captive facility and 77% in a sample of 210 free ranging white tailed deer. While the retropharyngeal lymph node remains the tissue of choice for early diagnostic testing, RAMALT biopsy may provide a suitable adjunct, particularly for antemortem testing of herds of farmed deer with potential exposure to the disease.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=233205





Chronic Wasting Disease National Program for Farmed and Captive Cervids Update

Patrice N. Klein, National Center for Animal Health Programs, USDA-APHISVS

In FY2010, APHIS received approximately $16.8 million in appropriated funding for the CWD Program, including $1.0 million in congressional earmarks. The FY2011 President’s proposed budget for the CWD Program is $14.2 million (exclusive of any congressional earmarks). In the first quarter of FY2011, the federal government is operating on a Continuing Resolution based on a quarterly percentage of the FY10 budget. CWD Rule Update: Public comments received on the proposed amendments to the 2006 CWD rule were categorized, reviewed, and responses were drafted. Issues that may impact the amended final rule and CWD Program implementation include the President’s Memo on federal preemption (May 20, 2009), budgetary constraints, and ongoing need for additional research to better understand the science for prevention and control of CWD. A draft of the amended CWD final rule is in clearance in November 2010. Surveillance testing: Through FY2009, VS conducted surveillance testing on more than 23,000 farmed and captive cervids by the immunohistochemistry (IHC) standard protocol. In FY2010, approximately 20,000 farmed and captive cervids were tested by IHC for CWD with funding to cover lab costs provided through NVSL. Status: CWD was detected in one captive white-tailed deer (WTD) herd in Missouri in February 2010. To date, 50 farmed/captive cervid herds have been identified in 11 states: CO, KS, MI, MN, MO, MT, NE, NY, OK, SD, WI. Thirty-seven were elk herds and 13 were WTD herds. At this time, six CWD positive elk herds remain in Colorado and one WTD herd remains in MO. VS has continued to offer indemnity for appraised value of the animals and to cover costs of depopulation, disposal, and testing of CWD-positive and exposed herds. Indemnity is provided based on availability of federal funding.

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

Controlling Disease at the Fence: Research Questions, Answers, and on to More Questions

Kurt VerCauteren, National Wildlife Research Center, USDA-APHIS-WS

In recent years the National Wildlife Research Center has collaborated with many privately owned elk and deer producers to investigate many aspects regarding the potential for disease transmission between freeranging and captive cervids. A suite of studies began with a fencelineinteraction evaluation designed to determine if and to what extent interactions occurred along perimeter fences. We found through 1 year of video monitoring that interactions between captive and free-ranging whitetailed deer (Odocoileus virginianus) were relatively rare (2 direct contacts and 7 indirect contacts). Interactions between captive and free-ranging elk (Cervus elaphus), though, were relatively common (77 direct contacts and 274 indirect contacts). To address this issue, we proceeded to design and evaluate a cost-effective baited-electric fence that could be added to an existing single perimeter fence to minimize potential interactions. Our case study documented that once exposed to the electric fence individual elk learned to respect it and were completely deterred thereafter. The ambiguous question of how high white-tailed deer can jump was next on our list of pursuits to further evaluate risk associated with perimeter fences.

Following a controlled evaluation involving 43 white-tailed deer motivated to jump progressively higher fences, we determined that a 2.1-m-high fence presents a considerable barrier. We also teamed up with colleagues to develop the rectal biopsy antemortem test for identifying CWD-infected individuals, collecting over 1,500 rectal biopsies from captive cervids to date. We have incorporated the procedure into our research and continue to work toward assessing its utility relative to management. To prepare for instances when disease is introduced into the wild at a pointsource, we initiated a study evaluating rapid containment of white-tailed deer and demonstrated the efficacy of 2.1-m-high polypropylene mesh fence for emergency containment. A study we hope to do will document how captive white-tailed deer respond following “escape” from a captive deer facility. The study would give us an understanding of how easily these deer can be recaptured and how readily they integrate into the local free-ranging deer herd. The progression of research that we have conducted to date has provided insight into what occurs along perimeter fences at captive cervid facilities and is enabling producers and management agencies to make more informed decisions relative to protecting valuable resources inside and outside fences. We will briefly discuss these studies and more.



http://www.usaha.org/Portals/6/Proceedings/USAHAProceedings-2010-114th.pdf





PLEASE STUDY THIS MAP !

SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. daaa.

http://wwwnc.cdc.gov/eid/article/18/3/11-0685-f1.htm



*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***

Saturday, February 18, 2012

Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease

CDC Volume 18, Number 3—March 2012

http://wwwnc.cdc.gov/eid/ahead-of-print/article/18/3/11-0685_article.htm



SNIP...

Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).

SNIP...

CWD Zoonotic Potential, Species Barriers, and Strains

Current Understanding of the CWD Species Barrier

Strong evidence of zoonotic transmission of BSE to humans has led to concerns about zoonotic transmission of CWD (2,3). As noted above, CWD prions are present nearly ubiquitously throughout diseased hosts, including in muscle, fat, various glands and organs, antler velvet, and peripheral and CNS tissue (2,14,15). Thus, the potential for human exposure to CWD by handling and consumption of infectious cervid material is substantial and increases with increased disease prevalence.

Interspecies transmission of prion diseases often yields a species-barrier effect, in which transmission is less efficient compared with intraspecies transmission, as shown by lower attack rates and extended incubation periods (3,28). The species barrier effect is associated with minor differences in PrPc sequence and structure between the host and target species (3). Prion strain (discussed below) and route of inoculation also affect the species barrier (3,28). For instance, interspecies transmission by intracerebral inoculation is often possible but oral challenge is completely ineffective (29).



