Monday, August 8, 2011

Susceptibility of Domestic Cats to CWD Infection

Oral.29: Susceptibility of Domestic Cats to CWD Infection

Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†

Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu

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

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



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.[3] 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.[38] 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.[3]



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.[39] 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.[40]



http://en.wikipedia.org/wiki/Cougar




Oral.22:



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: nddenk@colostate.edu



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: davis.seelig@colostate.edu



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: wilfred.goldmann@roslin.ed.ac.uk



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.



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




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 ;



http://www.aphis.usda.gov/wildlife_damage/nwrc/publications/10pubs/vercauteren108.pdf





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




snip...




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









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




snip...




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.




snip...






(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)








INCINERATION TEMPS


Requirements include:


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;


snip...


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.


full text;








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 ...


BSE INQUIRY


Statement of behalf of the Environment Agency


Concerning Thruxted Mill


By


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


Soil clay content underlies prion infection odds

 
 







Monday, February 14, 2011



THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER



NO, NO, NOT NO, BUT HELL NO !



Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011



http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html




Monday, August 8, 2011



Susceptibility of Domestic Cats to CWD Infection



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




UPDATED DATA ON 2ND CWD STRAIN



Wednesday, September 08, 2010



CWD PRION CONGRESS SEPTEMBER 8-11 2010



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




Sunday, November 01, 2009



American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases



http://chronic-wasting-disease.blogspot.com/2009/11/american-crows-corvus-brachyrhynchos.html




Monday, July 13, 2009



Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease



http://chronic-wasting-disease.blogspot.com/2009/07/deer-carcass-decomposition-and.html




(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 ;



2005



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



GTN: FAX:



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)



HOUND STUDY



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.



http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf




76 pages on hound study;



http://web.archive.org/web/20030327022236/http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf




The signs of canine cognitive dysfunction syndrome or "old dog syndrome" commonly seen in dogs are:



snip...see full text ;



http://caninespongiformencephalopathy.blogspot.com/2010/03/canine-spongiform-encephalopathy-aka.html




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: fdadockets@oc.fda.gov



http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html




http://www.mad-cow.org/zoo_cites_annotated.html#ccc





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




http://www.mad-cow.org/zoo_cites_annotated.html#tig





http://www.mad-cow.org/zoo_cites_annotated.html#bbb





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.



http://www.mad-cow.org/zoo_cites_annotated.html#aaab





Thursday, December 25, 2008

Lions and Prions and Deer Demise

snip...

Greetings,

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 ?

snip...

see full text ;

http://chronic-wasting-disease.blogspot.com/2008/12/lions-and-prions-and-deer-demise.html




Friday, August 6, 2010

Is the presence of abnormal prion protein in the renal glomeruli of feline species presenting with FSE authentic?

Correspondence

http://felinespongiformencephalopathyfse.blogspot.com/2010/08/correspondence-is-presence-of-abnormal.html




Wednesday, April 1, 2009

Immunohistochemical study of PrPSc distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy

Research article

http://felinespongiformencephalopathyfse.blogspot.com/2009/04/immunohistochemical-study-of-prpsc.html





Saturday, September 5, 2009

Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah

http://felinespongiformencephalopathyfse.blogspot.com/2009/09/possible-case-of-maternal-transmission.html



Tuesday, September 02, 2008

Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease

http://chronic-wasting-disease.blogspot.com/2008/09/fecal-transmission-of-aa-amyloidosis-in.html


http://felinespongiformencephalopathyfse.blogspot.com/



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



http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/canadian-researchers-receive-29-million.html




http://bse-atypical.blogspot.com/




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




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




http://scrapie-usa.blogspot.com/




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




http://creutzfeldt-jakob-disease.blogspot.com/




http://sporadicffi.blogspot.com/




http://kuru-tse.blogspot.com/




http://prionopathy.blogspot.com/




http://betaamyloidcjd.blogspot.com/




http://transmissiblespongiformencephalopathy.blogspot.com/




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




http://www.mad-cow.org/~tom/animals.html




TSS

Friday, August 6, 2010

Is the presence of abnormal prion protein in the renal glomeruli of feline species presenting with FSE authentic?

Correspondence


Is the presence of abnormal prion protein in the renal glomeruli of feline species presenting with FSE authentic?


Stephane Lezmi , Thierry GM Baron and Anna A Bencsik

BMC Veterinary Research 2010, 6:41doi:10.1186/1746-6148-6-41

Published: 4 August 2010

Abstract (provisional) In a recent paper written by Hilbe et al (BMC vet res, 2009), the nature and specificity of the prion protein deposition in the kidney of feline species affected with feline spongiform encephalopathy (FSE) were clearly considered doubtful. This article was brought to our attention because we published several years ago an immunodetection of abnormal prion protein in the kidney of a cheetah affected with FSE. At this time we were convinced of its specificity but without having all the possibilities to demonstrate it. As previously published by another group, the presence of abnormal prion protein in some renal glomeruli in domestic cats affected with FSE is indeed generally considered as doubtful mainly because of low intensity detected in this organ and because control kidneys from safe animals present also a weak prion immunolabelling. Here we revisit these studies and thought it would be helpful to relay our last data to the readers of BMC Vet res for future reference on this subject. Here we come back on our material as it is possible to study and demonstrate the specificity of prion immunodetection using the PET-Blot method (Paraffin Embedded Tissue - Blot). It is admitted that this method allows detecting the Proteinase K (PK) resistant form of the abnormal prion protein (PrPres) without any confusion with unspecific immunoreaction. We re-analysed the kidney tissue versus adrenal gland and brain samples from the same cheetah affected with TSE using this PET-Blot method. The PET-Blot analysis revealed specific PrPres detection within the brain, adrenal gland and some glomeruli of the kidney, with a complete identicalness compared to our previous detection using immunohistochemistry. In conclusion, these new data enable us to confirm with assurance the presence of specific abnormal prion protein in the adrenal gland and in the kidney of the cheetah affected with FSE. It also emphasizes the usefulness for the re-examination of any available tissue blocks with the PET-Blot method as a sensitive complementary tool in case of doubtful PrP IHC results.

