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Soil clay content underlies prion infection odds

Posted Feb 25 2011 10:05pm
Soil clay content underlies prion infection odds



W. David Walter 1 , * , Daniel P. Walsh 2 , * , Matthew L. Farnsworth 3 , Dana L. Winkelman 1 & Michael W. Miller 2

1 United States Department of the Interior, United States Geological Survey, Colorado Cooperative Fish and Wildlife Research Unit , Fort Collins , Colorado

80523-1484, USA. 2 Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, Colorado 80526-2097, USA. 3 United States Department

of Agriculture, Animal and Plant Health Inspection Services, Veterinary Services, Centers for Epidemiology and Animal Health , Fort Collins , Colorado

80526-8117 , USA . * These authors contributed equally to this work. Correspondence and requests for materials should be addressed to M.W.M.

(email: mike.miller@state.co.us ) .

Received 6 Sep 2010 | Accepted 19 Jan 2011 | Published 15 Feb 2011 DOI: 10.1038/ncomms1203



Environmental factors — especially soil properties — have been suggested as potentially important in the transmission of infectious prion diseases. Because binding to montmorillonite (an aluminosilicate clay mineral) or clay-enriched soils had been shown to enhance experimental prion transmissibility, we hypothesized that prion transmission among mule deer might also be enhanced in ranges with relatively high soil clay content. In this study, we report apparent influences of soil clay content on the odds of prion infection in free-ranging deer. Analysis of data from prion-infected deer herds in northern Colorado, USA, revealed that a 1 % increase in the clay-sized particle content in soils within the approximate home range of an individual deer increased its odds of infection by up to 8.9 % . Our findings suggest that soil clay content and related environmental properties deserve greater attention in assessing risks of prion disease outbreaks and prospects for their control in both natural and production settings.



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The capacity of clay minerals and clay-laden soils to capture and enhance infectivity of shed or deposited prions 19,20,25 – 27 and the common tendency of ruminants to ingest soil both deliberately and incidentally in the course of foraging and grooming 12,44,45 provide an elegantly simple hypothetical mechanism for indirect prion transmission, as follows: infected individuals propagate infectious prions in mucosa-associated lymphoid tissues and shed prions into ingesta and saliva; ingested and environmental soil microparticles with a high phyllosilicate (especially smectite) content bind to, sequester and enhance infectivity of prions both before and after leaving the host; microparticle-bound prions are incorporated into surface soil; susceptible individuals consume contaminated soil and some become infected. (Also see Supplementary Figure S1 .) This mechanism may underlie the apparent importance of indirect transmission in explaining observed patterns of prion infection among captive mule deer 10,11 , and perhaps among sheep 3,4,6,7 . In light of these and others ’ findings, soil clay content and related environmental properties deserve greater attention in assessing local and regional risks of prion disease outbreaks and prospects for their control in natural and production settings.


http://www.nature.com/ncomms/journal/v2/n2/pdf/ncomms1203.pdf



PRION 2010

International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria

PRION 2010 is the top Global Annual TSE Conference in prion research, following a sequence of PRION meetings that were originally organized by the EU Network of Excellence NeuroPrion. In this proud tradition, PRION 2010 covers all aspects of this fascinating scientific area. PRION 2010 is a meeting of greatest interest for neuroscientists, protein structural biologists, geneticists, medical specialists including neurologists, neuropathologists, hygiene experts and blood product providers, veterinarians, epidemiologists, laboratory technicians, industry developers, risk assessors and managers. An outstanding list of Plenary Lecture, Symposia and Workshop Speakers is complemented by the plethora of original input from Poster Presentations. Special consideration is given this year to two areas of major interest: the renewed discussion about the zoonotic potential of animal prion diseases, given the emergence of atypical BSE and scrapie strains, and the breakthrough work on synthetic prions by several groups simultaneously.



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PPo4-4
Survival and Limited Spread of TSE Infectivity after Burial

Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK

Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.

The authors gratefully acknowledge funding from DEFRA.



