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: , ,

Sunday, September 07, 2008

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

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

[QUOTE=xxxxxx]There is NO viable test for CWD on LIVE deer thus the entire herd was killed and tested.................which is also why there is a "mandatory" deer check in for any deer taken from the surrounding townships during hunting season..[/QUOTE]


http://www.michigan-sportsman.com/forum/showthread.php?t=249787&page=2



TESTING OF LYMPHOID TISSUE OBTAINED BY RECTAL BIOPSY WAS APPROVED BY USDA AS AN OFFICIAL LIVE-ANIMAL TEST ON JANUARY 11, 2008. ...

PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**



http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps



Biopsy of the rectal mucosal tissue, a site readily sampled in the restrained or chemically immobilized deer, provided an accurate diagnosis in 83% of the infected deer.



http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=218153



"The use of this new live test in the initial screening, surveillance, and monitoring of CWD will greatly aid in the management and control of the disease in the wild, as well as in captive settings," Dr. VerCauteren said.


http://www.avma.org/onlnews/javma/jul08/080715t.asp



“The key advantage to the rectal biopsy test is that it can be performed on live animals. Until now, there was no practical live test for CWD in elk,” said research wildlife biologist Dr. Kurt VerCauteren with APHIS’ Wildlife Services (WS) National Wildlife Research Center (NWRC). “With this technique we can detect CWD in animals not showing any signs of the disease and, thus, remove them so they are not left to infect other individuals and further contaminate the environment.”


http://www.aphis.usda.gov/newsroom/content/2008/05/cwdelktst.shtml



Greetings Michigan Hunters et al;

now, let's ponder a few things, shall we.

why quarantine a farm for 4 to 5 years due to an atypical TSE of foreign origin and due to potential serious animal and HUMAN health here in the USA there-from. then a few years later, discover the same damn TSE in the USA, home grown, and the same quarantine is not put in place. case in points, the mad sheep of mad river valley compared to those two atypical H-BSE cases in Texas and Alabama, and 6 cases to date of the atypical scrapie NOR-98 in six different states. why is the usda et al hiding behind some serum toxin act from decades ago, simply to NOT allow testing for BSE/TSE in the USA bovine i.e. Creekstone vs USDA ? and why is the same serum-toxin act not applying to the CWD testing in the States, with deer and elk? or does it? these are not trick questions, i really want to know. you cannot ignore these other TSEs, and the politics that surround them. well, the moderators can ;-) and that's their choice, and i will abide by whatever move they take. i am not trying to get off topic, but, these issues must not be ignored. that must not happen with CWD in Michigan. and remember, in Terms of TSE i.e. prion disease, Michigan has CWD, Scrapie, and the atypical Nor-98 scrapie, Michigan also has cattle$ remember, the first recorded case of scrapie in the US occurred on a ranch in Michigan in 1947, the year of the first TME outbreak in Wisconsin. riddle me this batman, riddle me this ???

see last link at bottome of page ; ''Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?''

kind regards, terry

xxxxxxxxxxx

Prof Collinge old findings, a key issue, the media always seems to forget about, states that BSE propagates as either variant CJD-like or sporadic CJD-like prion strains. funny how our health officials, governments, and such seem to conveniently ignore these findings, let alone the atypical TSE in cattle and sheep that do NOT look like nvCJD in the lab, but some sub-types of the sporadic CJD. all this goes ignored for one reason, and one reason only $$$ it's why the UKBSEnvCJD only theory was put forth in the first place, and it's why it is still set in stone $$$ to much science has been forth to date that proves that theory wrong.

PLEASE NOTE, the last two mad cows documented in the USA were H-type BSE, then the USDA quickly shut the testing down to a level of non-detection. it would be a miracle to find one case, from testing only 40,000 annually, from some 97,000,000 (that's 97 million head), and of that, some 37 million slaughtered, if i am not mistaken. and these cattle are cherry picked brains too, probably calves from USDA grain fed facilities, and don't think these corrupt people are not capable of doing it either. they are very capable, in fact, they did just that ;

"REDACTED is alleged to have provided possibly inaccurate test results involving diseased sheep. However, because the results were determined to be inconclusive, no actual violation was actually committed.''

snip...

Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.

snip...

I would note that the sample was taken in April, at which time the protocols allowed for a preservative to be used (protocols changed in June 2005). The sample was not submitted to us until last week, because the veterinarian set aside the sample after preserving it and simply forgot to send it in. On that point, I would like to emphasize that while that time lag is not optimal, it has no implications in terms of the risk to human health. The carcass of this animal was destroyed, therefore there is absolutely no risk to human or animal health from this animal.

snip...

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

snip...

4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half


http://www.usda.gov/oig/webdocs/sarc070619.pdf



full text ;



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



USDA: In 9,200 cases only one type of test could be used

WASHINGTON (AP)--The U.S. Department of Agriculture acknowledged Aug. 17 that its testing options for bovine spongiform encephalopathy were limited in 9,200 cases despite its effort to expand surveillance throughout the U.S. herd.

In those cases, only one type of test was used--one that failed to detect the disease in an infected Texas cow.

The department posted the information on its website because of an inquiry from The Associated Press.

Conducted over the past 14 months, the tests have not been included in the department's running tally of BSE tests since last summer. That total reached 439,126 on Aug. 17.

"There's no secret program," the department's chief veterinarian, John Clifford, said in an interview. "There has been no hiding, I can assure you of that."

Officials intended to report the tests later in an annual report, Clifford said.

These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC.

In the Texas case, officials had declared the cow free of disease in November after an IHC test came back negative. The department's inspector general ordered an additional kind of test, which confirmed the animal was infected.

Veterinarians in remote locations have used the preservative on tissue to keep it from degrading on its way to the department's laboratory in Ames, Iowa. Officials this year asked veterinarians to stop using preservative and send fresh or chilled samples within 48 hours.

The department recently investigated a possible case of BSE that turned up in a preserved sample. Further testing ruled out the disease two weeks ago.

Scientists used two additional tests--rapid screening and Western blot--to help detect BSE in the country's second confirmed case, in a Texas cow in June. They used IHC and Western blot to confirm the first case, in a Washington state cow in December 2003.

"The IHC test is still an excellent test," Clifford said. "These are not simple tests, either."

Clifford pointed out that scientists reran the IHC several times and got conflicting results. That happened, too, with the Western blot test. Both tests are accepted by international animal health officials.

Date: 8/25/05



http://www.hpj.com/archives/2005/aug05/aug29/BSEtestoptionswerelimited.cfm



""These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."

THIS WAS DONE FOR A REASON!

THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS

USDA 2003

We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip.............

Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.

Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .

Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.

snip...

FULL TEXT;

Completely Edited Version PRION ROUNDTABLE

Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado

2005

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

CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006

The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.

The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.

These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.

"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."

Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.

USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.

"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end



http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r




CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...



http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm



PLEASE NOTE ;

179 Page 10 of 17

BSE cattle may need to be reexamined.

T. Kitamoto (Ed.) PRIONS Food and Drug Safety

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

ALSO from the International Symposium of Prion Diseases held in Sendai, October 31, to November 2, 2004; Bovine spongiform encephalopathy (BSE) in Japan

snip...

"Furthermore, current studies into transmission of cases of BSE that are atypical or that develop in young cattle are expected to amplify the BSE prion" NO. Date conf. Farm Birth place and Date Age at diagnosis 8. 2003.10.6. Fukushima Tochigi 2001.10.13. 23 9. 2003.11.4. Hiroshima Hyogo 2002.1.13. 21

Test results # 8b, 9c cows Elisa Positive, WB Positive, IHC negative, histopathology negative b = atypical BSE case c = case of BSE in a young animal b,c, No PrPSc on IHC, and no spongiform change on histology International Symposium of Prion Diseases

held in Sendai, October 31, to November 2, 2004. Tetsuyuki Kitamoto Professor and Chairman Department of Prion Research Tohoku University School of Medicine 2-1 SeiryoAoba-ku, Sendai 980-8575, JAPAN TEL +81-22-717-8147 FAX +81-22-717-8148 e-mail; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:kitamoto@mail.tains.tohoku.ac.jp Symposium Secretariat Kyomi Sasaki TEL +81-22-717-8233 FAX +81-22-717-7656 e-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:kvomi-sasaki@mail.tains.tohoku.ac.ip