Most epidemiologic studies and experimental work have suggested that the potential for CWD transmission to humans is low, and such transmission has not been documented through ongoing surveillance (2,3). In vitro prion replication assays report a relatively low efficiency of CWD PrPSc-directed conversion of human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are resistant to CWD infection (31); these findings indicate low zoonotic potential. However, squirrel monkeys are susceptible to CWD by intracerebral and oral inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans than squirrel monkeys, are resistant to CWD infection (32). Regardless, the finding that a primate is orally susceptible to CWD is of concern.



Interspecies transmission of CWD to noncervids has not been observed under natural conditions. CWD infection of carcass scavengers such as raccoons, opossums, and coyotes was not observed in a recent study in Wisconsin (22). In addition, natural transmission of CWD to cattle has not been observed in experimentally controlled natural exposure studies or targeted surveillance (2). However, CWD has been experimentally transmitted to cattle, sheep, goats, mink, ferrets, voles, and mice by intracerebral inoculation (2,29,33).



CWD is likely transmitted among mule, white-tailed deer, and elk without a major species barrier (1), and other members of the cervid family, including reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD infection. Black-tailed deer (a subspecies of mule deer) and European red deer (Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34). Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation (35). Continued study of CWD susceptibility in other cervids is of considerable interest.



Reasons for Caution

There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD.



Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation.



Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified,

SNIP...




*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***




Saturday, February 18, 2012

Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease

CDC Volume 18, Number 3—March 2012

http://wwwnc.cdc.gov/eid/ahead-of-print/article/18/3/11-0685_article.htm




see much more here ;

http://chronic-wasting-disease.blogspot.com/2012/02/occurrence-transmission-and-zoonotic.html





50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE CWD

2012

Tuesday, December 20, 2011

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

> > > The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.

However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.

Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < <

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf





SNIP...SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html





Thursday, February 09, 2012

50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE

http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html





see what CWD did with first and second passage of testing in the lab to cattle ;

first passage ;

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




second passage

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.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=178318




Chronic Wasting Disease CWD cervids interspecies transmission

Wednesday, January 5, 2011

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

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

+ Author Affiliations

1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu

SNIP...

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





MARCH 1, 2011

UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON 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

====================END...TSS==============




SNIP...SEE FULL TEXT ;

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




please remember, CWD has mutated into a second strain already, i.e. THE WISCONSIN STRAIN CWD.

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.

PPo2-22:

CWD Strain Emergence in Orally Inoculated White-tailed Deer (Odocoileus virginianus) with Different PRNP Genotypes

Camilo Duque-Velasquez,1 Chad Johnson,2 Allen Herbst,1 Judd Aiken1 and Debbie McKenzie1 1Centre for Prions and Protein Folding Diseases; University of Alberta; Edmonton, Alberta Canada; 2Department of Soil Science; University of Wisconsin; Madison, Wisconsin USA

Key words: CWD, strains, emergence

Chronic wasting disease (CWD) is a prion disease affecting captive and free-ranging cervids in North America. We have previously demonstrated that specific Prnp polymorphisms are linked to susceptibility/resistance to CWD infection in free-ranging white-tailed deer populations. The “wild-type” alleles (with glutamine at aa 95 and a Glycine at aa 96) were over-represented in the infected deer while the polymorphisms at aa 95 (Q95H) and 96 (G96S) were under-represented in the CWD-positive animals. Experimental oral infection of white-tailed deer with known Prnp genotypes (with inocula from CWD-positive wt/wt deer) confirmed this link between Prnp primary sequence and incubation period. All orally infected animals became clinically positive for CWD. The wt/wt had the shortest incubation period (693 dpi) and the Q95H/G96S the longest (1596 dpi). Brain homogenates prepared from clinically affected deer of each genotype were treated with proteinase K and resolved by western blot; differences in the glycosylation pattern and PK resistance were observed and are suggestive of different PrPSc isoforms. Subsequent experiments regarding biochemical properties like detergent solubility, structural stability, host range and the stability of these characteristics upon serial passages will allow us to further define potential CWD strain emergence in white-tailed deer.

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

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




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




Friday, February 03, 2012

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html




Saturday, February 04, 2012

Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html




Thursday, February 09, 2012

Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html




Monday, February 13, 2012

Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild Deer Herd oppose HB3164

http://chronic-wasting-disease.blogspot.com/2012/02/stop-white-tailed-deer-farming-from.html




Tuesday, February 14, 2012

Oppose Indiana House Bill 1265 game farming cervids

http://chronic-wasting-disease.blogspot.com/2012/02/oppose-indiana-house-bill-1265-game.html




Wednesday, February 15, 2012

West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE WARNED CWD

http://chronic-wasting-disease.blogspot.com/2012/02/west-virginia-deer-farming-bill-backed.html




Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html




Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html




Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html






layperson

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net

Labels: , ,

Emergency Conservation Program Restores Idaho Deer Farm ?

Emergency Conservation Program Restores Idaho Deer Farm



Posted by Candy Moore, Idaho FSA Communications Coordinator and Debbie Carlock, County Executive Director, on February 28, 2012 at 11:15 AM


Ivan and Wilmina Phelps are the proud operators of a European Fallow Deer farm in scenic McCall, Idaho where national forests are the border for many farms. Their story is a tale of hard work, love of the land, care for their animals and survival of the fittest, as the couple recovered from a disaster with help from the Farm Service Agency (FSA).



The Phelps Family raises the deer for venison that they sell at area farmers markets. They also sell to restaurants, stores and direct to consumers. The business started in 1998 with only seven does and one buck. In 2000, the Phelps’ purchased an additional 54 heads and now have a herd of 150.



