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SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Draft minutes of the 96th meeting held on 20th February 2007 ITEM 9 – ANY OTHER BUSINESS 54. The Chair noted that a paper had been provided to update the committee on an ongoing study on the susceptibility of red deer to BSE. To date, BSE had transmitted to four ic challenged deer, however no orally challenged deer had succumbed to the disease. http://www.seac.gov.uk/minutes/96.pdf ----- Original Message ----- Subject: SEAC 93rd MEETING ON THURSDAY 6TH JULY 2006 'AGENDA' (cwd) Draft minutes of the open session of the 92nd meeting held on 28th April 2006 ISSUE 1. At SEAC 85, SEAC reviewed the possible public and animal health implications of chronic wasting disease (CWD) in UK deer and produced a position statement. The committee concluded that CWD currently poses relatively little risk to human health, or to the health of cattle, sheep or goats in the UK. Nevertheless, as a risk cannot be excluded a watching brief should be maintained. In response to the recommendation that a watching brief be maintained, the SEAC secretariat have produced a review of the research on CWD published since 2004. BACKGROUND 2. CWD is the only known transmissible spongiform encephalopathy (TSE) to occur naturally in cervids. The disease is endemic in a number of captive and free-ranging cervid species (mule deer, white-tailed deer, Rocky Mountain elk and moose) in many areas of North America. With the exception of deer imported into South Korea, CWD has not been detected elsewhere in the world. CWD is naturally transmissible from infected to susceptible cervids and although the primary route(s) of infection remain unclear it is possible that it may be transmitted via contaminated environments. The origins of the disease are unknown. 3. CWD is experimentally transmissible to non-cervid species by intracerebral inoculation. However, oral transmission of CWD has only been successful to North American cervid species. It is unclear whether CWD could be naturally transmitted to other cervid and non-cervid species. 4. There have been no reported cases of transmission of CWD to humans through the consumption of infected venison. There is however limited epidemiological data on possible transmission of CWD to humans through this route. 5. It is probable that captive and free-ranging deer species in the UK were exposed to contaminated mammalian meat and bone meal 2 © SEAC 2006 prior to its ban in 1996. Studies investigating experimental transmission of BSE to cervids are ongoing. Although no TSEs have been detected in deer populations in the UK or elsewhere in Europe, surveillance data are limited. As such it remains possible that BSE may have been transmitted to UK deer which could present a risk to consumers of venison. PREVIOUS SEAC ADVICE 6. At SEAC 85, SEAC considered the possible public and animal health implications of CWD in UK deer based on a review of published, and some unpublished, research on CWD, together with surveillance data on TSEs in European cervids and information on UK cervid populations. The committee also considered the possibility that BSE may be present in UK deer. A position statement summarising SEAC's consideration was produced1. REVIEW OF CWD RESEARCH 7. To address a recommendation made in the SEAC position statement on CWD to keep a watching brief on emerging research on CWD, a review of the published scientific literature from October 2004 to May 2006 on CWD has been prepared by the SEAC Secretariat (see Annex 1). The original literature review is also provided at Annex 4 for ease of reference. Summary of new research 8. In summary the new information shows that: • to date, only one strain of CWD has been identified conclusively however, limited research had shown the possible presence of a further strain. • the geographical distribution of CWD in cervids continues to widen in North America. No cases of TSE infection have been identified in surveys elsewhere in Europe or elsewhere in the world with the exception of an imported case of CWD in South Korea, although the surveys in deer have been limited. • the host range broadened with confirmation of a first case of CWD in free ranging moose in September 2005. 