Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†
Colorado State University; Fort Collins, CO USA†Presenting author; Email: firstname.lastname@example.org
Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.
Hunting and diet
A successful generalist predator, the cougar will eat any animal it can catch, from insects to large ungulates (over 500 kg). Like all cats, it is an obligate carnivore, feeding only on meat. The mean weight of vertebrate prey (MWVP) was positively correlated (r=0.875) with puma body weight and inversely correlated (r=-0.836) with food niche breadth in all America. In general, MWVP was lower in areas closer to the Equator. Its most important prey species are various deer species, particularly in North America; mule deer, white-tailed deer, elk, and even large moose are taken by the cat. Other species such as Bighorn Sheep, wild horses of Arizona, domestic horses, and domestic livestock such as cattle and sheep are also primary food bases in many areas. A survey of North America research found 68% of prey items were ungulates, especially deer. Only the Florida Panther showed variation, often preferring feral hogs and armadillos.
Shown eating. Cougars are ambush predators, feeding mostly on deer and other mammals. Investigation in Yellowstone National Park showed that elk, followed by mule deer, were the cougar's primary targets; the prey base is shared with the park's gray wolves, with whom the cougar competes for resources. Another study on winter kills (November–April) in Alberta showed that ungulates accounted for greater than 99% of the cougar diet. Learned, individual prey recognition was observed, as some cougars rarely killed bighorn sheep, while others relied heavily on the species.
Transmission and Pathogenesis of Chronic Wasting Disease in Cervid and Non-Cervid Species
Edward Hoover,† Candace K. Mathiason, Nicholas J. Haley, Timothy D. Kurt, Davis M. Seelig, Amy V. Nalls, Mark D. Zabel, Glenn C. Telling Department of Microbiology, Immunology, and Pathology; Colorado State University; Fort Collins, CO; Department of Microbiology, Immunology and Molecular Genetics and Neurology; University of Kentucky Medical Center; Lexington, KY USA †Presenting author
Now recognized in 18 states in the US, two Canadian provinces, and one Asian country, efficient horizontal transmission is a signature trait of chronic wasting disease (CWD) of cervids. The facile spread of CWD appears linked to the prion/host relationship facilitating efficient mucosal uptake, peripheral lymphoreticular amplification, and horizontal dissemination exploiting excretory tissues and their products. In addition, recent studies suggest the likelihood of early life mother to offspring transmission. Growing evidence from studies of cervid CWD exposure by natural routes indicate that the incubation period for overt infection detection and disease onset (if any) may be much longer than originally thought. Whether non-cervid species (including humans) may be susceptible to CWD infection and/or act as reservoirs for infection in nature remains unknown. In vitro and in vivo studies of the CWD species barrier indicate the potential for a host range extending beyond cervid species, although no evidence for this has thus far been detected in nature. Interestingly, rodent and mustelid species sympatric with free ranging cervids have been shown susceptible to CWD prions and such trans-species infection broadens the host range/strain characteristics of CWD prions. While the origins of CWD remain unknown, the relationship between sheep scrapie and CWD and the existence of multiple CWD prion strains/quasispecies remain interesting and merit further investigation.
Oral.26: Minor Oral Lesions Facilitate CWD Infection
Nathaniel D. Denkers,1,† Glenn C. Telling2 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Kentuckty; Lexington, KY USA †Presenting author; Email: email@example.com
Purpose: While the exact mechanisms of chronic wasting disease (CWD) prion transmission, entry, and trafficking remain incompletely elucidated, transmission by exposure of the oral and/or nasal mucous membranes seems certain. As part of foraging, cervids likely experience minor lesions in the oral mucous membranes; these could have impact on susceptibility to prion entry and subsequent infection. To explore this potential co-factor, we used cervid PrP transgenic mice to assess whether or not micro-abrasions to the tongue may enhance susceptibility to oral CWD infection and whether or not infectious CWD PrPCWD could be detected immediately after exposure.
Methods: Two sets of FVB mice transgenically expressing the normal cervid PrPC protein [Tg(CerPrP-E226)5037+/-], with or without abrasions on the lingual mucosa, were inoculated orally with 10µl of a 10% w/v brain homogenate from either CWD-positive or negative deer. Abrasions were created by lightly scratching the dorsal lingual epithelium with a 27g needle. Cohorts were sacrificed at either early [0, 1, and 4 h post inoculation (pi)] or late [3, 12, and 24 months pi] time points or when signs of neurologic disease were observed. Tongue, lymphoid tissue, and the brain were assessed by western blotting and tyramide signal amplification (TSA) immunohistochemistry to detect the CWD abnormal prion protein (PrPCWD).