Gradual expansion has now brought their operation to approximately 50 acres in deer fencing, with seven pastures and some small pens, including a special handling facility, as required by the state.



On June 29, 2010, the McCall area experienced strong windstorms that were unusual for the area. Winds, estimated at 60 to 70 miles per hour, tore through the valley, causing severe damage.



“It came through our farm, uprooting and snapping off over 70 pine trees, many of which were over 100 years old and left a massive mess and huge holes,” Ivan explained. “Most of the damage was to interior fences. But one field, where our un-bred does are kept, had exterior damage. This allowed our herd to escape, but we were able to capture them in two days.”



USDA recognizes that a strong farm safety net is important to sustain the success of American agriculture. To help keep American agriculture profitable, USDA immediately responds to disasters across the country, ranging from record floods, droughts and tropical storms, with direct support, disaster assistance, technical assistance, and access to credit.



The debris from the trees was also scattered throughout the individual pastures, effectively limiting grazing and proper irrigation and destroying several gates and much of the fencing.



The Phelps’ contacted their local FSA office, where they learned about FSA’s Emergency Conservation Program (ECP). Shortly thereafter, their application for emergency cost share under the ECP program was approved.



The Phelps’ had most of the equipment to start on the debris




The Emergency Conservation Program helped the Phelps family save their deer farm after a windstorm.





cleanup. Ivan and his son worked for two months to clear all of the fallen trees and repair the fences and gates. They also had friends who came and helped cut and haul away downed trees. Several of the trees left large root holes that were too big for the Phelps to handle on their own so they had to hire equipment and an operator to clean up the stumps and roots, fill the holes and haul everything away.



“Because we are a small farm, the assistance from the Farm Service Agency was invaluable in helping with the cost of material and the many hours of debris removal,” said Wilmina. “With the dollars we received we were able to get new wire and posts so the work could be completed in a much shorter time frame. We also rotated the deer from field to field more often to allow us to complete the work needed in each area.”



Ivan added, “Without the assistance through the Farm Service Agency we would still be working on the early stages of the wind damage and fencing as the costs and work involved was more than we could handle ourselves.”



Landowners, individuals and communities have endured incredible hardships because of the intensity and volume of natural disasters that have threatened their livelihoods these past few years. The emergency assistance offered by USDA helps to rebuild communities, sustain and spur job creation, and keeps our farmers and ranchers productive and profitable.





Tags: Conservation, Emergency Conservation Program, FSA, Idaho, McCall









http://blogs.usda.gov/2012/02/28/emergency-conservation-program-restores-idaho-deer-farm/









>>> This allowed our herd to escape, but we were able to capture them in two days.<<<




disturbing is an understatement for the above comment, in relations to CWD.


see why ;


SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS.



http://wwwnc.cdc.gov/eid/article/18/3/11-0685-f1.htm




*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***



Saturday, February 18, 2012 Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease CDC Volume 18, Number 3—March 2012




http://wwwnc.cdc.gov/eid/ahead-of-print/article/18/3/11-0685_article.htm





SNIP...



Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).



SNIP...



CWD Zoonotic Potential, Species Barriers, and Strains


Current Understanding of the CWD Species



Barrier Strong evidence of zoonotic transmission of BSE to humans has led to concerns about zoonotic transmission of CWD (2,3). As noted above, CWD prions are present nearly ubiquitously throughout diseased hosts, including in muscle, fat, various glands and organs, antler velvet, and peripheral and CNS tissue (2,14,15). Thus, the potential for human exposure to CWD by handling and consumption of infectious cervid material is substantial and increases with increased disease prevalence. Interspecies transmission of prion diseases often yields a species-barrier effect, in which transmission is less efficient compared with intraspecies transmission, as shown by lower attack rates and extended incubation periods (3,28). The species barrier effect is associated with minor differences in PrPc sequence and structure between the host and target species (3). Prion strain (discussed below) and route of inoculation also affect the species barrier (3,28). For instance, interspecies transmission by intracerebral inoculation is often possible but oral challenge is completely ineffective (29). Most epidemiologic studies and experimental work have suggested that the potential for CWD transmission to humans is low, and such transmission has not been documented through ongoing surveillance (2,3). In vitro prion replication assays report a relatively low efficiency of CWD PrPSc-directed conversion of human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are resistant to CWD infection (31); these findings indicate low zoonotic potential. However, squirrel monkeys are susceptible to CWD by intracerebral and oral inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans than squirrel monkeys, are resistant to CWD infection (32). Regardless, the finding that a primate is orally susceptible to CWD is of concern. Interspecies transmission of CWD to noncervids has not been observed under natural conditions. CWD infection of carcass scavengers such as raccoons, opossums, and coyotes was not observed in a recent study in Wisconsin (22). In addition, natural transmission of CWD to cattle has not been observed in experimentally controlled natural exposure studies or targeted surveillance (2). However, CWD has been experimentally transmitted to cattle, sheep, goats, mink, ferrets, voles, and mice by intracerebral inoculation (2,29,33). CWD is likely transmitted among mule, white-tailed deer, and elk without a major species barrier (1), and other members of the cervid family, including reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD infection. Black-tailed deer (a subspecies of mule deer) and European red deer (Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34). Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation (35).



Continued study of CWD susceptibility in other cervids is of considerable interest. Reasons for Caution There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of 2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD.






Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation.







Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified,




SNIP...






*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***


Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012



http://wwwnc.cdc.gov/eid/ahead-of-print/article/18/3/11-0685_article.htm








see much more here ;




http://chronic-wasting-disease.blogspot.com/2012/02/occurrence-transmission-and-zoonotic.html










Can J Vet Res. 2011 April; 75(2): 152–156.