http://www.biomedcentral.com/1746-6148/6/41/abstract


Discussion

These new results enable us to confirm confidently the presence of specific abnormal prion protein in the adrenal gland and in the kidney of the cheetah affected with FSE. This question is important because it becomes evidenced that urine may sustain transmission of certain forms of the transmissible spongiform encephalopathy (TSE) diseases, such as hamsters carrying infectious particles. More recently the kidney was found to accumulate abnormal PrP in other species too such as sheep [17, 18], and the urinary secretion of pathological form of PrP is seriously considered [19, 20]. Even if the origin of the production of this infectious prion particles are not yet clearly identified, the specific detection of PrPres within the glomeruli of the kidney of cheetah with FSE is in total accordance with this point.

snip...see full text ;

http://www.biomedcentral.com/content/pdf/1746-6148-6-41.pdf


Subject: CWD/POTENTIAL SOURCE/URINE/HUNTERS ? (Mrs. Doe Pee Doe in Estrus)

Date: Sun, 14 Jul 2002 08:42:51 -0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de

######## Bovine Spongiform Encephalopathy #########

1: Hum Reprod 2002 Jul;17(7):1676-80 Bye-bye urinary gonadotrophins?: Is there a risk of prion diseaseafter the administration of urinary-derived gonadotrophins?

Balen A.

Department of Reproductive Medicine, The General Infirmary, LeedsLS2 9NS, UK. E-mail: adam.balen@leedsth.nhs.uk

Concern has been raised recently about the possibility of prionproteins appearing in the urine of animals and, possibly, humansaffected by prion disease [scrapie, bovine spongiform encephalopathy(BSE) and Creutzfeldt Jakob disease (CJD)]. A debate has started inwhich the suggestion has been made that the purification of human urinefor the provision of gonadotrophins should be discontinued. Thealternative would be to use recombinantly-derived gonadotrophinpreparations. The recombinant products, however, rely upon bovine serumduring the cell culture process and could potentially also be exposed toabnormal prion proteins. It is reassuring that the different types ofgonadotrophin preparations that are currently available are producedwith either urine or bovine serum that is sourced from countries that atthe present time appear to be free of BSE and new variant CJD. We cantherefore be reassured that the gonadotrophins that we usetherapeutically appear to be equally safe.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12093821&dopt=Abstract


what about the 100% deer urine they use to atract deer ?

just one example of many below;

CWD/POTENTIAL SOURCE/URINE/HUNTERS ?

Mrs. Doe Pee Doe in Estrus

Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urinecollected at the peak of the rut, blended with Fresh Doe Urine for anextremely effective buck enticer. Use pre-rut before the does come intoheat. Use during full rut when bucks are most active. Use duringpost-rut when bucks are still actively looking for does. 1 oz.

http://www.gamecalls.net/huntingproducts/deerlures.html


ELK SCENT/SPRAY BOTTLE * Works anytime of the year* 100 % Cow Elk-in-Heat urine (2oz.)* Economical - mix with water in spray mist bottle* Use wind to your advantage Product Code WP-ESB $9.95 http://www.elkinc.com/Scent.asp

prions in urine? [PDF] A URINE TEST FOR THE IN-VIVO DIAGNOSIS OF PRION DISEASES

http://www.sigov.si/vurs/PDF/diagnoastika-bse-urin.pdf


snip...

see full text ;

Wednesday, March 18, 2009

Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay

http://chronic-wasting-disease.blogspot.com/2009/03/detection-of-cwd-prions-in-urine-and.html


Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease

Beiru Zhang*†, Yumi Une‡, Xiaoying Fu*, Jingmin Yan*, FengXia Ge*, Junjie Yao*§, Jinko Sawashita*, Masayuki Mori*, Hiroshi Tomozawa¶, Fuyuki Kametani , and Keiichi Higuchi*‡** *Department of Aging Biology, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, and ¶Division of Laboratory Animal Research, Research Center for Human and Environmental Science, Shinshu University, 3-1-1, Asahi, Matsumoto 390-8621, Japan; †Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, China; ‡Laboratory of Veterinary Pathology, School of Veterinary Medicine, Azabu University, 1-17-71 Fuchinobe, Sagamihara, Kanagawa 229-8501, Japan; §The Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Tokyo 183-8508, Japan; and Tokyo Institute of Psychiatry, Tokyo Metropolitan Organization for Medical Research, Tokyo 156-8585, Japan Edited by Reed B. Wickner, National Institutes of Health, Bethesda, MD, and approved April 1, 2008 (received for review January 16, 2008)

AA amyloidosis is one of the principal causes of morbidity and mortality in captive cheetahs (Acinonyx jubatus), which are in danger of extinction, but little is known about the underlying mechanisms. Given the transmissible characteristics of AA amyloidosis, transmission between captive cheetahs may be a possible mechanism involved in the high incidence of AA amyloidosis. In this study of animals with AA amyloidosis, we found that cheetah feces contained AA amyloid fibrils that were different from those of the liver with regard to molecular weight and shape and had greater transmissibility. The infectious activity of fecal AA amyloid fibrils was reduced or abolished by the protein denaturants 6 M guanidine HCl and formic acid or by AA immunodepletion. Thus, we propose that feces are a vehicle of transmission that may accelerate AA amyloidosis in captive cheetah populations. These results provide a pathogenesis for AA amyloidosis and suggest possible measures for rescuing cheetahs from extinction.

snip...