Results: Between 296 and 515 dpi, 9 of the 9 CWD-inoculated mice with lingual lesions developed clinical signs of neurologic dysfunction mandating euthanasia. Only the brain in all nine mice was positive for PrPCWD by western blot and TSA immunohistochemistry. Conversely, all mice without oral lesions remained asymptomatic for >700 dpi and no evidence of PrPCWD was detected in these mice terminally. Moreover, no evidence of PrPCWD could be detected when the micro-abrasion sites were examined at 0, 1, or 4 h after oral exposure or at any pre-terminal time point thereafter.
Conclusions: Micro-abrasions to the lingual surface substantially facilitated CWD transmission, suggesting that minor oral mucosal lesions may be a significant co-factor facilitating infection in foraging cervids or other species.
Oral.27: Identification of PrPCWD in the Salivary Gland Epithelium of White-Tailed Deer: Novel Insights Into Mechanisms of CWD Horizontal Transmission
Davis Seelig,1,† Gary Mason,1 Glenn Telling2 and Edward Hoover1
1Colorado State University; Fort Collins, CO USA; 2University of Kentucky; Lexington, KY USA†Presenting author; Email: firstname.lastname@example.org
Background. Chronic wasting disease (CWD) of cervids is characterized by its efficient transmission among animals. Although bioassay and in vitro amplification studies have confirmed the infectious nature of saliva, urine, blood and feces, uncertainties remain regarding the mechanisms of this facile horizontal transmission. Notable among these is a specific understanding of the means by which prion infectivity is transferred to a body fluid or excretion.
Objectives. The chief objective of this work was to provide tissue-level insights into the process of prion shedding via the salivary glands by means of enhanced immunohistochemistry (IHC).
Methods. Formalin fixed, paraffin-embedded tissues from CWD-infected white-tailed deer (WTD) were evaluated for the presence of PrPCWD using sensitive amplified immunohistochemistry (IHC) methods employing, citrate buffer-based heat-induced epitope retrieval, tyramide signal amplification (TSA), and a polyclonal anti-prion protein antisera.
Results. Here we show that enhanced IHC techniques are capable of detecting pathogenic prion protein (PrPCWD) in the salivary glands of infected WTD. Utilizing optimized TSA we have detected granular to clumped, intra-cytoplasmic PrPCWD deposits in parotid and mandibular salivary gland ductular epithelial cells of WTD infected with CWD for 19 to 27 months. Salivary PrPCWD was not detected in sham-inoculated or naïve WTD. PrPCWD was not identified in any other salivary gland cell types.
Discussion. We present immunohistochemical evidence for PrPCWD accumulation in the salivary gland ductules, which provides a tissue level correlate to the infectivity present in cervid saliva and may explain the manner by which prions transit to saliva, and thereby facilitate the high degree of CWD horizontal transmission. These findings complement work by Haley et al. (this symposium) demonstrating the presence of CWD prions in salivary glands through the in vitro amplification assay PMCA.
Oral.44: Genetic Variability and Association with Prion Disease Susceptibility of the Prion Gene in the Mammalian Order Carnivora
Paula Stewart,1 Karen Griffin,8 Jon E. Swenson,2 Jens Persson,11 Olof Liberg,11 Jon M. Arnemo,3, 4 Thierry Baron,5 Martin Groschup,6 Danielle Gunn-Moore,9 Simon Girling,10 Michael W. Miller,8 Michael Tranulis7 and Wilfred Goldmann,1,†
1The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh; Easter Bush, Midlothian, UK; 2Department of Ecology and Natural Resources Management, Norwegian University of Life Sciences; As, Norway; 3Department of Forestry and Wildlife Management, Hedmark University College; Campus Evenstad, Norway; 4Department of Wildlife, Fish and Environmental Studies, Faculty of Forest Sciences, Swedish University of Agricultural Sciences; Umea, Sweden; 5Agence Française de Sécurité Sanitaire des Aliments; Lyon, France; 6Friedrich Loeffler Institut; Riems, Germany; 7Department of Basic Sciences & Aquatic Medicine, Norwegian School of Veterinary Science; Oslo, Norway; 8Wildlife Research Center, Colorado Division of Wildlife; Fort Collins, CO USA; 9Small Animal Hospital, Royal (Dick) School of Veterinary Studies, University of Edinburgh; Edinburgh, UK; 10The Royal Zoological Society of Scotland, Edinburgh Zoo; Edinburgh, UK; 11Grimsö Wildlife Research Station, Department of Ecology, Swedish University of Agricultural Sciences ; Riddarhyttan, Sweden†Presenting author; Email: email@example.com
Carnivores are exposed to significant levels of CWD in some regions of the US and Canada. Indeed it has been proposed recently that mountain lions prey selectively on prion–infected mule deer. It is likely that predators have also at least occasionally been exposed to other prion diseases, such as sheep scrapie in other countries. How susceptible are predators and scavengers to prion diseases? It is well known that the prion protein sequence is important as a major modulator of susceptibility and pathogenesis of prion disease. For example, prion disease susceptibility in sheep, goats and deer is modulated by at least 15 different polymorphisms of the PrP protein. PrP sequencing of carnivore species has not been done in great numbers and the degree of genetic variation of their PrP in wild and domesticated populations has not been addressed in any detail. However, to estimate the genetic risk of populations to diseases such as CWD one needs to understand the genetic variation of the target species.
