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

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






TSS