1 SEAC (2004) Chronic wasting disease in UK deer. http://www.seac.gov.uk/statements/state180105.htm 3 © SEAC 2006 • it is possible that TSEs may be transmitted via contaminated soils lending support to existing evidence on the possibility of environmental transmission of the CWD. • the susceptibility to, and incubation period of, CWD in elk is influenced by polymorphisms in codon 132 of the elk prion protein gene. • after more than 7 years following oral inoculation of cattle with CWD-infected brain tissue, cattle show no clinical signs of CWD. • cattle intracerebrally (ic) inoculated with CWD infected brain tissue develop neuropathological patterns distinct from those of BSE infection. • PrPCWD can be detected in the skeletal muscles of CWD infected cervids by bioassays using transgenic mice expressing the cervid PrP. • CWD has been transmitted to non-human primates but not to humanised mice after ic inoculation of brain material from CWD infected cervids. FSA RESEARCH ON TSEs IN DEER 9. A FSA funded study continues to investigate whether UK red deer are susceptible to BSE infection by oral or ic challenge (Annex 2). The study is set for completion in 2007. To determine the preclinical status of deer a rectal biopsy method has been employed with samples taken every 6 months from all remaining animals in the study. To date, there are no clinical or pathological signs of BSE in orally or ic challenged animals at 26 and 20 months respectively. Please note that Annex 2 has not been circulated outside the committee as it contains new scientific data that has not yet been published in a scientific journal. ADVICE SOUGHT FROM THE COMMITTEE programme for Chronic Wasting Disease in the European Union Question N° EFSA-Q-2003-088 Adopted on 3rd June 2004 programme for Chronic Wasting Disease in the EU http://www.efsa.eu.int 1 of 32 Annex: Report of the EFSA working group on a surveillance program for Chronic Wasting Disease (CWD) in the EU TABLE OF CONTENTS 1 Preamble..........................................................................................................................1 2 Introduction.....................................................................................................................2 3 Diagnosis..........................................................................................................................4 4 Review Of The Different Screening Tests Used For The Diagnosis Of CWD............7 5 Surveillance of TSE in European cervid......................................................................10 6 Conclusions....................................................................................................................11 7 Recommendations..........................................................................................................13 8 Documentation provided to EFSA ...............................................................................14 9 Scientific Panel members ..............................................................................................14 10 Acknowledgement..........................................................................................................14 11 References......................................................................................................................15 Review of research published since November 2004 June 2006, SEAC Secretariat from CWD-infected mule deer with three calves kept as controls (Hamir et al, 2005). After six years, two of the inoculated animals showed clinical signs of infection. PrPres was found in the CNS of five inoculated animals however, the microscopic lesions expected in spongiform encephalopathy (SE) were subtle in three cases and absent in two cases. The eight remaining inoculated animals and three controls all tested negative for signs of infection. The study suggests that CWD may be weakly transmissible to cattle after ic inoculation. 16. In a follow-up study, six calves were inoculated ic with brain tissue derived from the PrPCWD positive cattle described in paragraph 15 (Hamir et al, 2006a). At 16.5 months, all six inoculated cattle showed acute clinical signs of disease resulting in the termination of the experiment. Although microscopical SE-type lesions were not observed in any of the cattle, PrPres was detected in CNS tissues. The authors noted that these findings were similar to those in a study of cattle inoculated with the scrapie agent where, in the absence of SE lesions, cattle showed clinical signs of infection and PrPres was found in CNS tissues. The authors suggest that distinct differences exist between CWD and BSE in cattle enabling clear identification of both diseases if natural transmission of CWD to cattle were to occur. likely that CWD arose from a spontaneous change of endogenous PrP resulting in a disease-associated and laterally-transmissible form of PrP, although direct data to support this hypothesis ___are lacking___. 6. The known natural hosts for CWD are mule deer (Odocoileus hemionus hemionus), black-tailed deer (Odocoileus hemionus columbianus), white-tailed deer (Odocoileus virginianus), Rocky Mountain elk (Cervus elaphus nelsoni) and moose (Alces alces). The prevalence and geographical distribution of CWD in these species appears to be increasing in North America in a manner which is unlikely to be due simply to increased surveillance. 