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

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.



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