PPo8-14


Enzymatic Digestion of Chronic Wasting Disease Prions Bound to Soil

Samuel E. Saunders,1 Jason C. Bartz,2 Kurt C. Vercauteren3 and Shannon L. Bartelt-Hunt1 1Department of Civil Engineering; University of Nebraska-Lincoln; Peter Kiewit Institute; Omaha, Nebraska USA; 2Department of Medical Microbiology and Immunology; Creighton University; Omaha, Nebraska USA; 3USDA; Animal and Plant Health Inspection Service; Wildlife Services; National Wildlife Research Center; Fort Collins, CO USA

Chronic wasting disease (CWD) and sheep scrapie can be transmitted via indirect environmental routes, and it is known that soil can serve as a reservoir of prion infectivity. Given the strong interaction between the prion protein (PrP) and soil, we hypothesized that binding to soil enhances prion resistance to enzymatic digestion, thereby facilitating prion longevity in the environment and providing protection from host degradation. We characterized the performance of a commercially available subtilisin enzyme, the Prionzyme, to degrade soil-bound and unbound CWD and HY TME PrP as a function of pH, temperature, and treatment time. The subtilisin enzyme effectively degraded PrP adsorbed to a wide range of soils and soil minerals below the limits of detection. Signal loss occurred rapidly at high pH (12.5) and within 7 d under conditions representative of the natural environment (pH 7.4, 22°C). Serial PMCA of treated soil samples suggests a greater than 6-log decrease in infectious titer compared with controls. We observed no apparent difference in enzyme effectiveness between bound and unbound CWD PrP. Our results show that although adsorbed prions do retain relative resistance to enzymatic digestion compared with other brain homogenate proteins, they can be effectively degraded when bound to soil. Our results also suggest a topical application of a subtilisin enzyme solution may be an effective decontamination method to limit disease transmission via environmental ‘hot spots’ of prion infectivity.


PPo8-13


Degradation of Pathogenic Prion Protein and Prion Infectivity by Lichens

Christopher J. Johnson,1 James P. Bennett,1 Steven M. Biro,1,2 Cynthia M. Rodriguez,1,2 Richard A. Bessen3 and Tonie E. Rocke1

1USGS National Wildlife Health Center; 2Department of Bacteriology; University of Wisconsin, Madison; 3Department of Veterinary Molecular Biology; Montana State University; Bozeman, MT USA

Key words: prion, lichen, bioassay, protease, degradation

Few biological systems have been identified that degrade the transmissible spongiform encephalopathy (TSE)-associated form of the prion protein (PrPTSE) and TSE infectivity. Stability of the TSE agent allows scrapie and chronic wasting disease agents to persist in the environment and cause disease for years. Naturally-occurring or engineered processes that reduce infectivity in the environment could aid in limiting environmental TSE transmission. We have previously identified that species of at least three lichens, unusual, symbiotic organisms formed from a fungus and photosynthetic partner, contain a serine protease capable of degrading PrPTSE under gentle conditions. We tested the hypothesis that lichen extracts from these three species reduce TSE infectivity by treating infected brain homogenate with extracts and examining infectivity in mice. We found lichen extracts diminished TSE infectious titer by factors of 100 to 1,000 and that reductions in infectivity were not well-correlated with the extent of PrPTSE degradation observed by immunoblotting. For example, treatment of brain homogenate with Cladonia rangiferina extract caused <100-fold reduction in PrP immunoreactivity but ~1,000-fold decrease in infectivity, suggesting that some PrPTSE remaining after extract treatment was rendered uninfectious or that the lichen protease favors more infectious forms of PrPTSE. Our data also indicate that lichen species closely related to those with prion-degrading protease activity do not necessarily degrade PrPTSE. Characterization of the lichen species-specificity of PrPTSE degradation within the genera Cladonia and Usnea and comparison with known lichen phylogeny has yielded clusters of species on which to focus searches for anti-prion agents.