PMCID: PMC3062927


Copyright and/or publishing rights held by the Canadian Veterinary Medical Association


Experimental transmission of chronic wasting disease (CWD) from elk and white-tailed deer to fallow deer by intracerebral route: Final report


Amir N. Hamir, Justin J. Greenlee, Eric M. Nicholson, Robert A. Kunkle, Juergen A. Richt, Janice M. Miller, and Mark Hall


National Animal Disease Center (NADC), Agricultural Research Service (ARS), United States Department of Agriculture (USDA), 1920 Dayton Avenue, PO Box 70, Ames, Iowa (Hamir, Greenlee, Nicholson, Kunkle, Richt, Miller); and Pathobiology Laboratory, NVSL, USDA, 1920 Dayton Road, Ames, Iowa (Hall)


Address all correspondence to Dr. Hamir; telephone: (713) 792-2797; fax: (713) 794-4546; e-mail: ahamir@mdanderson.org


Dr. Hamir’s current address is Department of Veterinary Medicine and Surgery — Unit 63, M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Room 4055C, Houston, Texas 77030, USA.


Dr. Richt’s current address is Department of Diagnostic Medicine and Pathobiology, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506, USA.


Received February 23, 2010; Accepted May 9, 2010.


Other Sections▼




Abstract



Final observations on experimental transmission of chronic wasting disease (CWD) from elk (Cervus elaphus nelsoni) and white-tailed deer (Odocoileus virginianus) to fallow deer (Dama dama) are reported herein. During the 5-year study, 13 fawns were inoculated intracerebrally with CWD-infected brain material from white-tailed deer (n = 7; Group A) or elk (n = 6; Group B), and 3 other fawns were kept as uninoculated controls (Group C). As described previously, 3 CWD-inoculated deer were euthanized at 7.6 mo post-inoculation (MPI). None revealed presence of abnormal prion protein (PrPd) in their tissues. At 24 (Group A) and 26 (Group B) MPI, 2 deer were necropsied. Both animals had a small focal accumulation of PrPd in their midbrains. Between 29 and 37 MPI, 3 other deer (all from Group A) were euthanized. The 5 remaining deer became sick and were euthanized between 51 and 60 MPI (1 from Group A and 4 from Group B). Microscopic lesions of spongiform encephalopathy (SE) were observed in only these 5 animals; however, PrPd was detected in tissues of the central nervous system by immunohistochemistry, Western blot, and by commercial rapid test in all animals that survived beyond 24 MPI. This study demonstrates that intracerebrally inoculated fallow deer not only amplify CWD prions, but also develop lesions of spongiform encephalopathy.




http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3062927/







Tuesday, February 14, 2012


White House budget proposes cuts to ag programs including TSE PRION disease aka mad cow type disease


http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/white-house-budget-proposes-cuts-to-ag.html








50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE CWD




2012


Tuesday, December 20, 2011


CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011



> > > The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.


Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.


However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.


Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < <




http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf








SNIP...SEE FULL TEXT ;



http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html







Thursday, February 09, 2012


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE


http://chronic-wasting-disease.blogspot.com/2012/02/50-game-farms-to-date-in-usa-infected.html








Friday, February 03, 2012


Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al


http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html






Saturday, February 04, 2012


Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised


http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html







Thursday, February 09, 2012


Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al


http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html






Tuesday, February 14, 2012


Oppose Indiana House Bill 1265 game farming cervids


http://chronic-wasting-disease.blogspot.com/2012/02/oppose-indiana-house-bill-1265-game.html






Monday, February 13, 2012


Stop White-tailed Deer Farming from Destroying Tennessee's Priceless Wild Deer Herd oppose HB3164


http://chronic-wasting-disease.blogspot.com/2012/02/stop-white-tailed-deer-farming-from.html






Wednesday, February 15, 2012


West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE WARNED CWD


http://chronic-wasting-disease.blogspot.com/2012/02/west-virginia-deer-farming-bill-backed.html







Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission


http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html







now, a few things to ponder about those said double fences that will supposedly stop those deer from escaping.




what about water that drains from any of these game farms. surrounding water tables etc., are the double fences going to stop the water from becoming contaminated? where does it drain? who's drinking it?




Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area




65




Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- tracy.a.nichols@aphis.usda.gov




Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.




snip...




The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.




snip...end...full text at ;



http://www.landesbioscience.com/






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






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






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







what about rodents there from? 4 American rodents are susceptible to CWD to date. are those double fences going to stop these rodents from escaping these game farms once becoming exposed to CWD?




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.







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






please see ;


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









Oral.29: Susceptibility of Domestic Cats to CWD Infection




Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu




Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.





www.landesbioscience.com Prion






http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf







http://felinespongiformencephalopathyfse.blogspot.com/2011/08/susceptibility-of-domestic-cats-to-cwd.html








see what CWD did with first and second passage of testing in the lab to cattle ;





first passage ;



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







second passage


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.



http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=178318








Chronic Wasting Disease CWD cervids interspecies transmission



Wednesday, January 5, 2011




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




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




+ Author Affiliations




1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu






SNIP...



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




MARCH 1, 2011




UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON 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




====================END...TSS==============








SNIP...SEE FULL TEXT ;


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








Monday, October 10, 2011


EFSA Journal 2011 The European Response to BSE: A Success Story


snip...



EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.



snip...





http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1






http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf








see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;





http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html







Thursday, February 16, 2012




Bovine Spongiform Encephalopathy BSE




31 USA SENATORS ASK PRESIDENT OBAMA TO HELP SPREAD MAD COW DISEASE 2012




http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/bovine-spongiform-encephalopathy-bse-31.html






kind regards,
terry




layperson


Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518
flounder9@verizon.net





http://blogs.usda.gov/2012/02/28/emergency-conservation-program-restores-idaho-deer-farm/

Labels: , , ,

Thursday, February 09, 2012

50 GAME FARMS (to date) IN USA INFECTED WITH CHRONIC WASTING DISEASE

50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE




2010




Chronic Wasting Disease


The Federal Chronic Wasting Disease (CWD) herd-certification program for farmed cervids operations has been in development since late 2003. A CWD final rule was published in the Federal Register in 2006 but was not implemented in response to several petitions. The CWD rule was amended in 2010 following the publication of proposed changes. The amended rule will set minimum standards for interstate movement and establish the Federal CWD Herd Certification Program (HCP).


The Federal CWD HCP for farmed cervids is intended to be a cooperative State-Federal-industry program. The CWD program goals are to control CWD in farmed cervid herds and to encourage State and Tribal wildlife agencies to conduct CWD surveillance in wild cervids.


The number of farmed cervids tested for CWD has increased steadily since FY 2003 from approximately 12,000 animals tested to nearly 20,000 in FY 2010. From FY 1997 through FY 2010, CWD was identified in 37 farmed elk herds and 13 farmed white-tailed deer herds in 11 States (Table 3.2). Three new farmed cervid herds were found to have animals diagnosed as positive for CWD in 2010.





Table 3.2: Number of farmed cervid herds with animals positive for CWD by State,




FY 1997–FY 2010




State FY 1997–2010 FY 2010 ( FY 1997–2010)




Colorado 18 18




Kansas 1 1




Michigan 1 1




Minnesota 4 4




Missouri 1 1




Montana 1 1




Nebraska 5 5




New York 2 2




Oklahoma 1 1




South Dakota 7 7




Wisconsin 9 9




Total 49 1 50








Of the 50 CWD-positive herds identified as of September 30, 2010, 6 elk herds (all in Colorado) remained under State quarantine. One White-tailed deer herd in Missouri was identified as CWD positive in February 2010 and remained under State quarantine through 2010 pending depopulation.




Since 2002, most States have been participating in CWD surveillance in free-ranging deer, elk, and more recently, moose. By September 30, 2010, 13 States had reported detecting CWD in wild cervids (Colorado, Illinois, Kansas, Nebraska, North Dakota, New Mexico, New York, South Dakota, Utah, Virginia, West Virginia, Wisconsin, and Wyoming). From the 2002 through the 2010 hunting seasons, an approximate total of 773,400 hunter-harvested and targeted wild cervids were tested with an average of 95,600 samples each season (Figure 3.4). Wildlife surveillance strategies have also evolved over the years from broad active surveillance of hunter-harvested animals to targeted and weighted surveillance of wild cervids considered to be at greater risk of CWD (based on our knowledge and understanding of CWD transmission in those populations).







Figure 3.4: Surveillance testing of hunter-killed and targeted wildlife for CWD






U.S. Wild Cervid CWD Surveillance
(Reported to VS through 03/26/2010)






http://www.aphis.usda.gov/animal_health/animal_health_report/2010/ahr2010_chapter3.pdf







Friday, February 03, 2012

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html






Saturday, February 04, 2012

Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-16-age-limit-on-testing-dead.html






Thursday, February 09, 2012

Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al



http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html









CANADA, USA, CWD UPDATE 2011





Summary of Chronic Wasting Disease Workshop in Edmonton on Feb. 9-10, 2011


and Alberta’s CWD Update as of March 23, 2011


By Blair Rippin and Dr. Margo Pybus




snip...


Jurisdictional Summaries


! Dr. Michael Miller, Colorado Division of Wildlife


- CWD known in Colorado in captive cervids since 1967 and in wild cervids since early 1980s but intensive study done only since 2001.


- no evidence of occurrence in other domestic ruminants nor other wild mammals.


- prevalence high in many local mule deer populations.


- patterns of infections influenced by time since introduction, herd demographics, movement and congregation patterns, land use, soil characteristics, and management strategies.


- attempts to control or contain CWD deemed ineffective and abandoned, partly because of lack of public support.


- surveillance through directing hunt pressure and testing hunter kills continues.


Dr. Michael Samuel, Department of Forest and Wildlife Ecology, University of Wisconsin


- CWD identified in Wisconsin wild cervids in 2002 (white-tailed deer) but it’s estimated that it may have been there for 2 or 3 decades.


- early eradication attempts deemed ineffective and abandoned 3 years ago


- present management aimed only at containment through directing hunt pressure, testing and monitoring.


- spread estimated to be 2 -3 miles per year.


- genetic research indicates some evidence of developing resistence but it is a very slow to occur and estimated to take in the order of 200 years to make a difference.


Dr. Trent Bollinger, University of Saskatchewan


- CWD brought in from the US in late 1980s via imported game farm animals and now found in three populations of wild cervids.


- over the past decade CWD became wide spread in the province and occurs in both deer species and wild elk.


- containment efforts by directing hunt pressure have been unsuccessful and there is fear that caribou may become infected.


- management currently focused on tracking movements of the disease.


- considerable concern that if CWD crosses the species barrier (i.e. to domestic stock and/or humans) there will be far reaching negative economic and social consequences.


- largely depending on research to result in effective management programs.


Dr. Greg Douglas, Chief Veterinary Officer, Saskatchewan Ministry of Agriculture


- game farms and hunt farms involving 54,000 cervids is currently worth $60 million annually to Saskatchewans economy.