Discussion It is currently accepted that systemic AA amyloidosis is an increasingly important cause of morbidity and mortality in captive cheetah populations (14). For conservation of this species, therefore, it is critical to elucidate the etiology of AA amyloidosis. As with sheep scrapie and cervid CWD, the routes of transmission are among the most debated and intriguing issues. InfectiousCWDprions in saliva have been identified to be involved in transmission in high-density captive situations (19, 20). Recently, available evidence indicates that an environmental reservoir of infectivity contributes to the continuation of these diseases in affected populations. These infectious agents can be transmitted by flesh flies (21) or hay mites (22) and can directly enter the environment from decomposing carcasses of infected animals (23). Environmental contamination by excreta from infected cervids has also seemed the most plausible explanation for the dissemination of CWD (24). Scrapie-infected hamsters and Creutzfeldt–Jakob disease (CJD) patients were reported to excrete urinary protease-resistant PrP isoform (25), indicating that urinary excretion from infected animals may provide a vector for horizontal transmission. However, there are studies that are not consistent with these findings (26, 27). Perhaps unrecognized nephritic conditions may underlie these discrepant observations, because it has been reported that urinary prion excretion is found only in scrapie-infected mice with lymphocytic nephritis (28). In this study, we observed several bands with high molecular weights that reacted with anti-cheetah AA antiserum in the whole urine sample, but not in the urine pellet in whichAAamyloid fibrils should be recovered. We thought that the possibility for a transmission pathway through urine might be low, but it could not be ruled out. In addition to urine, the alimentary shedding route has been considered as a possible transmission pathway (29). Abnormal prion protein is present in gut-associated lymphoid tissues of mule deer infected with CWD, consistent with an alimentary shedding route (30). In this study, we showed that the fecal fraction from a cheetah with amyloidosis had AA amyloid fibrils and possessed high transmissibility. In mouse AApoAII amyloidosis, regarded recently as another transmissible amyloidosis (5–7), we also demonstrated that the feces could serve as an agent to induce amyloidosis in recipient mice (31). These results shed new light on the etiology involved in the high incidence of AA amyloidosis in cheetahs. In this study, we unexpectedly found that the amyloid fibril fraction from feces had smaller amyloid fibrils and higher sensitivity to denaturation treatment than the liver amyloid fibril fraction. In mammalian prion, it has been demonstrated that there is a very strong correlation between seeding capability and amyloid fibril conformation (32, 33). Similarly, in yeast prion, it also has been indicated that [PSI ] with stronger infectivity typically have less stable fibrils in vivo than strains with weaker infectivity (34), and the prion strain with relatively smaller prion particles is always associated with greater frangibility and increased sensitivity to denaturants (35). The enhanced frangibility is presumably involved in the increase in seeding efficiency and prion infectivity, while the high sensitivity probably results from structural differences in inter-molecular contacts and a shorter, less stable amyloid core. The divergent ultrastructure between the fecal and the liver fibrils identified by transmission electron microscopy may be responsible for the different characteristics of transmissibility and sensitivity to denaturation treatment, analogous to prion protein. It has been reported that AA amyloidosis can be experimentally induced by i.v. or i.p. administration of AA amyloid fibrillar extracts in recipient mice (10). A few recent studies have shown that AA-containing extracts also had amyloid-inducing activity when administered orally to mice (36, 37). In AApoAII amyloidosis, we orted that an oral administration of AApoAII amyloid fibrils induced amyloidosis in recipient mice (38). Thus, it is plausible that oral ingestion of AA-containing fecal matter caused amyloid deposition in the cheetah population. At this juncture, the manner in which fecal matter is initially absorbed by the cheetahs is not clear. This may occur during mutual grooming (licking of the fur contaminated by fecal matter). Recently it was shown that a prion agent could bind to whole soil and common soil minerals and retain infectivity for a prolonged period (23, 39). Thus, soil may act as a reservoir capable of contaminating both food and fur. It is also unknown how AA fibril proteins enter the feces. Because AA amyloidosis was also in the small intestines of AA amyloidosis cheetahs, it is possible that AA proteins enter the feces through exfoliated mucosa. In conclusion, we found that cheetahs with amyloidosis pass fecal matter that had strong seeding efficiency and should be regarded as a transmission medium. To control the incidence of AA amyloidosis and reduce the likelihood of the animal’s extinction, prevention of the transmission with excretion from cheetahs with amyloidosis should be considered along with reduction of precursor SAA levels.

Materials and Methods

snip...end

http://www.pnas.org/content/105/20/7263.full.pdf+html


http://betaamyloidcjd.blogspot.com/2008/05/fecal-transmission-of-aa-amyloidosis-in.html



Tuesday, September 02, 2008

Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease

http://chronic-wasting-disease.blogspot.com/2008/09/fecal-transmission-of-aa-amyloidosis-in.html



Saturday, September 5, 2009

Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah

http://felinespongiformencephalopathyfse.blogspot.com/2009/09/possible-case-of-maternal-transmission.html



http://felinespongiformencephalopathyfse.blogspot.com/



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



http://betaamyloidcjd.blogspot.com/



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



http://www.mad-cow.org/~tom/animals.html



TSS

Saturday, September 5, 2009

Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah

Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah


Anna Bencsik1*, Sabine Debeer1¤, Thierry Petit2, Thierry Baron1

1 Unité ATNC, Agence Française de Sécurité Sanitaire des Aliments (AFSSA), Lyon, France, 2 Zoo de La Palmyre, Les Mathes, France