================================= 9/13/2005 --------------------------------------------------------------------------------


Page 11 of 17

From: TSS () Subject: Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Date: August 26, 2005 at 10:24 am PST Atypical Proteinase K-Resistant Prion Protein (PrPres) observed in an Apparently Healthy 23-Month-Old Holstein Steer Jpn. J. Infect. Dis., 56, 221-222, 2003 Laboratory and Epidemiology Communications Atypical Proteinase K-Resistant Prion Protein (PrPres) Observed in an Apparently Healthy 23-Month-Old Holstein Steer Yoshio Yamakawa*, KenÕichi Hagiwara, Kyoko Nohtomi, Yuko Nakamura, Masahiro Nishizima ,Yoshimi Higuchi1, Yuko Sato1, Tetsutaro Sata1 and the Expert Committee for BSE Diagnosis, Ministry of Health, Labour and Welfare of Japan2 Department of Biochemistry & Cell Biology and 1Department of Pathology, National Institute of Infectious Diseases, Tokyo 162-8640 and 2Miistry of Health, Labour and Welfare, Tokyo 100-8916 Communicated by Tetsutaro Sata (Accepted December 2, 2003) *Corresponding author: Mailing address: Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Toyama 1-23-1, Shinjuku-ku, Tokyo 1628640, Japan. Tel: +81-3-5285-1111, Fax: +81-3-5285-1157, E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:yamakawa@nih.go.jp

Since October 18, 2001, 'bovine spongiform encephalopathy (BSE) examination for all cattle slaughtered at abattoirs in the country' has been mandated in Japan by the Ministry of Health, Labour and Welfare (MHLW). 'Plateria' ELISA-kit (Bio-Rad Laboratories, Hercules, Calif., USA) is routinely used at abattoirs for detecting proteinase K (PK)-resistant prion protein (PrPSc) in the obex region. Samples positive according to the ELISA screening are further subjected to Western blot (WB) and histologic and immunohistochemical examination (IHC) at the National Institute of Infectious Diseases (NIID) or Obihiro University. If PrPSc is detected either by WB or by IHC, the cattle are diagnosed as BSE. The diagnosis is approved by the Expert Committee for BSE Diagnosis, MHLW. From October 18, 2001 to September 30, 2003, approximately 2.5 million cattle were screened at abattoirs. A hundred and ten specimens positive according to ELISA were subjected to WB/IHC. Seven showed positive by both WB and IHC, all exhibiting the typical electrophoretic profile of a high content of the di-glycosylated molecular form of PrPSc (1-3) and the distinctive granular deposition of PrPSc in neuronal cells and neuropil of the dorsal nucleus of vagus. An ELISA-positive specimen from a 23 month-old Holstein steer slaughtered on September 29, 2003, in Ibaraki Prefecture (Ibaraki case) was sent to the NIID for confirmation. The animal was reportedly healthy before slaughter. The OD titer in ELISA was slightly higher than the 'cut-off' level given by the manufacturer. The histology showed no spongiform changes and IHC revealed no signal of PrPSc accumulation typical for BSE. However, WB analysis of the homogenate that was prepared from the obex region and used for ELISA revealed a small amount of PrPSc with an electrophoretic profile different from that of typical BSE-associated PrPSc (1-3). The characteristics were (i) low content of the di-glycosylated molecular form of PrPSc, (ii) a faster migration of the non-glycosylated form of PrPSc on SDS-PAGE, and (iii) less resistance against PK digestion as compared with an authentic PrPSc specimen derived from an 83-month-old Holstein (Wakayama case) (Fig. 1). Table 1 summarizes the relative amounts of three distinctive glycoforms (di-, mono, non-glycosylated) of PrPSc calculated by densitometric analysis of the blot shown in Fig. 1. As 2.5 mg wet weight obex-equivalent homogenate of the Ibaraki case (Fig. 1, lane 4) gave slightly stronger band intensities of PrPSc than an 8 mg wet weight obex-equivqlent homogenate of a typical BSE-affected Wakayama case (Fig. 1, lane 2), the amount of PrPSc accumulated in the Ibaraki case was calculated to be 1/500 - 1/1000 of the Wakayama case. In the Ibaraki case, the PrPSc bands were not detectable in the homogenates of the proximal surrounding region of the obex. These findings were consistent with the low OD value in ELISA, i.e., 0.2 -0.3 for the Ibaraki case versus over 3.0 for the Wakayama case. The DNA sequence of the PrP coding region of the Ibaraki case was the same as that appearing in the database (GenBank accession number: AJ298878). More recently, we encountered another case that resembled the Ibaraki case. It was a 21-monthold Holstein steer from Hiroshima Prefecture. WB showed typical BSE-specific PrPSc deposition though IHC did not detect positive signals of PrPSc (data not shown). Though the clinical onset of BSE is usually at around 5 years of age or later, a 20-month-old case showing the clinical signs has been reported (4). Variant forms of BSE similar to our cases, i.e., with atypical histopathological and/or biochemical phenotype, have been recently reported in Italy (5) and in France (6). Such variant BSE was not associated with mutations in the prion protein (PrP) coding region as in our case (5,6). The Ministry of Agriculture, Forestry and Fisheries of Japan (MAFF) announced a ban of feeding ruminants with meat bone meal (MBM) on September 18, 2001, and a complete ban was made on October 15 of the same year. According to the recent MAFF report, the p ous seven cases of BSE in Japan were cattle born in 1995 - 1996 and possibly fed with cross-contaminated feed. However, the two cattle in this report were born after the complete ban. Whether contaminated MBM was implicated in the present cases remains to be investigated.

