Research Project: Detection of Transmissible Spongiform Encephalopathy Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: Foodborne Contaminants Research
2008 Annual Report
1a.Objectives (from AD-416) We will develop highly sensitive diagnostic tests to detect transmissible spongiform encephalopathy (TSE) in livestock and wildlife animal species prior to the onset of clinical disease. We will also develop tests to confirm the presence or absence of TSE disease agents in ingredients of animal origin and decontaminated environments.
1b.Approach (from AD-416) The threat of BSE continues to affect export economics for US meat. Meanwhile scrapie continues to influence sheep profits and herd biosecurity, and CWD is spreading throughout North America. Thus U.S. animal industry stakeholders have identified detection of the TSE infectious agent (prions) as a priority biosecurity research issue essential for prevention of TSE diseases. We will build on our previous successes using mass spectrometry (MS) for high-sensitivity and specificity in detection of PrPsc as a marker for TSE infectivity in blood using a hamster scrapie model. We will also develop a novel PrP-null mouse strain and related myeloma cell culture system for production of monoclonal antibodies (MAb), which may be specific for PrPsc. We will then choose MS or MAb and validate our novel diagnostic for preclinical diagnosis of scrapie in sheep blood. Whereas MS and MAb methods rely on dissolved samples, contamination of agricultural products and environmental surfaces is associated with solid samples. So we will produce a cell culture based assay for TSE infectivity that is surface-adsorbed. After using the relatively convenient hamster model for early development, we will validate this technology for detection of scrapie in sheep brain on meat-and-bone meal and stainless steel. Replacing 5325-32000-007-00D (3/19/2008).
3.Progress Report At this point in the Project, in general, we are completing preliminary studies using our relatively convenient hamster and mouse models, and are starting to work with more agriculturally relevant sheep and deer tissues. We are finding the cervid tissues quite different from rodent tissues, in their requirements for sample workup (e.g., amount and quality of lipid and fiber) and in their expression of TSE infectivity and presence of markers. OSQR required us to establish a new collaboration with a reputable cell biologist, to assist with our cell-based scrapie assay. We now have a new MTA with Dr. Charles Weissmann (Scripps), under which we are sharing cell lines and laboratory protocols. We have completed one part of our speed congenics project to develop PrP-null (disease-resistant) mice for use in antibody generation. After conceiving a new procedure for immunogen enrichment, we performed experimental vaccination of these animals in our facilities. This project relates to NP103 Component 8: Prevention and control of transmissible spongiform encephalopathies. Problem statement 9A: Scrapie; 9B Chronic Wasting Disease (CWD); and 9C: Bovine Spongiform Encephalopathy (BSE).
4.Accomplishments 1. Proteinase K-free method for preparation of samples facilitates TSE blood assay.
The most widely used and regulatory approved methods for detection of Transmissible Spongiform Encephalopathy (TSE) contain a step in which the sample is subjected to digestion by a very strong enzyme, proteinase K, which degrades almost all proteins in the sample except for an Infectious isoform of the normal cellular prion protein, a prion (PrPsc). Although PrPsc has served well as a marker for brain disease, infectivity in the blood is mostly not proteinase K resistant. The proteinase K-free technique developed by ARS scientists in the Foodborne Contaminants Research Unit in Albany, CA will allow scientists to detect infectivity in blood. These efforts will lead to diagnostic tests that will save farmers and ranchers money and resources by allowing them to identify infected animals prior to purchase, sale or slaughter, and keep TSE-infected animals out of the US food supply. This accomplishment addresses NP103 Component 8: Prevention and Control of Transmissible Spongiform Encephalopathies; Problem Statement 9A: Scrapie; 9B: Chronic Wasting Disease (CWD); and 9C: Bovine Spongiform Encephalopathy (BSE).