Abstract Top Feline spongiform encephalopathy (FSE) is considered to be related to bovine spongiform encephalopathy (BSE) and has been reported in domestic cats as well as in captive wild cats including cheetahs, first in the United Kingdom (UK) and then in other European countries. In France, several cases were described in cheetahs either imported from UK or born in France. Here we report details of two other FSE cases in captive cheetah including a 2nd case of FSE in a cheetah born in France, most likely due to maternal transmission. Complete prion protein immunohistochemical study on both brains and peripheral organs showed the close likeness between the two cases. In addition, transmission studies to the TgOvPrP4 mouse line were also performed, for comparison with the transmission of cattle BSE. The TgOvPrP4 mouse brains infected with cattle BSE and cheetah FSE revealed similar vacuolar lesion profiles, PrPd brain mapping with occurrence of typical florid plaques. Collectively, these data indicate that they harbor the same strain of agent as the cattle BSE agent. This new observation may have some impact on our knowledge of vertical transmission of BSE agent-linked TSEs such as in housecat FSE, or vCJD.

Citation: Bencsik A, Debeer S, Petit T, Baron T (2009) Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah. PLoS ONE 4(9): e6929. doi:10.1371/journal.pone.0006929

Editor: Neil Mabbott, University of Edinburgh, United Kingdom

Received: May 27, 2009; Accepted: August 12, 2009; Published: September 7, 2009

Copyright: © 2009 Bencsik et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work was supported by the Agence Francaise de Securite Sanitaire des Aliments. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

* E-mail: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000243/!x-usc:mailto:a.bencsik@afssa.fr

¤ Current address: INSERM Unité 851, Immunité Infection Vaccination, Tour CERVI, Lyon, France


SNIP...


Discussion Top Here are reports of two cases of feline spongiform encephalopathy (FSE) in 2 female cheetahs, one imported from Great Britain, the other born in France, that most likely constitute the first description of a possible maternal transmission of this disease in that species. FSE is a transmissible spongiform encephalopathy (TSE) of the felidae, identified for several years now, in domestic and in captive wild felids, for the most part in cheetahs [21], [22]. In captivity, all these felidae could have been exposed to infected tissues from cattle from early in their lives and the most probable explanation of the occurrence of FSE is consequently a contamination by oral route with the infectious agent of the bovine spongiform encephalopathy (BSE). For FSE cases in domestic cats only, a link between BSE and FSE agent was demonstrated by the similarity of mean incubation periods and lesion profiles in FSE and BSE cases transmitted to wild-type mice [3], [23]. Here we report the transmission of the FSE case 1 (the mother of case 2) into the Tg(OvPrP4) mouse model that has been demonstrated as sensitive to and efficient at detecting the BSE strain of agent [2], [15], [16]. When BSE agent is transmitted in this model, at first passage the mean incubation periods may vary depending on the species of the host harboring the BSE agent (cattle, sheep etc.), and was reported to be from 300 d.p.i. +/-50 (mean +/- standard error) to 475 +/-69 d.p.i. (and even up to 500 d.p.i. +/-110 for an experimental ovine BSE in an ARR/ARR genotype sheep) [2], [15], [17].

For both passages reported in the present study, the mean incubation periods of FSE are totally in accordance with this previously reported range of data obtained in BSE agent transmission studies in TgOvPrP4 mice. It is likely that the slight differences between the incubation periods reported here in BSE and FSE transmissions resulted from the different species and different titre of infectious agent present in the inoculum. This was also suggested in other BSE transmission studies in RIII or C57Bl mouse lines, for which quite a wide range of mean incubation times has also been reported (range 393–909 days in BSE transmissions to C57Bl mice) [24]. At second passage, the incubation period for FSE appeared slightly longer, but this was not statistically different from the mean incubation period of the first passage experiment. The reason for this tendency is unclear but it had already been reported for ovine BSE transmitted to this model (296 d.p.i at first passage to 365 d.p.i at 2nd passage) [17]. However, it remained within the range of expected duration for BSE agent transmitted to this transgenic mouse model.

The comparison of FSE and BSE lesion profiles indicates clear resemblance in the shape and severity of vacuolation of the nine referential gray matter sites, consistent with the hypothesis of similarity between the infectious agents responsible for these TSE cases. In the same way, the systematic assessment of PrPd-accumulation sites and type revealed additional supportive arguments: PrPd depositions were also found in the cortex, septum, hippocampus, thalamus, hypothalamus, midbrain and brain stem, in structures all previously identified as accumulation sites in past experiments using different BSE sources [2], [15]–[17]. More characteristically in this transgenic mouse model, the typical amyloid florid plaques detected in each group indicated that the infectious agent present in the case of the mother cheetah was similar to the one responsible for the BSE in cattle. Collectively, these transmission data therefore clearly signified that the FSE case 1 was linked to the classical BSE agent.

As established for other species such as mink affected with transmissible mink encephalopathy [25], oral contamination appeared as the most obvious cause in that case. It is likely that this case, born in 1989 in a UK zoo, like other previously-described FSE cases in cheetah (born before 1986 and fed with cattle carcasses) [10]), was exposed to a BSE risk mainly during the first year of her life, before being exported in 1993 to Peaugres Safari Park in France. Contamination with another TSE source such as scrapie appears less likely, since scrapie is not transmittable to domestic cats, at least via the intracerebral route [26].