REFERENCES Collinge, J., Sidle, K. C. L., Meads, J., Ironside, J. and Hill, A. F. (1996): Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature, 383, 685690. Bruce, M. E., Will, R. G., Ironside, J. W., McConnell, I., Drummond, D., Suttie, A., McCardle, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. J. (1997): Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature, 389, 498-501. Hill, A. F., Desbruslais, M., Joiner, S., Sidle, K. C. L., Gowland, I. and Collinge, J. (1997): The same prion strain causes vCJD and BSE. Nature, 389, 448-450. Matravers, W., Bridgeman, J. and Smith, M.-F. (ed.)(2000): The BSE Inquiry. p. 37. vol. 16. The Stationery Office Ltd., Norwich, UK. Casalone, C., Zanusso, G., Acutis, P. L., Crescio, M. I., Corona, C., Ferrari, S., Capobianco, R., Tagliavini, F., Monaco, S. and Caramelli, M. (2003): Identification of a novel molecular and neuropathological BSE phenotype in Italy. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen, October 8-10. Bicaba, A. G., Laplanche, J. L., Ryder, S. and Baron, T. (2003): A molecular variant of bovine spongiform encephalopatie. International Conference on Prion Disease: from basic research to intervention concepts. Gasreig, Munhen, October 8-10. Asante, E. A., Linehan, J. M., Desbruslais, M., Joiner, S., Gowland, I., Wood, A. L., Welch, J., Hill, A. F., Lloyd, S. E., Wadsworth, J. D. F. and Collinge, J. (2002). BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J., 21, 6358-6366. 9/13/2005 Page 12 of 17 SEE SLIDES IN PDF FILE;


http://www.nih.go.jp/JJID/56/221.pdf



http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf




THE SEVEN SCIENTIST REPORT ***



http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf



***

WELL, someone did call me from Bio-Rad about this, however it was not Susan Berg. but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;

Bio-Rad, TSS phone conversation 12/28/04

Finally spoke with ;

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX

at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.

my question;

Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???

ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.

again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there. "very difficult to answer"

"very political"

"very loaded question"

outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing. said something about Dr. Houston stating; any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives? said something about ''just look at the sheep that tested IHC- but were positive''. ...