- described the challenges in efforts (mainly involving surveillance and culling) to eradicate CWD from Saskatchewan game farms via mechanisms to improve traceability, inventory, and surveillance.


Dr. Stephane McLachlan and Misty Potts-Sanderson, University of Manitoba


- CWD not present in Manitoba to date but is approaching from eastern Saskatchewan


- First Nations very concerned about “corralling” or “penning” (game farming) wild animals.


- considerable concern expressed about the decline in environmental quality from industrial sources and its effect on wildlife, indicating that CWD may be a symptom of a much larger problem.


- considerable concern expressed about the lack of effective communication between scientific community and First Nations.


Impacts of CWD presence on society


Dr. Vic Adamowicz, Department of Rural Economy, University of Alberta


- presented results of questionnaires designed to investigate how CWD affects recreational hunting.


- further work will determine the effects of CWD presence on the province’s economy.


- found awareness of CWD varied among societal cohorts, particularly urban/rural differences.


- CWD presence resulted in greater change in hunting venue among urban as opposed to rural dwellers.


Helen Cote-Quewezance, Cote First Nations, Saskatchewan


- outlined the importance of healthy wildlife to First Nations people in the form of sustenance, health, and spirituality.


- very concerned that CWD will likely degrade that aspect of aboriginal life.


- is willing to share knowledge with scientific community but asked for a forum that includes an effective understanding of aboriginal culture.


Dr. Ellen Goddard, et al, Department of Rural Economy, University of Alberta


- Canadians in general currently have a very limited understanding of CWD, however, it is somewhat greater than that of Americans.


- concern that CWD constitutes a significant human health risk is very low in both countries (i.e. much lower ranking than concerns about BSE or other known meat borne pathogens).


- Canadians support efforts to eradicate CWD much more than Americans.


Research initiatives


Dr. Michael Coulthart, et al, Public Health Agency of Canada


- although not occurring to date, he estimates that report of just one probable case of human CWD could trigger a public health crisis in North America.


- epidemiological studies so far indicate the probability is very slight, however, prion agents and their transmission properties are highly mutable and adaptable and the possibility can not be ruled out.


- suggests those involved in human prion disease surveillance should consider the possibility of human CWD and develop a readiness to deal with it.


Dr. Margit Westphal, McLaughlin Centre for Population Health Risk Assessment, University of Ottawa


- CWD identified in captive research animals in 1967 has now spread to 18 US states and 2 Canadian provinces in farmed and free ranging cervids.


- complicating development of an effective plan to combat CWD are the facts that it has a very long latency period, extended environmental persistence, and it lacks a quick and sensitive diagnostic anti-mortem test.


- “Effective management of CWD requires the development and application of an integrated risk management framework based on sound principles of risk assessment and management, and the harmonization of regulation that align trans-border management efforts”.




Judd Aikens et al, Centre for Protein Folding Diseases, University of Alberta


- have identified two prion protein gene variants in Alberta white-tailed deer that are linked to disease prolongation.


- implications could lead to possible development of resistence but would likely take a very long time.




Scott Adams and Scott Napper, University of Saskatchewan




- testing is currently underway to determine the effectiveness of a newly developed injectable CWD vaccine that has shown considerable promise.


- an effective vaccine could be used to prevent CWD in game farm animals but additional study would be required to determine an effective application method in the wild.




Conclusions drawn from the workshop presentations and discussions




CWD is a newly invasive and fatal neurodegenerative prion disease of cervids known in North America only since 1967 (45 years) and hosts have not had time to adapt. To date it is present in 18 US states and 2 Canadian provinces.


$ Attempts to eradicate CWD via intensive culling has generally proved to be ineffective except where infection is very recent. Evidence of recent timing of infection was shown in Alberta by lymph node positive but brain negative in tested specimens.


$ In wild cervids the two deer species are most commonly involved. Of those, mule deer are most heavily infected in western jurisdictions while in east-central states, where mule deer are absent, white-tails are the only host. Further, of the various cohorts, adult males are most commonly infected and regulations aimed at providing trophy antlers may be exacerbating efforts to control CWD prevalence and spread.


$ Culling by management agencies and/or by directing hunting pressure was shown to be ineffective in eradicating and even the in halting the spread of the disease.


$ Surveillance for prevalence and degree of spread via testing hunter-killed animals is currently the most common management method in practice. It has also been shown that public awareness, understanding, and attitudes are critical factors to consider when embarking on control activities.




$ Factors complicating the control or management of CWD are:




- CWD has a very long latency period.


- Currently the only tests for diagnosing CWD in living animals is to collect tonsil or rectal lymph biopsy tissues.


- Prions will bind with clay particles in soil and thus remain persistent in areas containing infected animals.


- Although there are some signs of developing immunity or resistence in hosts it will take very long time (i.e. > 200 years) to manifest itself.


-In infected foci, close relatedness appears to be a factor in increase prevalence, which could also result from mule deer being more gregarious and exhibiting clumping behavior, particularly during winter when CWD transmission is most likely to occur.


- Some mule deer are migratory, which further complicates CWD containment efforts.


$ CWD is slow to show population effects but with time it is predicted to result in significant reductions in density and distributions of ecologically, economically, socially important cervids in all jurisdictions with CWD infections.




Presently there are only speculative indications of CWD crossing species barrier but on the slim chance human CWD occurs, it is predicted there will be general public panic and adverse repercussions to recreational and First Nation’s use of cervids and subsequent negative effects on economies in several jurisdictions.


$ Social science is directing further effort into determining probable effects of CWD presence on public understanding, awareness, and attitudes toward control efforts and in turn how this may influence hunter behavior, food safety, and the economy.