We have analyzed the prion protein sequence of over 450 samples from over 20 species/subspecies of the suborders feliformia (cat-like) and caniformia (dog-like) representing ~320 samples from wild populations (US, Europe), ~110 samples from companion animals and ~25 samples from zoo collections. Within these samples were nine FSE cat cases, including the index case from the UK and six FSE cheetahs.
We established the PrP protein variants in our sample set and conclude that the number of PrP variants is small, with slightly more variability in caniformia than feliformia. All feline prion sequences have a characteristic alanine change in their repeat region that is not seen in any other species; all canine PrP encode aspartic acid in position 163, which is not present in any other species with the exception of wolverines. We hypothesis that these differences may explain some of the difference observed in prion disease susceptibility. The analysis of the FSE cases revealed no additional mutations therefore excluding the possibility of particularly susceptible PrP genotypes.
Although the general susceptibility of predators to CWD has not been established, we predict that it is unlikely that species such as mountain lion and black bear will be protected by resistant alleles, whereas wolf and wolverine may have a slightly higher susceptibility threshold.
W.G. and P.S. supported by Institute Strategic Grant funding from the BBSRC, UK.
Enzymatic Digestion of Chronic Wasting Disease Prions Bound to Soil
S A M U E L E . S A U N D E R S , † J A S O N C . B A R T Z , ‡ K U R T C . V E R C A U T E R E N , § A N D S H A N N O N L . B A R T E L T - H U N T * , †
Department of Civil Engineering, Peter Kiewit Institute, University of NebraskasLincoln, Omaha, Nebraska 68588, Department of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska 68178, and USDA Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, Fort Collins, Colorado 80521 Received November 19, 2009. Revised manuscript received April 5, 2010. Accepted April 24, 2010.
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, Prionzyme, to degrade soil-bound and unbound CWD and HY TME PrP as a function of pH, temperature, and treatment time. The subtilisinenzymeeffectively 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 days under conditions representative of the natural environment (pH 7.4, 22 °C). We observednoapparent difference inenzymeeffectivenessbetween 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. see full text study here ;
CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the CWD TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the CWD TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
CWD TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Paul Brown*,dagger , Edward H. RauDagger , Bruce K. Johnson*, Alfred E. Bacote*, Clarence J. Gibbs Jr.*, and D. Carleton Gajdusek§ * Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, and Dagger Environmental Protection Branch, Division of Safety, Office of Research Services, National Institutes of Health, Bethesda, MD 20892; and § Institut Alfred Fessard, Centre National de la Recherche Scientifique, 91198 Gif sur Yvette, France Contributed by D. Carleton Gajdusek, December 22, 1999
see full text:
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Cathrin E. Bruederle,1* Robert M. Hnasko,1 Thomas Kraemer,2 Rafael A. Garcia,3 Michael J. Haas,3 William N. Marmer,3 and John Mark Carter1 1USDA-ARS WRRC, Foodborne Contaminants Research Unit, Albany, California, United States of America 2Forensic Toxicology, Institute of Legal Medicine, Saarland University, Homburg/Saar, Germany 3USDA-ARS ERRC, Fats, Oils and Animal Coproducts Research Unit, Wyndmoor, Pennsylvania, United States of America Neil Mabbott, EditorUniversity of Edinburgh, United Kingdom *
Wednesday, October 14, 2009
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
T.A. Nichols,1,2 Bruce Pulford,1 A. Christy Wyckoff,1,2 Crystal Meyerett,1 Brady Michel,1 Kevin Gertig,3 Edward A. Hoover,1 Jean E. Jewell,4 Glenn C. Telling5 and Mark D. Zabel1,*
1Department of Microbiology, Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort Collins, CO USA; 2National Wildlife Research Center; Wildlife Services; United States Department of Agriculture; Fort Collins, CO USA; 3Fort Collins Utilities; Fort Collins; CO USA; 4Department of Veterinary Sciences; Wyoming State Veterinary Laboratory; University of Wyoming; Laramie, WY USA; 5Department of Microbiology, Immunology, Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky; Lexington, KY USA
The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.
OLD BSE TSE PRION HISTORY
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
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.