The occurrence of the second case reported here is of great interest since for this female cheetah the meat source was exclusively from rabbits and hens freshly killed or beef (minced steak fit for human consumption), every effort being made to avoid any possible risk of oral contamination with the BSE agent. In April 1996, immediately after the identification of the first cases of vCJD in the UK and France, essential precautionary measures were implemented, with a ban on the introduction of specified risk materials (SRM), including bovine brain and spinal cord, into the human and animal food chain. In addition, cheetahs are threatened with extinction and the species is classified as Vulnerable on the IUCN Red List, with subspecies venaticus and hecki classified as Critically Endangered. They appear on Annex I of the Convention on International Trade in Endangered Species of Wild Fauna and Flora (CITES). Captive specimens are managed in the context of breeding and conservation programs (EEP in Europe) where participating zoos including La Palmyre and Peaugres work in cooperation.

Moreover, lack of genetic diversity and the difficulty of breeding them in captivity make these animals very precious in zoological collections and they receive special care from the staff, including their diet which is evaluated for nutritional and sanitary risks. In addition, this female cheetah was not in contact with any other identified FSE-affected cheetah, except her mother. It therefore seems most likely that this female cheetah was contaminated through the vertical transmission of a prion agent related to BSE. The mother started to express the first clinical symptoms of FSE about 2 months before giving birth, suggesting that during the gestation as well as the suckling periods the little cheetah could have been exposed to the infectious agent from the mother. At the very least, these critical periods were those when the mother accumulated a maximum of PrPd. It is not possible to determine the precise way (in utero, via placenta, at birth, after birth via colostrums/milk) by which the infectious agent may have contaminated the young female cheetah. Anatomically, in the cheetah as in other carnivores, there is an endothelio-chorial placenta, a type of placenta facilitating exchanges between the mother and the fetus, in particular thanks to the proximity of their vascular elements. This is not the case of ruminants, which have an epithelio-chorial placenta and for which the risk of this type of transmission is thus very low. The mother gave birth to 5 individuals and 2 little cheetahs died in the first days after birth. At present, the 2 brothers of the FSE case 2 are still alive and healthy, living in 2 other, different French zoos, suggesting that the dose of infectious agent must not have been very high. In that context, the hypothesis of transmission of the disease via colostrums or milk is also credible, first because cellular as well as pathological forms of PrP have been detected in ruminant mammary glands [27], [28], second because PrPc (the acknowledged protein substrate for PrPd conversion) exists in the milk of domestic ruminants [27] and third because the possibility of transmitting the disease through milk and colostrums has recently been shown in the sheep species [29], [30]. In that hypothesis, the fact that PrPd was detectable in the lymph nodes of this cheetah is also remarkable because the lymphoreticular system seems to play a substantial role in facilitating neuroinvasion in the event of low doses of infective agent as demonstrated in a scrapie infection model of hamsters [31]. The age for onset of the disease (between 6 and 7 years) as well as the clinical symptoms seem to be comparable for the two FSE cases, and the fact that the incubation period was not shortened in the daughter is in accordance with the hypothesis of a low dose infection.

The comparison of PrPd brain mapping and type of deposition does not reveal obvious differences either in the brain structures affected or in the intensity of PrPd accumulation. The thalamo-cortical PrPd labeling might explain the sensorial dysfunctions observed in both cases, and the strong PrPd accumulation seen in the cerebellum may be at least a contributor to the loss of equilibrium. Finally the transmission studies of this second FSE case to TgOvPrP4 should make it possible to establish whether or not the parameters of the BSE strain reported here for the mother are stable.

In summary, although oral contamination by the BSE agent could not be totally excluded, the elements reported in the present article indicate collectively that the 2nd case of cheetah FSE, concerning an animal born in France, is most likely due to maternal transmission from a cheetah harboring the same strain of agent as the cattle BSE agent.

Beside the epidemiological significance of this finding (and this may have some impact on our knowledge of FSE cases in domestic cats in which the possibility of a maternal transmission should be taken into account) it may have some incidence on the question of vertical transmission of other TSEs, especially those linked to the BSE agent. In the case of BSE in sheep, it appears that maternal transmission can occur [32], [33]. In cattle, there is no evidence of vertical transmission of either natural or experimental BSE even though the risk has been analyzed [34], but the peripheral pathogenesis of the BSE agent is also much more restricted, compared to the case of sheep or humans. Prion protein immunostaining and infectivity have been reported in lymphoreticular tissues in vCJD cases, as in the present FSE cases. Despite this, vertical transmission had not been found until now in vCJD cases. This question is still a current issue and a recent article underlines the caveats and difficulties in excluding this possibility, principally due to the limited availability of data concerning children in vCJD cases and a relatively short period of observation [35]. In this context, our article should bring additional elements for consideration in the hypothesis of a vertical transmission of the human disease linked to the BSE agent.

Materials and Methods Top Cases history Case 1.A female cheetah (Acinonyx jubatus) born in September 1989 at Whipsnade Wild Animal Park in UK was exported in May 1993 to Safari Parc de Peaugres in France. Like other previously-described FSE cases in cheetah, this animal may have been exposed to a BSE agent contamination through its food. In mid-June 1997, she was suspected of developing a spongiform encephalopathy as she showed abnormal neurological signs. Locomotor abnormalities such as incoordination, symmetrical hindlimb ataxia with staggering, robotic movements of the forelimbs and also postural difficulties were observed. She also presented alimentary disorders such as polydypsia and polyphagia and she was over-weight, but slowly lost weight from eight months before the onset of the nervous signs even though she continued eating normally. The female became anxious for several months before giving birth in April 1997. Her maternal behavior was completely different from that expressed at the time of her first litter, when she had been an excellent mother. Despite the development of the disease she was left to raise the litter for as long as possible and she continued suckling the young during this period until, after 5 weeks, euthanasia became unavoidable in July 1997.