Identified needs for future efforts to manage CWD


snip...




Chronic Wasting Disease (CWD) Surveillance Update: March 23, 2011


All heads of deer and elk received to date from the fall hunting seasons have been tested, although a few heads continue to dribble into the lab. Herein we provide the summary of the 2010 fall surveillance. However, the ongoing CWD Surveillance Program will continue to test heads whenever they are received throughout the year.


From September 1, 2010 to March 23, 2011 we tested 5062 heads (primarily deer heads) and detected nineteen (0.4%) new cases of CWD in wild deer in Alberta. Seventeen of the positive deer were mule deer: twelve males, five females The two remaining positive deer were white-tail males All positive deer were harvested by hunters and were in very good to excellent body condition.


All but one positive deer were adults. The remaining positive deer was a yearling in the early stages of infection.


Many of the infected deer were near previous known CWD cases, largely in the Battle River and Ribstone Creek drainages in the north and the Red Deer River drainage in the south.


A cluster of infected deer was found north and west of Dinosaur Provincial Park in WMU 152 – a significant extension of the disease westward along the Red Deer River.


Of particular significance, the positive yearling mule deer buck was the first case of CWD found in the North Saskatchewan River valley in Alberta. This is strong evidence of recent expansion of the disease into or within the valley.


As anticipated, additional infected deer were found in CFB Wainwright in association with the Battle River valley.


The 19 new hunter-kill cases are in addition to the road-kill case found in February 2010, thus the annual total for 2010 is 20 cases.


Ongoing NEGATIVE test results were posted to AlbertaRelm and made available to individual hunters. To date, approximately 50% of the test results have been read by the hunter.


Ongoing POSITIVE test results were provided by phone directly to the hunter who harvested the infected deer.


As in previous years, hunters who harvest a CWD-infected deer were given the options of


! keeping the meat


! turning in the meat and receiving a replacement licence for this year (if the season was still open where the infected deer was harvested)


! turning in the meat and receiving a replacement licence for next year for the same species and location as the infected deer


The total number of CWD cases detected in wild deer in Alberta since September 2005 is 94.


As part of the ongoing provincial surveillance program, we also are testing a random sample of emaciated cervids associated with severe winter conditions occurring in various parts of Alberta


To learn more about CWD in Alberta, visit:





http://srd.alberta.ca/BioDiversityStewardship/WildlifeDiseases/ChronicWastingDisease/




Attention Hunters!

If you have frozen deer heads that you would like to submit to the ongoing CWD
surveillance program, please drop them off at any Fish and Wildlife office during
regular office hours. For more details, visit:


http://srd.alberta.ca/FishingHuntingTrapping/Hunting/ChronicWastingDisease-









CWD Map and Statistics



MAP:


http://srd.alberta.ca/BioDiversityStewardship/WildlifeDiseases/ChronicWastingDisease/CWDUpdates/documents/CWD-PositiveMap-Mar18-2011.pdf







LIST:




http://srd.alberta.ca/BioDiversityStewardship/WildlifeDiseases/ChronicWastingDisease/CWDUpdates/documents/CWD-PositiveList-Mar18-2011.pdf








snip...see full text ;





http://joomla.wildlife.org/Alberta/images/Documents/Cons_committee/cwd%20update%202011.pdf







now, a few things to ponder about those said double fences that will supposedly stop those deer from escaping.



what about water that drains from any of these game farms. surrounding water tables etc., are the double fences going to stop the water from becoming contaminated? where does it drain? who's drinking it?



Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area




65


Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- tracy.a.nichols@aphis.usda.gov

Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.

snip...

The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.

snip...end...full text at ;



http://www.landesbioscience.com/





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




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





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








what about rodents there from? 4 American rodents are susceptible to CWD to date. are those double fences going to stop these rodents from escaping these game farms once becoming exposed to CWD?






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.



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









please see ;



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









Oral.29: Susceptibility of Domestic Cats to CWD Infection



Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu



Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.




www.landesbioscience.com Prion





http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf






http://felinespongiformencephalopathyfse.blogspot.com/2011/08/susceptibility-of-domestic-cats-to-cwd.html







Avian Scavengers as Vectors of Prion Disease—
Mechanisms for the spread of CWD in North American
deer and other cervids are not completely understood.
NWRC researchers hypothesize that avian
scavengers may play a role in translocating CWD in
the wild, potentially encountering CWD-infected
carcasses, consuming infected tissue, and transporting
it over long distances before depositing feces. In
a recent study, researchers inoculated 100 mice with
fecal extracts obtained from American crows (Corvus
brachyrhynchos) that were force-fed material infected
with mouse scrapie (PrPSc). These mice showed
severe neurological dysfunction 196 to 231 days post
inoculation and tested positive for PrPSc. These results
demonstrate that a common, migratory North American
scavenger can pass infective prions in feces and,
therefore, could play a role in the geographic spread
of CWD in the environment.



http://www.aphis.usda.gov/wildlife_damage/nwrc/publications/NWRC%202010%20Ann%20Report_Final.pdf







Distribution and Epizootiology of CWD in
Nebraska Deer—Western Nebraska is considered
part of the core endemic area of CWD, yet little is
known about prevalence rates or the factors affecting
the distribution of CWD in this area. NWRC
researchers used data on the occurrence of CWD
collected from 2000 to 2007 throughout Nebraska
to calculate prevalence rates and investigate
the role that key spatial, temporal, demographic,
and environmental factors have on the distribution
of this disease. Researchers conducted analyses
at two spatial scales, including the Panhandle
region of western Nebraska and Statewide.
Results show that the dynamics of CWD were
similar between the different spatial scales. CWD
was more prevalent in mule deer (Odocoileus
hemionus) than in white-tailed deer (Odocoileus
virginianus), in male deer than in female deer, and
in adult deer than in fawns. Overall prevalence has
increased from 0.3 to 1.4 percent in the Panhandle
and from 0.2 to 0.5 percent Statewide. The sex of
the animal and the interaction of latitude and longitude
had the most influence when predicting CWD
occurrence in Nebraska at both spatial scales. Age,
year collected, and soil texture were also predictors.
These results concur with studies conducted
in other areas of the CWD core endemic area, suggesting
that CWD dynamics are governed by similar
processes throughout the disease’s range.