PPo8-20

The Anti-prion Activity of Soil Organic Compounds Humic and Fulvic Acids

Joanna Narkiewicz,1,2 Ai H.N. Tran,1 Gabriele Giachin,1 Liviana Leita2 and Giuseppe Legname1, 1Neurobiology Sector; Scuola Internazionale Superiore di Studi Avanzati; International School for Advanced Studies; Bonomea, Trieste Italy; 2Agricultural Research Council (CRA); Research Centre for Soil-Plant System; Trieste, Gorizia Italy

A notable feature of prion diseases, as scrapie in sheep and chronic wasting disease in mule deer and elk, is horizontal transmission between grazing animals, suggesting that contaminated environment may contribute significantly to disease transmission. Increasing evidence suggests that soil may present natural reservoir of prion infectivity. Recent studies have shown that prions may persist in contaminated soil and remain infectious for years. As the mechanism of prion retention and persistence in soil is unknown, it is necessary to understand which soil components may interact with prions and thus contribute to disease transmission. Several reports indicate that prion have potential to interact with soil minerals, however the contribution of soil organic fraction in adsorption to prions has been neglected. Here, we present strong evidence for soil humic substances (HS) interaction with prions. We show that two HS, classified as humic and fulvic acids, interact with recombinant prion proteins in vitro. Moreover, we show that both HS possess anti-prion activity, both in vivo and in vitro. Both compounds induced elimination of PrPSc from chronically scrapie-infected GT1 mouse hypothalamic cells (ScGT1) in a dose-dependent manner. ScGT1 cells treatment with HS at concentration of 20mg/mL eliminated more than 95% of PrPSc and did not affect cell viability. Moreover, both HS induced inhibition of prion fibril formation in vitro, as determined by thioflavin T assay. Our results suggest that HS may contribute significantly to prion inactivation in natural soil environments.



PPo8-21

Detection of PrPCWD in Rocky Mountain Elk Feces Using Protein Misfolding Cyclic Amplification

Bruce E Pulford,1 Terry Spraker,1 Jenny Powers,2 Margaret Wild2 and Mark D. Zabel1 1Department of Microbiology; Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; 2Biological Resource Management Division; United States National Park Service; CO, USA

Key words: CWD, feces, PMCA, elk

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy affecting cervids, including mule and white-tailed deer (Odocoileus hemionus and virginianus), elk (Cervus elaphus nelsoni) and moose (Alces alces shirasi). The method of CWD transmission between hosts is unclear, though there is evidence that feces excreted by infected animals may play a role. Recently, CWD prions was detected in feces using bioassays in cervidized mice, which took many months to produce results. In this study, we use a more rapid procedure, protein misfolding cyclic amplification (PMCA), to test elk feces for the presence of PK-resistant cervid PrP (PrPCWD). Feces were collected from symptomatic and asymptomatic elk in several northern Colorado locations, homogenized, mixed with normal brain homogenate from Tg5037 mice (expressing cervid PrP) and subjected to up to 9 rounds of PMCA (1 round = 40 secs sonication/30 mins at 70% maximum power, 24 hours). Western blots were used to detect PrPCWD using BAR-224 anti-PrP antibody. Rectal and CNS tissue from the elk were IHC-labeled and examined for the presence of PrPCWD. Fecal samples from symptomatic and asymptomatic elk that tested positive by IHC showed characteristic PrPCWD bands on western blots following PMCA. In addition, PMCA detected PrPCWD in 25% of fecal samples from IHC-negative animals. These data suggest that PMCA may (1) prove useful as a non-invasive method to supplement or even replace IHC testing of cervids for CWD, and (2) identify additional asymptomatic carriers of CWD, the prevalence of which may be underestimated using IHC.



http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099




Wednesday, September 08, 2010



CWD PRION CONGRESS SEPTEMBER 8-11 2010



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



COMERCIAL IN CONFIDENCE

SPREADING OF UNPROCESSED BLOOD ON LAND

http://web.archive.org/web/20040315202749/www.bseinquiry.gov.uk/files/yb/1991/02/15003001.pdf