The animal was brought for diagnosis to the French National Reference Laboratory for animal TSEs (AFSSA-Lyon). The lymph nodes, tonsils and the brain were quickly removed; eight coronal slices were cut from the forebrain to the C1 spinal cord segment. All these slices were then dissected mid-sagitally, one half being rapidly frozen and kept at -20°C for later use in molecular diagnosis, the other being fixed by immersion in a buffered formalin solution (10%, pH 7.4) for histopathological examination.

Case 2.One of the three young cheetahs born in April 1997 was sent in December 2002 to another French zoo, La Palmyre, at Les Mathes (Charente-Maritime). This young female was suckled until the death of the mother and was then fed exclusively, at Peaugres as well as in La Palmyre zoo, with freshly-killed rabbits and hens or with beef (minced steak fit for human consumption). In La Palmyre zoo, she was in contact with other female cheetahs and occasionally with males but none were FSE positive.

Posterior lameness started at the end of January 2004 and FSE was suspected only five days later because of the occurrence of ataxia and increasing lateral decubitus. The symptoms then evolved very quickly with additional signs of FSE such as head trembling, hyper salivation and difficulty in standing. In early March, hyper-excitability, loss of equilibrium in a stationary state and clear loss of weight were also present, and euthanasia was programmed roughly 2 months after occurrence of the first symptoms. Brain and other tissues (lymph nodes, spleen, tonsils, a piece of intestine) were either fixed by immersion in a buffered formalin solution (10%, pH 7.4) or frozen and kept at -20°C.

Transmission studies in Tg(OvPrP4) mice A first passage of cheetah FSE was carried out on a first group of 10 female Tg(OvPrP4) mice -4 to 6 weeks-old – injected by the intracerebral (i.c.) route with 20 µl of 10% (in a saline buffered solution containing 5% glucose) from the brainstem of the cheetah FSE case 1. A second passage was carried out on a second group of 10 female Tg(OvPrP4) mice -4 to 6 weeks-old – injected by the i.c. route with 20 µl of 1% brain homogenates from a first passage diseased mouse. The control groups consisted of 10 female Tg(OvPrP4) mice, i.c. injected with cattle BSE (1st passage) and a Tg(OvPrP4) mouse infected with classical cattle BSE (2nd passage).

Mice were housed in a temperature-controlled (22°C) room on a 12 hr light/12 hr dark cycle. Food and drinking solution were available ad libitum. All procedures were carried out in compliance with the French Ethical Committee (Decree 87–848) and European Community Directive 86/609/EEC and were authorized (No. 98) by the CREEA (Regional Committee for Ethical Experimentation on Animals).

The mice were sacrificed at clinical end-point. The incubation period for each transgenic mouse was calculated as the interval between injection and death. Brains were removed and fixed in buffered formalin solution (10%, pH 7.4) for histopathological assessment (n = 5 to 6 per group). Statistical analyses of survival periods were performed using the log-rank test; p values <0.05 href="mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000243/!x-usc:http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0006929">http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0006929




http://felinespongiformencephalopathyfse.blogspot.com/


ALSO, see ;



1: Schweiz Arch Tierheilkd. 1998;140(6):250-4. Links

[182 offspring of cows with bovine spongiform encephalopathy (BSE) in Switzerland. 2. Epidemiology and pathological findings] [Article in German]


Fatzer R, Ehrensperger F, Heim D, Schmidt J, Schmitt A, Braun U, Vandevelde M. Institut für Tierneurologie, Universität Bern.


In order to detect lesions of a spongiform encephalopathy and/or accumulation of the protease resistant prion protein (PrPres), 182 offspring of cows affected with BSE were examined neuropathological and immunohistochemically. Neither spongiform encephalopathy nor PrPres accumulation were found. In seven animals other neuropathological lesions were seen, significant ones in three. Because of the small risk of exposure to contaminated feed in these animals, nearly all of which were born after the introduction of the protein feed ban for ruminants, the occurrence of spongiform encephalopathy in this series of BSE offspring would be suggestive of maternal transmission. However, the value of the study in this respect is quite limited. Only half of the animals were old enough to develop clinical and pathological evidence of the disease. If a maternal effect on the risk for the offspring is only to be expected during the last 6 months of the incubation of the dam as suggested by British investigations, only few animals in this study would fulfil the requirement of having been born during this critical period. Since it cannot be entirely excluded that the BSE agent transiently invades extraneural tissues in the early stages of infection, the above mentioned restriction to the final 6 months of the incubation time of the dam would not necessarily be applicable to all situations. We concluded that this study supports previous observations according to which maternal transmission of BSE is at best a rare event.


http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=Retrieve&list_uids=9646714&dopt=abstractplus



TSS

Wednesday, April 1, 2009

Immunohistochemical study of PrPSc distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy

Research article

Immunohistochemical study of PrPSc distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy


Monika M Hilbe , Guido G Soldati , Kati K Zlinszky , Sabina S Wunderlin and Felix F Ehrensperger

BMC Veterinary Research 2009, 5:11doi:10.1186/1746-6148-5-11

Published: 31 March 2009

Abstract (provisional) Background Two domestic shorthair cats presenting with progressive hind-limb ataxia and increased aggressiveness were necropsied and a post mortem diagnosis of Feline Spongiform Encephalopathy (FSE) was made. A wide spectrum of tissue samples was collected and evaluated histologically and immunohistologically for the presence of PrPSc. Result Histopathological examination revealed a diffuse vacuolation of the grey matter neuropil with the following areas being most severely affected: corpus geniculatum medialis, thalamus, gyrus dentatus of the hippocampus, corpus striatum, and deep layers of the cerebral and cerebellar cortex as well as in the brain stem. In addition, a diffuse glial reaction involving astrocytes and microglia and intraneuronal vacuolation in a few neurons in the brain stem was present. Heavy PrPSc immunostaining was detected in brain, retina, optic nerve, pars nervosa of the pituitary gland, trigeminal ganglia and small amounts in the myenteric plexus of the small intestine (duodenum, jejunum) and slightly in the medulla of the adrenal gland.