TSS

-------- Original Message -------- Subject: Your questions Date: Mon, 27 Dec 2004 15:58:11 -0800 From: To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:flounder@wt.net

Hi Terry:

............................................snip Let me know your phone number so I can talk to you about the Bio-Rad BSE test. Thank you

Regards

Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: =================================

END...TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########



http://madcowtesting.blogspot.com/




Executive Summary

In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.



http://www.aphis.usda.gov/lpa/issues/bse/epi-updates/bse_final_epidemiology_report.pdf




Greetings again Michigan Hunters et al ;

i know how some don't like to get political, but cwd, mad cow disease (all strains), TME, Scrapie, and cjd i.e. human and animal TSE, that's all they are are political. bush has failed us terribly, clinton before him failed us terribly, and whomever gets in office next will do the same damn thing, in terms of human and animal TSE. it was said long ago ;

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.



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




PLEASE NOTE, ''FANATICAL INCIDENT TO BE AVOIDED IN THE US AT ALL COSTS.''

AND they meant it. i have watched this nightmare unfold daily for over a decade. i was told long ago, by an old wise person, that the deer and elk industry, was used as a scapegoat, or was sacrificed by the USDA et al, to get the monkey off their backs i.e. livestock, commodities, and futures, i.e. global trade. mere words of wisdom i suppose, but why does the USDA et al refuse to test to find. everything they have done in the past, was done just the opposite. it's been proven. i.e. the USDA, OIE, BSE MRR policy gave birth to that. i give you this data only as history, so as to maybe not to repeat itself. who knows? you can file it away, but i dont care to debate it, there is nothing to debate in my mind, the data speaks for itself. YOU, anyone one of you do not think our Government is capable of doing such a think, i only say two words, tobacco and asbestos. decades of cover-up by big industry. i have seen it repeated time and time again, to date. and i really dont see a new regime in Washington doing anything different, from either party. the only way to do that would be to get the industry out of Washington, and this will not happen $$$

The EMBO Journal Vol. 21 No. 23 pp. 6358±6366, 2002

BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein

Emmanuel A.Asante, Jacqueline M.Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L.Wood, Julie Welch, Andrew F.Hill, Sarah E.Lloyd, Jonathan D.F.Wadsworth and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:j.collinge@prion.ucl.ac.uk Variant Creutzfeldt±Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSEderived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure. ...snip...end...TSS

Molecular Features of the Protease-resistant Prion Protein (PrPres) in H-type BSE

Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden

Western blot analyses of PrPres accumulating in the brain of BSE-infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H-type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C-terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans. ...end

USA MAD COW STRAIN MORE VIRULENT TO HUMANS THAN UK STRAIN

18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.

snip...

64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE.

Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. *** A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.

snip...



http://www.seac.gov.uk/minutes/95.pdf



AND WHAT ABOUT THOSE atypical NOR-98 scrapie cases in the USA, now documented at 6 cases in the past two years, and the risk thereof to humans as sporadic CJD ???

P03.141

Aspects of the Cerebellar Neuropathology in Nor98

Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,

Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

INFECTED AND SOURCE FLOCKS

There were 20 scrapie infected and source flocks with open statuses (Figure 3) as of April, 30, 2008. Twenty eight new infected and source flocks have been designated in FY 2008 (Figure 4); three source flocks were reported in April. ...snip

POSITIVE SCRAPIE CASES

As of April 30, 2008, 122 new scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2008 (Figure 6). Of these, 103 were field cases and 19* were Regulatory Scrapie Slaughter Surveillance (RSSS) cases (collected in FY 2008 and reported by May 20, 2008). Positive cases reported for April 2008 are depicted in Figure 7. Eighteen cases of scrapie in goats have been confirmed by NVSL since implementation of the regulatory changes in FY 2002 (Figure 8). The most recent positive goat case was confirmed in February 2008 and originated from the same herd in Michigan as the other FY 2008 goat cases. ...snip

CAPRINE SCRAPIE PREVALENCE STUDY (CSPS)

snip...

However, four positive goats have been identified this fiscal year through field investigations. One was a clinical suspect submitted for testing and the other three originated from the birth herd of the clinical case.