The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences & Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s Hospital London and William Harvey Hospital Ashford April 1999

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88. Natural decay: Infectivity persists for a long time in the environment. A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep, after they had grazed on land which had previously been grazed by scrapie-infected sheep, even though the land had lain fallow for three years before the healthy sheep were introduced. Brown also quoted an early experiment of his own (1991), where he had buried scrapie-infected hamster brain and found that he could still detect substantial infectivity three years later near where the material had been placed. 89. Potential environmental routes of infection: Brown discusses the various possible scenarios, including surface or subsurface deposits of TSE-contaminated material, which would lead to a build-up of long-lasting infectivity. Birds feeding on animal remains (such as gulls visiting landfill sites) could disperse infectivity. Other animals could become vectors if they later grazed on contaminated land. "A further question concerns the risk of contamination of the surrounding water table or even surface water channels, by effluents and discarded solid wastes from treatment plants. A reasonable conclusion is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge numbers of uncertainties and assumptions that attend each stage of the disposal process". These comments, from a long established authority on TSEs, closely echo my own statements which were based on a recent examination of all the evidence. 90. Susceptibility: It is likely that transmissibility of the disease to humans in vivo is probably low, because sheep that die from scrapie and cattle that die from BSE are probably a small fraction of the exposed population. However, no definitive data are available.

91. Recommendations for disposal procedures: Brown recommends that material which is actually or potentially contaminated by BSE should be: 1) exposed to caustic soda; 2) thoroughly incinerated under carefully inspected conditions; and 3) that any residue should be buried in landfill, to a depth which would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source.

92. This review and recommendations from Brown have particular importance. Brown is one of the world's foremost authorities on TSEs and is a senior researcher in the US National Institutes of Health (NIH). It is notable that such a respected authority is forthright in acknowledging the existence of potential risks, and in identifying the appropriate measures necessary to safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical distribution of variant CJD in the UK (excluding Northern Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41 (02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD (variant CJD) might live closer to rendering factories than would be expected by chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were studied. The incubation period of vCJD is not known but by analogy with other human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure to rendering products, such exposure might plausibly have occurred 8-10 years before the onset of symptoms. The authors were able to obtain the addresses of all rendering plants in the UK which were in production in 1988. For each case of vCJD, the distance from the place of residence on 1st January 1998 to the nearest rendering plant was calculated

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http://web.archive.org/web/20030326042814/http://www.bseinquiry.gov.uk/files/ws/s019b.pdf



Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).

http://europa.eu.int/comm/food/fs/sc/ssc/out58_en.pdf



PAUL BROWN SCRAPIE SOIL TEST

http://collections.europarchive.org/tna/20080102120203/http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf



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Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

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




Chronic Wasting Disease—Prion Disease in the Wild

Citation: Bunk S (2004) Chronic Wasting Disease—Prion Disease in the Wild. PLoS Biol 2(4): e121. doi:10.1371/journal.pbio.0020121

Published: April 13, 2004

In 1967, mule deer in a research facility near Fort Collins, Colorado, in the United States apparently began to react badly to their captivity. At least, that was the guess of researchers working on the natural history and nutrition of the deer, which became listless and showed signs of depressed mood, hanging their heads and lowering their ears. They lost appetite and weight. Then they died—of emaciation, pneumonia, and other complications—or were euthanized. The scientists dubbed it chronic wasting disease (CWD), and for years they thought it might be caused by stress, nutritional deficiencies, or poisoning. A decade later, CWD was identified as one of the neurodegenerative diseases called spongiform encephalopathies, the most notorious example of which is bovine spongiform encephalopathy (BSE), more commonly known as mad cow disease. Nowadays, CWD is epidemic in the United States. Although no proof has yet emerged that it's transmissible to humans, scientific authorities haven't ruled out the possibility of a public health threat. The media have concentrated on this concern, and politicians have responded with escalated funding over the past two years for fundamental research into the many questions surrounding this mysterious disease.