2. Demonstrated conversion of a non-infectious normal cellular prion protein (PrP) into disease isoform in cell culture.
Although Transmissible Spongiform Encephalopathy (TSE) infectivity can be detected using animal models and mass spectroscopy, a cell culture system offers increased speed and throughput. ARS scientists in the Foodborne Contaminants Research Unit in Albany, CA developed conditions for growth and infection of existing cell cultures and cultures expressing transgenic PrP genes, observing conversion to the disease-associated PrPsc isoform. This method will be further developed to detect infectivity that is adsorbed onto surfaces, such as stainless steel and soil. These efforts will lead to diagnostic tests that will save farmers and ranchers money and resources by allowing them to identify infected areas and equipment before these areas or items can infect their animals. This accomplishment addresses NP103 Component 8: Prevention and Control of Transmissible Spongiform Encephalopathies; Problem Statement 9A: Scrapie; 9B: Chronic Wasting Disease (CWD); and 9C: Bovine Spongiform Encephalopathy (BSE).
5.Significant Activities that Support Special Target Populations None.
6.Technology Transfer Number of New Commercial Licenses Executed 1
Review Publications Bruederle, C.E., Hnasko, R.M., Kraemer, T., Garcia, R.A., Haas, M.J., Marmer, W.N., Carter, J.M. 2008. Prion infected Meat-and-Bone Meal is still infectious after biodiesel production. PLoS Pathogens. Available:
http://dx.plos.org/10.1371/journal.pone.0002969Onisko, B.C., Chen, N., Napoli, J. 2008. The Nuclear Transcription Factor RAR Associates with Neuronal RNA Granules and Suppresses Translation. Journal of Biological Chemistry. 283(30):20841-20847.
Sajnani, G., Pastrana, M.A., Dynin, I.A., Onisko, B.C., Requena, J.R. 2008. Insights on scrapie prion protein (prpsc) structure obtained by limited proteolysis and mass spectrometry. Journal of Molecular Biology. 382(2008):88-98.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=413072&showpars=true&fy=2008FY2006: Tests for prion contamination in soil and water will be developed.
http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=405202&showpars=true&fy=2003???
Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years Bjoern Seidel1#*, Achim Thomzig2#, Anne Buschmann3#, Martin H. Groschup3, Rainer Peters1, Michael Beekes2, Konstantin Terytze4
1 Fraunhofer Institute for Molecular Biology und Applied Ecology (IME), Schmallenberg, Germany, 2 P24 -Transmissible Spongiform Encephalopathies, Robert Koch-Institut, Berlin, Germany, 3 Institute for Novel and Emerging Infectious Diseases, Friedrich-Loeffler-Institut, Insel Riems, Germany, 4 German Federal Environmental Agency (Umweltbundesamt, UBA), Dessau, Germany
Abstract The persistence of infectious biomolecules in soil constitutes a substantial challenge. This holds particularly true with respect to prions, the causative agents of transmissible spongiform encephalopathies (TSEs) such as scrapie, bovine spongiform encephalopathy (BSE), or chronic wasting disease (CWD). Various studies have indicated that prions are able to persist in soil for years without losing their pathogenic activity. Dissemination of prions into the environment can occur from several sources, e.g., infectious placenta or amniotic fluid of sheep. Furthermore, environmental contamination by saliva, excrements or non-sterilized agricultural organic fertilizer is conceivable. Natural transmission of scrapie in the field seems to occur via the alimentary tract in the majority of cases, and scrapie-free sheep flocks can become infected on pastures where outbreaks of scrapie had been observed before. These findings point to a sustained contagion in the environment, and notably the soil. By using outdoor lysimeters, we simulated a contamination of standard soil with hamster-adapted 263K scrapie prions, and analyzed the presence and biological activity of the soil-associated PrPSc and infectivity by Western blotting and hamster bioassay, respectively. Our results showed that 263K scrapie agent can persist in soil at least over 29 months. Strikingly, not only the contaminated soil itself retained high levels of infectivity, as evidenced by oral administration to Syrian hamsters, but also feeding of aqueous soil extracts was able to induce disease in the reporter animals. We could also demonstrate that PrPSc in soil, extracted after 21 months, provides a catalytically active seed in the protein misfolding cyclic amplification (PMCA) reaction. PMCA opens therefore a perspective for considerably improving the detectability of prions in soil samples from the field.