Conclusions The PrPSc distribution within the brain was consistent with that described in other FSE-affected cats. The pattern of abnormal PrP in the retina corresponded to that found in a captive cheetah with FSE, in sheep with scrapie and was similar to nvCJD in humans.

snip...

In cattle orally infected with BSE immunostaining in the follicles of the distal ileum was observed only after the onset of clinical disease at 36, 38 and 40 months after exposure [27]. Neurons in the enteric nervous system were positive in only one animal from each of the groups killed 38 and 40 months after exposure, but even then the staining was sparse and confined to the myenteric plexus. In contrast none of the follicles in the distal ileum showed evidence of immunostaining for PrPSc and only a few animals showed sparse staining in the myenteric plexus in naturally affected cattle with BSE. The mesenteric lymph nodes were negative 6 months after exposure in the experimental animals. Some authors concluded that the restricted distribution of the BSE agent in the lymphoreticular system of cattle contrasts with the distribution of the scrapie agent in sheep which, in most cases, spreads rapidly after the initial early involvement of the system [27]. The restricted distribution of BSE appears to be also true for FSE. Mice inoculated intraperitoneally or intracerebrally with brain material from cats with FSE had progressive neurological signs similar to those seen in mice affected with scrapie or BSE. Moreover some authors postulate, that the distribution of vacuolar degeneration was identical to that seen in mice terminally infected with primary sources of BSE and the lesion profile in mice 12 inoculated with FSE resembles that observed in BSE, rather than scrapie. It was postulated, therefore, that BSE and FSE probably arose from a common source [10]. The source of infection at least in one cat presented here could have been canned food contaminated with nervous tissue of BSE infected cattle before the ban.

Conclusions In conclusion, the two FSE cases described here had essentially the same histological lesions and PrPSc distribution in the brain and the peripheral tissues as reported in earlier FSE cases. In addition we were able to demonstrate PrPSc accumulation in the retina, the neurohypophysis, trigeminal ganglion and in the adrenal medulla, but not in lymphatic tissues nor in the bone marrow. The kidneys showed random immunohistochemical staining in the mesangial glomerular tufts. This was seen in the kidneys of one FSE as well as in the control cats. Even though in experimentally infected Syrian hamsters and in scrapie infected sheep a possible prionuria and infectivity of urine is postulated, our findings confirm previously reported observations in the kidney of FSE cases, showing that immunohistochemical labelling of glomerular structures has to be regarded as unspecific. In summary, the distribution of PrPSc in FSE is similar to BSE but different from classical scrapie. In analogy, horizontal PrPSc transmission in FSE appears to be unlikely.

see full text ;




http://www.biomedcentral.com/content/pdf/1746-6148-5-11.pdf






see also ;



DIA-45

FELINE SPONGIFORM ENCEPHALOPATHY: FIRST CONFIRMED CASE REPORTED IN PORTUGAL

J.F. Silva1, J.J. Correia, 1 J. Ribeiro2, S. Carmo2 and L.Orge31 Faculdade de Medicina Veterinária (UTL), Lisbon, Portugal 2 Clínica Veterinária Ani+, Queluz, Portugal 3 Laboratório Nacional de Investigação Veterinária, Unidade de BSE, Lisbon, PortugalFeline spongiform encephalopathy (FSE), affecting domestic and captive feline species, is a prion disease considered to be related to bovine spongiform encephalopathy (BSE). Here we report the first case diagnosed in Portugal, highlighting the neuroapthological findings. In 2004 a 9-year old intact female Siamese cat was referred with chronic progressive behavioural changes, polydipsia, gait abnormalities and episodes of hypersalivation. Clinical signs progressed to tetraparesis and dementia and euthanasia was performed. At necropsy, brain and spinal cord had no significative changes. Tissue samples from brain, cerebellum, brainstem and spinal cord were collected for histopathology and immunohistochemistry for detection of PrPres. Histology revealed neuropil and neuronal perikarion vacuolation in several areas of the central nervous system together with gliosis and cell rarefaction at the granular layer of the cerebellum. Immunohistochemical detection of PrPres showed a strong and widespread PrPres accumulation as granular and linear deposits as well as associated with some neurons. These findings are supportive of FSE. To the authors knowledge this is the first confirmed case of FSE reported in Portugal.




http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf






HOUND STUDY

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.

snip…




http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf





2005 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

GTN: FAX:

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://web.archive.org/web/20010305222642/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

IN CONFIDENCE

CONCEPT NOT FOR FURTHER STUDY OF MATERIAL OBTAINED IN A SURVEY OF HOUNDS FOR EVIDENCE OF A SCRAPIE-LIKE SPONGIFORM ENCEPHALOPATHY (SE)

snip…

b) Fibrillar material closely similar to SAF, found in BSE/Scrapie, was observed in 19 (4.3%) cases, all of which were hounds > 7 years of age. 14/19 of these suspected SAF results correlated with cases in the unresolveable histopathological category.