Quite apart from how little is yet known about CWD, media interest is reason enough to step up investigation of it, says Mo Salman, a veterinary epidemiologist at Colorado State University in Fort Collins. He's been scientifically involved with BSE, since it was first discovered among cattle in the United Kingdom in 1986. He recalls predicting that lay interest in BSE would wane after five years. Instead, the disease was found in the mid-1990s to be capable of killing humans who ate tainted beef. “I was wrong, and it really changed my way of thinking, to differentiate between scientific evidence and the public perception,” Salman admits. “Because CWD is similar to BSE, the public perception is that we need to address this disease, to see if it has any link to human health.”

http://www.plosbiology.org/article/info:doi%2F10.1371%2Fjournal.pbio.0020121



* Williams reported in the same scientific paper that ``a few surplus deer and elk'' from CWD-infected state-run pens near Fort Collins had been released back into the wild. How many and in what years remains unclear. State officials say they can find few records.

http://www.highbeam.com/doc/1G1-87932644.html




Within the facilities, deer have had irregular and discontinuous contact with other wild ruminants and with domestic cattle, goats and sheep. In addition, other feral mammalian species either reside within or traverse the facilities’ pens.

Journal of Wildlife Diseases Vol. 16. No. 1, January, 1980 B Mice (Peromyscus sp., Mus musculus), rabbit (Lepus sp., Syluilagus sp.), raccoon (Procyon lotor), skunk (Mephitis

http://www.jwildlifedis.org/cgi/reprint/16/1/89




The Fort Collins facility became a CWD death trap. Between 1970 and 1981, 90 percent of the deer that stayed more than two years died from the disease or had to be euthanized. In 1980 the scourge emerged outside Colorado, at the Sybille Research Unit in southeastern Wyoming, 120 miles northwest of Fort Collins. The two facilities had exchanged deer for breeding purposes, thus indicating that the disease was infectious--even to a different species: soon the elk at the facilities contracted the disease. (Deer and elk both belong to the cervid family.)

For years, researchers thought CWD resulted from nutritional deficiencies, poisoning, or stress from confinement. But in 1977 Elizabeth S. Williams, studying for her doctorate at Colorado State University, discovered that this view was mistaken. When Williams looked at brain slices from infected animals, she saw that the tissue was full of microscopic holes. "I happened to be taking a course in neuropathology and had studied a lot of brain lesions," she recalls. The holes were unmistakably like scrapie, the sheep sickness that was the first documented spongiform encephalopathy.

In fact, CWD appears to have originated from scrapie. Richard E. Race of the National Institutes of Health Rocky Mountain Laboratories in Hamilton, Mont., conducted test tube studies that revealed no distinction between the malformed PrP of scrapie sheep and CWD cervids. Consistent with this discovery, Amir Hamir of the U.S. Department of Agriculture's National Animal Disease Center in Ames, Iowa, found no difference in the appearance of brain samples from elk with CWD and elk experimentally infected with scrapie. (BSE also probably arose from scrapie, after cows ate feed derived from infected sheep.)

Philip Yam is Scientific American's news editor. This article is adapted from his book, The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases, published in June. Overview/Chronic Wasting Disease

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How did CWD get started? 17 Mar 98 webmaster opinion My best guess as to what really happened

in the early days of the Ft. Collins facility, before they went to wild animal diseases, they studied scrapie and other diseases in sheep. The facility became contaminated, just like the pasture in Iceland. They hoped it wouldn't cross the species barrier.

Then they brought in mule deer. These became infected. No post-mortems were done, no tissues were saved, no records were kept; one worker there in 1967 wrote me to say they suspected scrapie at the time. They hoped it would go away.

The facility became grossly contaminated, 90% of the animals dying. No autopsies were supposedly done until 13 years into the disease, even though this was a disease research facility. They hoped it would go away.

Deer infected elk and other cervids. They hoped it would go away.