http://www.plosone.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0000435&representation=PDFPrions Adhere to Soil Minerals and Remain Infectious Christopher J. Johnson1,2, Kristen E. Phillips3, Peter T. Schramm3, Debbie McKenzie2, Judd M. Aiken1,2, Joel A. Pedersen3,4*
1 Program in Cellular and Molecular Biology, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 2 Department of Animal Health and Biomedical Sciences, School of Veterinary Medicine, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 3 Molecular and Environmental Toxicology Center, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 4 Department of Soil Science, University of Wisconsin Madison, Madison, Wisconsin, United States of America
Abstract An unidentified environmental reservoir of infectivity contributes to the natural transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) in sheep, deer, and elk. Prion infectivity may enter soil environments via shedding from diseased animals and decomposition of infected carcasses. Burial of TSE-infected cattle, sheep, and deer as a means of disposal has resulted in unintentional introduction of prions into subsurface environments. We examined the potential for soil to serve as a TSE reservoir by studying the interaction of the disease-associated prion protein (PrPSc) with common soil minerals. In this study, we demonstrated substantial PrPSc adsorption to two clay minerals, quartz, and four whole soil samples. We quantified the PrPSc-binding capacities of each mineral. Furthermore, we observed that PrPSc desorbed from montmorillonite clay was cleaved at an N-terminal site and the interaction between PrPSc and Mte was strong, making desorption of the protein difficult. Despite cleavage and avid binding, PrPSc bound to Mte remained infectious. Results from our study suggest that PrPSc released into soil environments may be preserved in a bioavailable form, perpetuating prion disease epizootics and exposing other species to the infectious agent.
Synopsis Transmissible spongiform encephalopathies (TSEs) are a group of incurable diseases likely caused by a misfolded form of the prion protein (PrPSc). TSEs include scrapie in sheep, bovine spongiform encephalopathy (“mad cow” disease) in cattle, chronic wasting disease (CWD) in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and CWD are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity, because PrPSc likely enters soil environments through urinary or alimentary shedding and decomposition of infected animals. In this manuscript, the authors test the potential for soil to serve as a reservoir for PrPSc and TSE infectivity. They demonstrate that PrPSc binds to a variety of soil minerals and to whole soils. They also quantitate the levels of protein binding to three common soil minerals and show that the interaction of PrPSc with montmorillonite, a common clay mineral, is remarkably strong. PrPSc bound to Mte remained infectious to laboratory animals, suggesting that soil can serve as a reservoir of TSE infectivity.
http://www.plospathogens.org/article/info:doi%2F10.1371%2Fjournal.ppat.0020032Direct Detection of Soil-Bound Prions Sacha Genovesi1, Liviana Leita2, Paolo Sequi3, Igino Andrighetto4, M. Catia Sorgato1,5, Alessandro Bertoli1*
1 Dipartimento di Chimica Biologica, Università di Padova, Padova, Italy, 2 Istituto Sperimentale per la Nutrizione delle Piante, Gorizia, Italy, 3 Istituto Sperimentale per la Nutrizione delle Piante, Roma, Italy, 4 Istituto Zooprofilattico Sperimentale delle Venezie, Legnaro, Italy, 5 CNR Istituto di Neuroscienze, Padova, Italy
Abstract Scrapie and chronic wasting disease are contagious prion diseases affecting sheep and cervids, respectively. Studies have indicated that horizontal transmission is important in sustaining these epidemics, and that environmental contamination plays an important role in this. In the perspective of detecting prions in soil samples from the field by more direct methods than animal-based bioassays, we have developed a novel immuno-based approach that visualises in situ the major component (PrPSc) of prions sorbed onto agricultural soil particles. Importantly, the protocol needs no extraction of the protein from soil. Using a cell-based assay of infectivity, we also report that samples of agricultural soil, or quartz sand, acquire prion infectivity after exposure to whole brain homogenates from prion-infected mice. Our data provide further support to the notion that prion-exposed soils retain infectivity, as recently determined in Syrian hamsters intracerebrally or orally challanged with contaminated soils. The cell approach of the potential infectivity of contaminated soil is faster and cheaper than classical animal-based bioassays. Although it suffers from limitations, e.g. it can currently test only a few mouse prion strains, the cell model can nevertheless be applied in its present form to understand how soil composition influences infectivity, and to test prion-inactivating procedures.
http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0001069now, something i have pondered long about, with the atypical BSE in Texas and Alabama, where, as far as i know, those farms WERE NOT quarantined for 5 years due to an atypical TSE. HOWEVER, the farms of the atypical scrapie from where the mad sheep of mad river valley occurred, these farms were quarantined. ...