(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)
PAUL BROWN SCRAPIE SOIL TEST
(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)
a. after burning to the range of 800 to 1000*C to eliminate smell; well heck, this is just typical public relations fear factor control. do you actually think they would spend the extra costs for fuel, for such extreme heat, just to eliminate smell, when they spread manure all over your veg's. i think not. what they really meant were any _TSE agents_.
b. Gas scrubbing to eliminate smoke -- though steam may be omitted; c. Stacks to be fitted with grit arreaters;
1.2 Visual Imact
It is considered that the requirement for any carcase incinerator disign would be to ensure that the operations relating to the reception, storage and decepitation of diseased carcasses must not be publicly visible and that any part of a carcase could not be removed or interfered with by animals or birds.
18. The EA’s assertion at the Thruxted planning inquiry that the precautionary principle does not apply in the case of Thruxted Mill in view of the low risk entailed by its effluent discharge is entirely unfounded. The source data presented by the EA at the Thruxted Inquiry derive in part from its assumptions concerning the segregation of infectivity to the various products of rendering. The EA also stipulates a minimum particle size of 1013 molecules for human infection and assumes there is a 2500-fold reduction of infectivity by rendering, filtration and biological treatment prior to discharge. In fact, the minimum particle size may be at least 1012 times lower. The reduction in the input levels of BSE infectivity prior to discharge will also be very substantially less than implied in the EA source data, and may indeed be minimal. The EA assumes that biological treatment of the rendering effluent will reduce or eliminate BSE infectivity. This is probably the exact opposite of what is actually likely to happen.
19. In his proof of evidence at the Thruxted Inquiry, Mr Young asserted that "effective filtering of clumps of material is likely". As already mentioned, infectious prions are known to pass
[PDF]BSE INQUIRY Statement of behalf of the Environment Agency ...
File Format: PDF/Adobe Acrobat - View as HTML
... his Statement of March 1998 to the BSE Inquiry ... systems subject to regular or intermittent
contamination by rapid movement of recharge water ...
Statement of behalf of the Environment Agency
Concerning Thruxted Mill
Mr C. P. Young
Principal Hydrogeologist, Soil Waste and Groundwater Group
WRc plc; Medmenham, Bucks
Friday, February 25, 2011
Soil clay content underlies prion infection odds
Friday, February 25, 2011
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
Monday, August 8, 2011
Susceptibility of Domestic Cats to CWD Infection
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Sunday, November 01, 2009
American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases
Monday, July 13, 2009
Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease
(please note, there has never been a documneted case of CSE i.e. mad dog disease, BUT, if you read the history, and the data sent to me by maff/defra, and the transmission studies did show something, but another cases of screwed up testing, and then a determination of simply not doing anymore studies because of money and the fact that so many other species came down with it, there was really no need to try and prove a case of canine spongiform encephalopathy due to media and hype. that was my take on it, read up the history and correspondense ;
DEFRA Department for Environment, Food & Rural Affairs
Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk
Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518
21 November 2001
Dear Mr Singeltary
TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less
critical. For more details see- http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH BSE CORRESPONDENCE SECTION
TSE & HOUNDS
GAH WELLS (very important statement here...TSS)
AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.
76 pages on hound study;
The signs of canine cognitive dysfunction syndrome or "old dog syndrome" commonly seen in dogs are:
snip...see full text ;
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Date: Fri, 16 May 2003 11:47:37 -0500
From: "Terry S. Singeltary Sr." To: firstname.lastname@example.org
Ravensden, Marwell, Chester, Port Lympne, London, Whipsnade, Woburn, and Edinburgh are 8 known BSE affected British zoos.
Woburn Safari Park apparently killed the lion by feeding it split cattle spinal cords and skulls.
Thursday, December 25, 2008
Lions and Prions and Deer Demise
A disturbing study indeed, but even more disturbing, the fact that this very study shows the potential for transmission of the TSE agent into the wild of yet another species in the USA. Science has shown that the feline is most susceptible to the TSE agent. Will CWD be the demise of the mountain lions, cougars and such in the USA? How many have ever been tested in the USA? I recall there is a study taking place ;
Review A prion disease of cervids: Chronic wasting disease Christina J. Sigurdson et al ;
Mountain lion (Puma concolor) susceptibility to experimental feeding of CWD prions is currently under investigation (M. Miller and L. Wolfe, personal communication).
WHAT about multiple strains of CWD ?
see full text ;
Friday, August 6, 2010
Is the presence of abnormal prion protein in the renal glomeruli of feline species presenting with FSE authentic?
Wednesday, April 1, 2009
Immunohistochemical study of PrPSc distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy
Saturday, September 5, 2009
Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah
Tuesday, September 02, 2008
Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease
Wednesday, July 20, 2011
Canadian Researchers Receive $2.9 Million to Protect Against Prion Disease Outbreaks, Develop Novel Therapies to Treat Alzheimer's, Parkinson's and ALS