Pre-clinical animals were shipped to Wyoming, zoos, game farms, and released back into the wild. Wild animals infected each other at winter feeding stations at much higher rates than anyone expected. They hoped it would go away.

Infected wild animals were brought into various facilities. No monitoring had been done on wild animals. They hoped it would go away.

Tens of thousands of hunters ate contaminated meat from venison pooled into sausage. They hoped hunters wouldn't get CJD.

Some hunters subsequently donated blood which were pooled into batches of 50,000 doses or more. They hoped medical recipients wouldn't get CJD.

CWD is not scrapie, though it was probably originally triggered by scrapie. It is a different prion, a different amino acid sequence, after initial passage. CWD is probably not caused or spread through rendered downer protein feed like BSE. Its properties in humans are entirely unknown, the symptoms might be quite different from known forms of CJD.

http://www.mad-cow.org/elk_cwd.html#ddd




But the blanket slaughter programmes achieve little more than masking the superficial evidence of TSE, since they are merely taking out those susceptible populations that are at high risk of developing TSE. Meanwhile, the causal prerequisites remain well and truly cemented as Lendemic' into the bedrock of the TSE cluster environment. A good example of this is illustrated by the Colorado Division of Wildlife's failed attempts to annihilate so-called Chronic Wasting Disease (CWD) when they bulldozed the top six inches of soil from their CWD endemic deer facility at Fort Collins. CWD still returned. ...

http://www.mad-cow.org/99feb_cwd_special.html




DOW/CSU has never disclosed what happened to the original captive mule deer in 1967 -- were they released into the wild after the experiment, did any escape, did they exchange animals with the Wyoming facility, what were they fed, had there been prior scrapie sheep in the enclosure? It is ludicrous that they have never released the details -- as if the people who worked didn't keep lab notebooks.

My guess is that relevent documents were shredded long ago when they realized that the disease had gotten out of their facility -- with potentially devastating consequences to game tag sales and hence the very revenues that pay their salaries, never mind the legal liability. Now they are in too deep to confess. Just like MAFF.

The only other scenario that makes sense to me is a western Stetsonville: winter-ranged protein-caked deer, some of these got accidentally brought into the captive study.

http://www.mad-cow.org/colorado_exp.html



Tuesday, June 16, 2009

Infectious Prions in Pre-Clinical Deer and Transmission of Chronic Wasting Disease Solely by Environmental Exposure

http://chronic-wasting-disease.blogspot.com/2009/06/infectious-prions-in-pre-clinical-deer.html




Wednesday, October 14, 2009



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


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


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



Saturday, January 29, 2011

Atypical L-Type Bovine Spongiform Encephalopathy (L-BSE) Transmission to Cynomolgus Macaques, a Non-Human Primate

Jpn. J. Infect. Dis., 64 (1), 81-84, 2011


http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/atypical-l-type-bovine-spongiform.html



http://transmissiblespongiformencephalopathy.blogspot.com/




Wednesday, February 16, 2011

IN CONFIDENCE SCRAPIE TRANSMISSION TO CHIMPANZEES

IN CONFIDENCE

http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html





Seven main threats for the future linked to prions


The NeuroPrion network has identified seven main threats for the future linked to prions.

First threat

The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed. Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.



Second threat


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http://www.neuroprion.org/en/np-neuroprion.html




Wednesday, March 31, 2010

Atypical BSE in Cattle


To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.

This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.

http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2


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please see all seven threats listed in the USA, and more...FULL TEXT ;



Thursday, August 12, 2010

Seven main threats for the future linked to prions

http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html


http://prionpathy.blogspot.com/





Friday, February 11, 2011

Creutzfeldt-Jakob disease (CJD) biannual update (2010/1) Emerging infections/CJD

http://creutzfeldt-jakob-disease.blogspot.com/2011/02/creutzfeldt-jakob-disease-cjd-biannual.html





Monday, February 7, 2011

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


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




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

TSS
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