ANIMALS SAMPLED FOR SCRAPIE TESTING

As of April 30, 2008, 26,703 animals have been sampled for scrapie testing: 23,378 RSSS, 1,517 goats for the CSPS study, 1,466 regulatory field cases, 270 regulatory third eyelid biopsies, and 72 regulatory rectal biopsies (chart 8).

TESTING OF LYMPHOID TISSUE OBTAINED BY RECTAL BIOPSY WAS APPROVED BY USDA AS AN OFFICIAL LIVE-ANIMAL TEST ON JANUARY 11, 2008. ...

PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**



http://www.aphis.usda.gov/animal_health/animal_diseases/scrapie/downloads/monthly_scrapie_rpt.pps



NOT to forget the 5 cases of the NOR-98 atypical scrapie documented in the USA in 2007, in five different states. WHICH pathologically looks like some sub-types of sporadic CJD, of which Stanely Prusiner warns of a public health risk ;

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.



http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf



Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)



http://www.pnas.org/cgi/content/abstract/0502296102v1



Tuesday, June 3, 2008

SCRAPIE USA UPDATE JUNE 2008 NOR-98 REPORTED PA



http://nor-98.blogspot.com/2008/06/scrapie-usa-update-june-2008-nor-98.html



NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 2007



http://nor-98.blogspot.com/2008/04/seac-spongiform-encephalopathy-advisory.html



http://nor-98.blogspot.com/



Nonambulatory Cattle as a Potential Source of TSE

In this study, Wisconsin was the only State in which mink producers were reported to receive nonambulatory cows directly from dairies. However, given the small number of surveyed herds this finding is likely a result of the sampling design. Because mink producers pay a premium for nonambulatory cows, it appears reasonable that the practice of feeding nonambulatory cows to mink could occur wherever both large numbers of dairy cows and mink are found. As many as 2,157(3) nonambulatory cows per million milk cows, or a total of 9,482 nonambulatory cows, could have been fed to mink in the 7 surveyed States in 1992. Based on the sample response, only half of those cows would have had an identifiable reason for being nonambulatory. This equates to an estimated 4,741 nonambulatory cows that were, hypothetically, a potential source of TSE in the surveyed States.

(3)This estimate does not account for any nonambulatory cows received from slaughter plants.

Page 23

The five reported outbreaks of TME in the U.S. reveal no discernable trend. Assuming an average of 2,000 mink farms in the U.S. during the last 50 years, one outbreak of TME has occurred per 20,000 mink farm-years. Extrapolating from the data gathered in this study, 66,374 nonambulatory cows have been fed to mink in the 7 surveyed States since the last reported outbreak of TME in 1985. Of those, 33,187 would have had no identifiable reason for being nonambulatory and were hypothetically a potential source of TSE. Given the severity of signs and number of mink affected by TME it is unlikely that outbreaks have gone unreported. If any form Of a TSE (infectious, spontaneous, or other) occurs in U.S. cattle that is transmissible to mink in the form of TME, then it must be exceedingly rare or the conditions for its transmission must be highly specific and unusual. Nonetheless, studies are underway at the State and Federal levels to further characterize the disposition of nonambulatory cows and usage on mink farms.

snip...

An estimated 4,741 nonambulatory cows hypothetically considered to be potential sources of TSE may have been fed to mink in the 7 surveyed States in 1992. This equates to 33,187 such cows fed to mink since the last reported outbreak of TME in mink. Given this large number of nonambulatory cows fed to mink, the historic and current mink population, and the infrequent occurrence of TME, if TSE exists in cattle in the U.S. it must be very rare or transmissible to mink only under very unusual conditions.



http://downercattle.blogspot.com/2008/08/quantitative-assessment-of-possible.html



To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle

R.F. Marsh* and G.R. Hartsough

•Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092

ABSTRACT

Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England.

snip...

OBSERVATIONS AND RESULTS

A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were “acting funny”, and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death.