Project Contact: Kurt VerCauteren




http://www.aphis.usda.gov/wildlife_damage/nwrc/publications/NWRC%202010%20Ann%20Report_Final.pdf







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







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, 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, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html








Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html







at least that’s my opinion. my intentions are NOT, and never has been to split up the hunters. it’s just been to inform them of the rest of the science. I cannot stress enough, it’s not just about you, and what you consume as hunters. I don’t care what you eat. but once you expose yourself to the TSE Prion via CWD infected deer and or elk, and then go have medical procedures done, surgical, dental, donate blood, tissue, etc., then you expose everybody with the TSE Prion disease. then it becomes everybody’s business. ...






kind regards, terry





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



Subject: Tracking spongiform encephalopathies in North America LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003


Date: Tue, 29 Jul 2003 17:35:30 –0500

From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

Volume 3, Number 8 01 August 2003


Newsdesk


Tracking spongiform encephalopathies in North America


Xavier Bosch


My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.



Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.


http://infection.thelancet.com/journal/journal.isa



http://www.thelancet.com/journals/laninf/article/PIIS1473309903007151/%20fulltext




http://www.thelancet.com/journals/laninf/issue/vol3no8/PIIS1473-3099(00)X0025-4






Greetings,


> he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. <




actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article.



Full Text


Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734.



http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama





http://jama.ama-assn.org/content/285/6/733.extract







2 January 2000


British Medical Journal


U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well


http://www.bmj.com/cgi/eletters/320/7226/8/b#6117






15 November 1999


British Medical Journal


vCJD in the USA * BSE in U.S.


http://www.bmj.com/cgi/eletters/319/7220/1312/b#5406






Singeltary submission to PLOS ;


No competing interests declared.


see full text ;




http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd






Tuesday, November 08, 2011



Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011 Original Paper


Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.


http://creutzfeldt-jakob-disease.blogspot.com/2011/11/can-mortality-data-provide-reliable.html






Saturday, January 2, 2010


Human Prion Diseases in the United States January 1, 2010 ***FINAL***


http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html






14th ICID International Scientific Exchange Brochure -


Final Abstract Number: ISE.114


Session: International Scientific Exchange


Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009


T. Singeltary


Bacliff, TX, USA


Background:


An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.


Methods:


12 years independent research of available data


Results:


I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.


Conclusion:


I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.




http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf







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






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. HOW long can this cover-up continue $$$


The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.



http://www.oie.int/boutique/extrait/06heim937950.pdf







SEE FULL TEXT AND MORE HERE ;


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





Thursday, January 26, 2012


Facilitated Cross-Species Transmission of Prions in Extraneural Tissue


Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659


http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html






Thursday, January 26, 2012


The Risk of Prion Zoonoses


Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167


http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html







THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;



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








NOR IS THE FDA 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








Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.



snip...



*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,



snip... full text ;



http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html








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

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

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

From: "Belay, Ermias"

To:

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

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

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS



Dear Sir/Madam,



In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.


That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.



Ermias Belay, M.D. Centers for Disease Control and Prevention



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



From:

Sent: Sunday, September 29, 2002 10:15 AM

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

Sunday, November 10, 2002 6:26 PM


......snip........end..............TSS



http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html








O.K. THE PRION GODS AT THE CDC SAY NO _STRONG_ EVIDENCE FOR CWD TO HUMANS YET ???




HOWEVER, COLORADO OFFICIALS CLAIM NO CASUAL RELATIONSHIP BETWEEN CWD AND HUMAN HEALTH PROBLEM ???



an oxymoron or what ???




To date, ongoing investigations by state and federal public health officials have shown no causal relationship between CWD and human health problems, for more information see CWD and Potential Transmission to Humans .



http://wildlife.state.co.us/hunting/biggame/cwd/Pages/CWDHome.aspx







Monday, November 14, 2011


WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011


http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wyoming-creutzfeldt-jakob-disease-cwd.html






Wednesday, November 16, 2011


Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011


http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wisconsin-creutzfeldt-jakob-disease-cwd.html






Sunday, November 13, 2011


COLORADO CWD CJD TSE PRION REPORTING 2011


http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/colorado-cwd-cjd-tse-prion-reporting.html






PLEASE SEE THE LETTER THE British Deer Farmers Association October 1994




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






PLEASE REMEMBER ;


The Akron, Ohio-based CJD Foundation said the Center for Disease Control revised that number in October of 2004 to about one in 9,000 CJD cases per year in the population group age 55 and older.

HAVE YOU GOT YOUR CJD QUESTIONNAIRE ASKING REAL QUESTIONS PERTAINING TO ROUTE AND SOURCE OF THE TSE AGENT THAT KILLED YOUR LOVED ONE ???

if not, why not...




Friday, November 30, 2007



CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION



http://cjdquestionnaire.blogspot.com/2007/11/cjd-questionnaire.html







http://cjdquestionnaire.blogspot.com/







TSS

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