----- Original Message -----
From: Terry S. Singeltary Sr.
To:
mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000169/!x-usc:mailto:Boyd.Rutherford@usda.govSent: Sunday, February 25, 2007 12:35 PM
Subject: FOIA REQUEST FOR ATYPICAL TSE INFORMATION ON VERMONT SHEEP
Greetings USDA,
I respectfully request the final results of the mouse bio-assays test that were to have supposedly began 2+ years late, 5 years ago, on the imported sheep from Belgium ?
WHAT happened to the test results and MOUSE BIO-ASSAYS of those imported sheep from Belgium that were confiscated and slaughtered from the Faillace's, what sort of TSE did these animals have ?
WERE they atypical scrapie, BSE, and or typical scrapie ?
HOW much longer will you refuse to give us this information ? and for what reason ?
WHY is it that the Farm of the Mad Sheep of Mad River Valley were quarantined for 5 years, but none of these farms from Texas and Alabama with Atypical TSE in the Bovine, they have not been quarantined for 5 years,why not, with the real risk of BSE to sheep, whom is to say this was not BSE ?
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full text ;
http://foiamadsheepmadrivervalley.blogspot.com/2008/04/re-foia-of-declaration-of-extraordinary.htmlMonday, September 1, 2008 RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES [No. 00-072-1] September 1, 2008
Greetings again BSE-L members,
I had a pleasant surprise this past Saturday. I got an unexpected package from O.I.G. on my old F.O.I.A. request, of the final test results of the infamous mad sheep of mad river valley. IF you all remember, back on Thu, 24 Apr 2008 15:00:20 -0500 I wrote ;
snip...full text ;
http://foiamadsheepmadrivervalley.blogspot.com/2008/09/re-foia-of-declaration-of-extraordinary.htmlhttp://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=12;t=000469http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=print_topic;f=12;t=000469i remember a few years back ???
that a study showed the prion uptake in a tomato plant, not that this would surprise me ;
56. Members considered that there is no evidence that crops grown on the land which received composted excreta from BSE-challenged animals pose a TSE risk to humans or animals. One member suggested that, as some of these animals are orally challenged with high doses of BSE-infected materials, and the distribution of infectivity in the digestive system is not completely understood, it might be premature to conclude that there is no infective agent in the manure. Furthermore, an unpublished study had indicated low level absorption of PrP from soil by tomato plants although it should be noted that this study had not been repeated. Details of this work would be sent to the SEAC Secretary. Dr Matthews explained that most of the manure from animals challenged with high doses of BSE had already been composted and used for coppicing. Members agreed that the risks from disposal of residual manure from experimental animals would be much less than historic risks of on farm contamination from naturally infected animals at the height of the BSE epidemic.