14. Epidemiological data on possible CWD infection of humans are very limited. The possibility that clinical symptoms of CWD in humans differ from those of Creutzfeldt-Jakob Disease (CJD) cannot be excluded. There is no significant difference between the prevalence of CJD in CWD endemic areas and other areas of the world. However, because CJD surveillance in the USA is relatively recent, not all CJD cases may have been identified. Additionally, detection of a small increase in prevalence of such a rare disease is very difficult. Investigation of six cases of prion disease in young people (< 30 years of age) in the USA found no definite causal link with consumption of venison from known CWD endemic areas. The disease characteristics in these cases were indistinguishable from sporadic CJD or Gerstmann-Sträussler-Scheinker syndrome. Likewise, in a study of three hunters (> 54 years of age) diagnosed with sporadic CJD, no link with consumption of venison from CWD endemic areas was found. No causal link was found in an investigation of three men with neurological illnesses who were known to partake in “wild game feasts”. Only one of these subjects was found to have a prion disease and this was also indistinguishable from sporadic CJD. Written by Dr Debra Bourne, Wildlife Information Network, October 2004, for SEAC 211. To date, no transmission of CWD has been reported in domestic species living in CWD endemic areas or in research facilities with CWD. Monitoring is ongoing (Gould et al., 2003; Williams & Miller 2002; Belay et al., 2004). It has been possible to infect domestic cattle, goats and sheep by intracerebral inoculation, although not in all inoculated individuals (Hamir et al., 2003a; Hamir et al., 2004a); see paragraphs 66-67. Data from intracerebral inoculation experiments show that diagnostic methods currently in use for BSE surveillance would detect the CWD agent in cattle and sheep if it were present (Hamir et al., 2003a). 212. Data from in vitro experiments suggests that there may be a considerable “species barrier” limiting transmission of CWD from cervids to domestic cattle and, to a lesser extent, to domestic sheep. In a cell-free conversion system, PrPCWD from elk, mule deer or whitetailed deer showed 5-to-12-fold lower conversion efficiency of bovine PrP-sen than for intercervid conversion reactions; conversion efficiency of ovine PrP-sen (ovine PrP-AQ) was also less than half as efficient as for homologous cervid reactions (Raymond et al., 2000). 213. There is a theoretical risk than CWD could be transmitted to cattle via incorporation of infected tissue from Cervidae into meat and bone meal. The risk for this occurring in the USA was considered [in 1992] to be small “because CWD is believed to be rare and localized, and the proportion of harvested Cervidae whose offal is rendered is probably small” [in the USA] (Saunders, 1994). The feeding of ruminant-derived protein to ruminants has been banned in Canada and the USA since 1997 (Kahn et al., 2004). The US Food and Drug Administration (FDA) has, since November 2002, banned the use of “material from Chronic Wasting Disease (CWD)-positive animals, or animals at high risk for CWD, to be used as an ingredient in feed for any animal species.” Animals considered to be at high risk for CWD were stated to include animals from CWD-positive captive herds, free-ranging animals from the CWDendemic area in Colorado and Wyoming, deer from the CWD eradication zone in Wisconsin and also “deer from any areas designated around any new foci of CWD infection that might be identified through surveillance or hunter harvest testing” (FDA, 2002). Such policies should minimise the potential oral exposure of domestic ruminants to CWD-agent in feed. Potential risk to other species 214. Since BSE appears to have been transmitted orally to various Felidae (Kirkwood et al., 1995; Bourne, 2004b), the possibility of CWD being transmitted to carnivores must be considered. 215. Experimentally, CWD has been successfully transmitted by intracerebral inoculation to domestic ferrets (Mustela putorius fero) and to American mink (Mustela vison), but not to common raccoons (Procyon lotor) (Williams, Young & Marsh 1982; Williams & Young, 1992; Williams et al., 1992; Hamir et al., 2003c; Sigurdson et al., 2003). Since raccoons are highly adaptable carnivores which may include carrion in their diet (Hamir et al., 2003c), the lack of success in transmission of CWD to raccoons even by intracerebral inoculation is encouraging. 216. There is no published data on transmission or attempted transmission of CWD to felids or canids. 