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. ***The rancher was a “dead stock” feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.***

snip...end



http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf



Epidemiology Epidemiologic studies suggest that animals contract the disease by external exposure to the infectious agent, such as by eating contaminated feed. No evidence suggests that the TME agent spreads by contact between unrelated mink or from mother to nursing young. The disease has been identified in both genders and all color phases in animals greater than 1 year old. The first documented TME outbreak in the United States occurred in 1947 on one ranch in Wisconsin and then on a ranch in Minnesota that had received mink from the Wisconsin ranch. In 1961, TME outbreaks occurred on five ranches in Wisconsin. In Factsheet Veterinary Services February 2002 APHIS 1963, outbreaks occurred in Idaho, Minnesota, and Wisconsin. Epidemiologic data from the Minnesota and Wisconsin outbreaks trace the cases in those States to one common purchased food source.

snip...

The 1985 Stetsonville Outbreak The most recent TME outbreak occurred on one mink ranch in Stetsonville, WI, in 1985. In the herd of 7,300 adult mink, 60 percent of the animals died. Clinical signs included tail arching, incoordination, and hyperexcitability. At the most advanced stages of the disease, the animals were in trancelike states and eventually died. The outbreak lasted 5 months. Microscopic examination of sections of the brain confirmed the spongelike changes characteristic of TME. Diagnostic tests identified the prion protein. The following year, mink born during the outbreak showed no signs of TME. The late Richard Marsh, a veterinary virologist at the University of Wisconsin who studied the transmission of TME and other TSE’s, investigated this outbreak. Marsh learned that the mink were fed a diet composed of fresh meat products from “downer cattle” and commercial sources of fish, poultry, and cereal. Downer cattle are nonambulatory and cannot rise because they are affected with a condition such as a metabolic disease, broken limbs, or a central nervous system disorder. Marsh theorized that the meat from these downer cattle introduced a TSE agent to the mink in which TME resulted. Although Marsh’s hypothesis is based on speculation and anecdotal evidence, in 1993 APHIS adjusted its national BSE surveillance program to include testing downer cattle for evidence of a TSE. The brains of more than 20,141 cattle have been examined at APHIS’ National Veterinary Services Laboratories and other State diagnostic laboratories. Not a single tissue sample has revealed evidence of BSE or another TSE in cattle.



http://www.aphis.usda.gov/publications/animal_health/content/printable_version/fs_ahtme.pdf



AND as everyone knows, the rest is history, those dead-stock downers, the most high risk cattle, were NOT tested, and in FACT, was a major source of YOUR CHILDRENS SCHOOL LUNCH PROGRAM, all across the Nation. sorry, these are the most high risk cattle for TSE aka mad cow disease, and i am a bit touchy about this topic. ...sorry. ...terry

DOWNER COW SCHOOL LUNCH PROGRAM



http://downercattle.blogspot.com/



IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?

In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.

We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.

snip...

PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986



http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf



http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf



NOW, back to those mad mink i.e. TME. let me throw a curve ball here ;

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* and Richard A. Bessen† Emerging Infectious

Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine- passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, Htype BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profi les, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME. The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE. Transmissible mink encephalopathy (TME) is a rare prion disease in ranch-raised mink (Mustela vison) in North America and Europe (1–4). Six outbreaks have been reported from 1947 through 1985 in North America, and several have been linked to contaminated commercial feed (1). Although contamination of feed with scrapie-infected sheep parts has been proposed as the cause of TME, the origin of the disease remains elusive. The idea that scrapie in sheep may be a source of TME infection is supported by fi ndings that scrapie-infected mink have a similar distribution of vacuolar pathologic features in the brain and the same clinical signs as mink with natural and experimental TME (5). However, mink are not susceptible to scrapie infection following oral exposure for up to 4 years postinoculation, which suggests that either the scrapie agent may not be the source of natural TME infection or that only specifi c strains of the scrapie agent are able to induce TME (6,7). Epidemiologic investigations in the Stetsonville, Wisconsin, outbreak of TME in 1985 suggested a possible cattle origin, since mink were primarily fed downer or dead dairy cattle but not sheep products (8). Experimental transmission of Stetsonville TME into cattle resulted in transmissible spongiform encephalopathy (TSE) disease with an incubation period of 18.5 months. Back passage of bovine TME into mink resulted in incubation periods of 4 and 7 months after oral or intracerebral inoculation, respectively, which was similar to that found following inoculation of Stetsonville TME into mink by these same routes (8). These fi ndings indicated that cattle are susceptible to TME, and that bovine-passaged TME did not result in a reduced pathogenicity for mink. These studies raised the question as to whether an unknown TSE in cattle was the source of TME infection in the Stetsonville outbreak. Several additional TME outbreaks in the United States have been associated with mink diet that contained downer or dead cattle (9). ...