snip…

The following proposals address the hypothesis that the hound survey observations represent a PrP related or scrapie-like disease of dogs in which the pathological response, and possible the spread of infectivity, is neuroanatomically localized. By inference this could also mean that the disorder is clinically silent and non-progressive.




http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1995/02/09001001.pdf





http://www.mad-cow.org/00/aug00_late_news.html#ggg





http://www.kxnet.com/getForumPost.asp?ArticleId=113652





http://www.keeneequinox.com/home/index.cfm?event=displayArticleComments&ustory_id=4d8de1c2-fa09-42dc-958a-7e94e16e22db





PET FOODS MAD CATS AND MAD DOGS BSE/TSEs

worse still, there is serious risk the media could get to hear of such a meeting…

snip…

Crushed heads (which inevitably involve brain and spinal cord material) are used to a limited extent but will also form one of the constituent raw materials of meat and bone meal, which is used extensively in pet food manufacturer…




http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1989/03/17004001.pdf





2. The Parliamentary Secretary said that he was concerned about the possibility that countries in which BSE had not yet been detected could be exporting raw meat materials (in particular crushed heads) contaminated with the disease to the UK for use in petfood manufacture…

snip…

YOU explained that imported crushed heads were extensively used in the petfood industry…




http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1989/04/14001001.pdf





In particular I do not believe one can say that the levels of the scrapie agent in pet food are so low that domestic animals are not exposed…




http://web.archive.org/web/20010305222642/www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf






HOWEVER, why ignore the old science and transmission studies to date ???

Species Born Onset/Died

Ocelot May 1987

Mar 1994

Ocelot Jul 1980 Oct 1995

Puma 1986 May 1991

Puma 1980 May 1995

Puma 1978 May 1995

Lion Nov 1986 Dec 1998

Tiger 1981 Dec 1995

Tiger Feb 1983 Oct 1998

Ankole 1987 May 1995

Ankole 1986 Feb 1991

Bison 1989/90 Oct 1996

Maff data on 15 May 99

kudu 6

gemsbok 1

nyala 1

oryx 2

eland 6

cheetah 9

puma 3

tiger 2

ocelot 2

bison 1

ankole 2

lion 1





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






Feline Spongiform Encephalopathy (FSE) FSE was first identified in the UK in 1990. Most cases have been reported in the UK, where the epidemic has been consistent with that of the BSE epidemic. Some other countries (e.g. Norway, Liechtenstein and France) have also reported cases.Most cases have been reported in domestic cats but there have also been cases in captive exotic cats (e.g. Cheetah, Lion, Asian leopard cat, Ocelot, Puma and Tiger). The disease is characterised by progressive nervous signs, including ataxia, hyper-reactivity and behavioural changes and is fatal.The chemical and biological properties of the infectious agent are identical to those of the BSE and vCJD agents. These findings support the hypothesis that the FSE epidemic resulted from the consumption of food contaminated with the BSE agent.The FSE epidemic has declined as a result of tight controls on the disposal of specified risk material and other animal by-products.References: Leggett, M.M. et al.(1990) A spongiform encephalopathy in a cat. Veterinary Record. 127. 586-588Synge, B.A. et al. (1991) Spongiform encephalopathy in a Scottish cat. Veterinary Record. 129. 320Wyatt, J. M. et al. (1991) Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.Gruffydd-Jones, T. J.et al.. (1991) Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.Pearson, G. R. et al. (1992) Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.Willoughby, K. et al. (1992) Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.Fraser, H. et al. (1994) Transmission of feline spongiform encephalopathy to mice. Veterinary Record 134. 449.Bratberg, B. et al. (1995) Feline spongiform encephalopathy in a cat in Norway. Veterinary Record 136. 444Baron, T. et al. (1997) Spongiform encephalopathy in an imported cheetah in France. Veterinary Record 141. 270-271Zanusso, G et al. (1998) Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. Lancet, V352, N9134, OCT 3, Pp 1116-1117.Ryder, S.J. et al. (2001) Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy. Veterinary Record 146. 437-441Kelly, D.F. et al. (2005) Neuropathological findings in cats with clinically suspect but histologically unconfirmed feline spongiform encephalopathy. Veterinary Record 156. 472-477.TSEs in Exotic Ruminants TSEs have been detected in exotic ruminants in UK zoos since 1986. These include antelopes (Eland, Gemsbok, Arabian and Scimitar oryx, Nyala and Kudu), Ankole cattle and Bison. With hindsight the 1986 case in a Nyala was diagnosed before the first case of BSE was identified. The TSE cases in exotic ruminants had a younger onset age and a shorter clinical duration compared to that in cattle with BSE. All the cases appear to be linked to the BSE epidemic via the consumption of feed contaminated with the BSE agent. The epidemic has declined as a result of tight controls on feeding mammalian meat and bone meal to susceptible animals, particularly from August 1996.References: Jeffrey, M. and Wells, G.A.H, (1988) Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet.Path. 25. 398-399Kirkwood, J.K. et al (1990) Spongiform encephalopathy in an Arabian oryx (Oryx leucoryx) and a Greater kudu (Tragelaphus strepsiceros) Veterinary Record 127. 418-429.Kirkwood, J.K. (1993) Spongiform encephalopathy in a herd of Greater kudu (Tragelaphus strepsiceros): epidemiological observations. Veterinary Record 133. 360-364Kirkwood, J. K. and Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record. 135. 296-303.Food and Agriculture Organisation (1998) Manual on Bovine Spongiform Encephalopathy.



http://www.defra.gov.uk/animalh/bse/othertses/index.html#fse






snip... full text ;




http://chronic-wasting-disease.blogspot.com/2008/12/lions-and-prions-and-deer-demise.html






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