http://www.seac.gov.uk/minutes/final91.pdfdisturbing to say the least. ...TSS
Tuesday, January 13, 2009
Antemortem detection of PrPCWD in preclinical, ranch-raised Rocky Mountain elk (Cervus elaphus nelsoni) by biopsy of the rectal mucosa Full Scientific Reports
http://chronic-wasting-disease.blogspot.com/2009/01/antemortem-detection-of-prpcwd-in.htmlSaturday, January 10, 2009
Chronic Wasting Disease Investigation Update Michigan December 18, 2008
http://chronic-wasting-disease.blogspot.com/2009/01/chronic-wasting-disease-investigation.htmlSunday, September 07, 2008
CWD LIVE TEST, and the political aspects or fallout of live testing for BSE in cattle in the USA
http://chronic-wasting-disease.blogspot.com/2008/09/cwd-live-test-and-political-aspects-or.html2008 CWD Laboratory Testing for Wild White-tailed Deer
http://www.michigan.gov/emergingdiseases/0,1607,7-186-25806-202922--,00.htmlWednesday, January 07, 2009
CWD to tighten taxidermy rules Hunters need to understand regulations
http://chronic-wasting-disease.blogspot.com/2009/01/cwd-to-tighten-taxidermy-rules-hunters.htmlMonday, January 05, 2009
CWD, GAME FARMS, BAITING, AND POLITICS
http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.htmlThursday, December 25, 2008 Lions and Prions and Deer Demise
http://chronic-wasting-disease.blogspot.com/2008/12/lions-and-prions-and-deer-demise.htmlTuesday, January 06, 2009
CWD Update 93 December 29, 2008
http://chronic-wasting-disease.blogspot.com/2009/01/cwd-update-93-december-29-2008.htmlTuesday, September 09, 2008 CWD MICHIGAN UPDATE September 5, 2008
http://chronic-wasting-disease.blogspot.com/2008/09/cwd-michigan-update-september-5-2008.htmlMonday, August 25, 2008 CWD FIRST DOCUMENTED IN MICHIGAN
http://chronic-wasting-disease.blogspot.com/2008/08/cwd-first-documented-in-michigan.htmlWhen Atypical Scrapie cross species barriers
Authors
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.
Content
Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.
The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.
http://www.neuroprion.org/resources/pdf_docs/conferences/prion2008/abstract-book-prion2008.pdfSCRAPIE USA
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)
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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.ppshttp://scrapie-usa.blogspot.com/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.
***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.pdfHere 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/0502296102v1NOR-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.htmlTuesday, 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.htmlhttp://nor-98.blogspot.com/Monday, December 1, 2008 When Atypical Scrapie cross species barriers
http://nor-98.blogspot.com/2008/12/when-atypical-scrapie-cross-species.htmlTo 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.
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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.***
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http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdfEpidemiology 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.
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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.pdfAND 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.
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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.pdfhttp://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdfNOW, 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). ...
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http://www.cdc.gov/EID/content/13/12/pdfs/1887.pdfhttp://transmissible-mink-encephalopathy.blogspot.com/SPORADIC CJD IN FARMERS, FARMERS WIVES,
http://bseinquiry.blogspot.com/2008/05/sporadic-cjd-in-farmers-farmers-wives.htmlMAD COW DISEASE BSE CJD CHILDREN VACCINES BSE, Children, CJD, Mad Cow Disease, VACCINES
http://bseinquiry.blogspot.com/2008/05/mad-cow-disease-bse-cjd-children.htmlBSE, CJD, and Baby foods (the great debate 1999 to 2005 )
http://bseinquiry.blogspot.com/2008/05/bse-cjd-and-baby-foods-great-debate.htmlBSE Inquiry DRAFT FACTUAL ACCOUNT DFA
http://bseinquiry.blogspot.com/2008/05/bse-inquiry-draft-factual-account-dfa.htmlTHE USDA CERTIFIED MAD COW DEBACLE, BLUNDER, AND COVER-UP
Thursday, October 18, 2007
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA, A REVIEW OF SORTS
http://madcowtesting.blogspot.com/2007/10/bse-base-mad-cow-testing-texas-usa-and.htmlBSE BASE MAD COW TESTING TEXAS, USA, AND CANADA
http://madcowtesting.blogspot.com/Sunday, December 28, 2008
MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy
http://bse-atypical.blogspot.com/2008/12/mad-cow-disease-usa-december-28-2008-8.htmlUSDA CERTIFIED DEADSTOCK DOWNER COW SCHOOL LUNCH PROGRAM
http://downercattle.blogspot.com/2008/12/evaluation-of-fsis-management-controls.htmlhttp://downercattle.blogspot.com/TSS
Labels: atypical bse, ATYPICAL SCRAPIE, bse, CWD, SCRAPIE