snip...full text ;



http://www.cdc.gov/EID/content/13/12/pdfs/1887.pdf



http://transmissible-mink-encephalopathy.blogspot.com/



3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle,

*** did not produce the same clinical signs of brain lesions characteristic of BSE.***



http://www.bseinquiry.gov.uk/pdf/volume2/chapter3.pdf



"the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine." <<< href="mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:http://www.vetres.org/">www.vetres.org DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article

snip...

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

snip...

Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) [23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland [56]. It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

full text 18 pages ;



http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf



please see full text ;



http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html



***Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.***

Progress Report from the National Prion Disease Pathology Surveillance Center

An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD

April 3, 2008



http://www.aan.com/news/?event=read&article_id=4397&page=72.45.45



Sunday, March 16, 2008

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE



http://bse-atypical.blogspot.com/2008/03/mad-cow-disease-terminology-uk-c-bse.html



HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008

snip...

Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

snip...



http://cjdmadcowbaseoct2007.blogspot.com/2008/06/human-and-animal-tse-classifications-ie.html



Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate



http://organicconsumers.org/forum/index.php?showtopic=1951



http://bse-atypical.blogspot.com/2008/08/atypical-bse-base-transmitted-from.html




Sunday, August 10, 2008

A New Prionopathy OR more of the same old BSe and sporadic CJD



http://creutzfeldt-jakob-disease.blogspot.com/2008/08/new-prionopathy-or-more-of-same-old-bse.html



PLEASE NOTE THE PARTIAL AND VOLUNTARY MAD COW FEED BAN OF AUGUST 4, 1997 nothing more than ink on paper ... TSS

Wednesday, April 23, 2008

FDA Strengthens Safeguards for Consumers of Beef Issues Regulation on Animal Feeds with Added Safeguards Against BSE



http://madcowfeed.blogspot.com/



CWD, is but a small piece, of a very big puzzle. and one of the main reasons this puzzle has not been solved, is the secrecy, cover-ups, and such. you must not ignore these facts. i did not want to believe this either. for years i was naive, but the facts speak for themselves.

it goes way back ;

Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?

August 20, 2008



http://bse-atypical.blogspot.com/2008/08/bovine-spongiform-encephalopathy-mad.html



Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0006 Public Submission Title Comment from Terry S Singletary Sr Views Add Comments How To Comment

snip...

MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???

go figure....

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



http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&d=APHIS-2006-0041-0006



From: Terry S. Singeltary Sr.



To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:FREAS@CBER.FDA.GOV

Cc: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:william.freas@fda.hhs.gov ; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000050/!x-usc:mailto:rosanna.harvey@fda.hhs.gov

Sent: Friday, December 01, 2006 2:59 PM

Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION

snip...

ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.

These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...

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

snip... 48 pages...



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8



Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy; Animal Identification and Importation of Commodities Docket Type Rulemaking Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions, Identification of Ruminants and Processing and Importation of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title Comment from Terry S Singletary



http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=09000064801e47e1



Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Docket Type Rulemaking Document APHIS-2007-0033-0001 Document Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Public Submission APHIS-2007-0033-0002.1 Public Submission Title Attachment to Singeltary comment



http://www.regulations.gov/fdmspublic/component/main?main=DocumentDetail&o=090000648027c28e



Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.



http://www.regulations.gov/fdmspublic/ContentViewer?objectId=090000648027c28e&disposition=attachment&contentType=pdf



i hope i have not bored anyone with all this, but you must know the history, and why we are where we are today. and where we are going in the future, in terms of Transmissible Spongiform Encephalopathy, as a whole, the bigger picture, TSEs in all species, and the ramifications thereof. NOT the infamous, bogus, UKBSEnvCJD only theory. ...

to be continued. ...

kindest regards, terry

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