10) HUMAN HEALTH CONCERNS 217. To date there are no known cases of human prion disease attributable to CWD transmitted to humans (Belay et al., 2004). While limited epidemiological investigations to date have not shown any links between CWD and humans with spongiform encephalopathies CWD Review / Dr Debra Bourne / October 2004 / For SEAC / Page 45 of 66 this data must be considered along with a caveat: “because CWD is a relatively new TSE, it is unlikely that enough people have consumed enough CWD-affected cervids to result in a clinically or pathologically recognizable disease attributable to CWD, especially considering the very long incubation periods characteristic of TSE diseases.” (Race et al., 2002) Epidemiological investigations 218. Epidemiological investigations have failed to show any links between cases of prion disease in unusually young people or in hunters in the USA and CWD (CDC, 2003). Two major epidemiological investigations have been carried out, one on cases of CJD in unusually young individuals in the USA, the second on a group of men from Wisconsin who developed neurological diseases. 219. The first study (Belay et al., 2001) focused on three individuals, two 28 years of age and the third 30 years old, diagnosed with CJD in the USA between 1st January 1997 and 31st May 2000, and without any established risk factors for CJD (family history, receipt of human growth hormone, receipt of grafts of dura mater or cornea, or previous neurological surgery) and concluded that there was no strong evidence for a causal link with CWD. None of the individuals had travelled to Europe (therefore a link with BSE was unlikely). Two of the individuals were hunters who regularly consumed game meat while the third (case 1) had, as a young child, regularly consumed venison from animals hunted by family members and on two occasions from a family friend. Two of the individuals (cases 1 and 2) had undergone tonsillar surgery as children; the third had never received any surgical treatment. One individual (case 1) had eaten venison mainly hunted in Maine, occasionally hunted in New Jersey, and, on two occasions at about six years old, elk meat which had probably been harvested in Wyoming. The second person (case 2) had hunted cervids mainly in Utah, but had harvested an elk in southwestern Wyoming on one occasion (less than three years before onset of clinical signs) and had hunted in British Columbia on one occasion nine years before onset of illness. The third person (case 3) had hunted close to home and never in Colorado or Wyoming although the plant where he took his carcasses for processing did also process some elk from Colorado each year. The clinical signs, duration of illness and histopathological findings for the three individuals showed no obvious similarities to one another. One individual was methionine/methionine homozygous at codon 129 of the PRNP (case 1), one was homozygous for valine at this gene (case 2) and the third (case 3) was heterozygous methionine/valine. Immunohistochemistry revealed strong staining with a “synaptic” pattern in the first individual and weak staining with a “synaptic” pattern in the second case; in case 3, based on a brain biopsy sample obtained at an early point in the illness, staining was questionable and possibly showed a synaptic pattern. Cases 2 and 3 showed a “Type 1” immunoblot pattern, this test had not been carried out for case 1. It was noted that none of these three individuals had a definite history of consumption of venison from the geographical areas in which CWD was known to be endemic in Colorado and Wyoming, and no CWD had been identified in 299 deer and sampled from the area in which most of the venison consumed by patient 1 had originated, nor in 404 deer and 196 elk sampled from the area in which most of the venison consumed by patient 2 had originated, nor in 138 deer samples from the area in which most of the venison consumed by patient 1 had originated. Additionally, there was no homogeneity in phenotypic expression of the disease and all three possible options for coding at codon 129 of the PRNP gene were represented. Since a survey had indicated that approximately 40% of blood donors in the USA consumed venison from wild cervids, it was considered most likely that coincidence explained why three of the four young (30 years old or younger) individuals with sporadic CJD reported in the USA after March 1996 had consumed such meat (Belay et al., 2001). CWD Review / Dr Debra Bourne / October 2004 / For SEAC / Page 46 of 66 220. The second major epidemiological investigation centred around three men from Wisconsin and Minnesota who had died from degenerative neurological illnesses and who had participated in “wild game feasts” in northern Wisconsin. Full investigation including examination of fixed brain tissue confirmed CJD in only one of the three individuals. Wild game eaten during the feasts was harvested mainly in Wisconsin but also in areas of Colorado, Wyoming and Montana; CWD was not known to be endemic in the areas where the game was hunted at the time that the game was harvested. Further investigations of other possible attendees of the feasts revealed 34 participants, all male, of whom a total of seven were deceased, including the three individuals in the initial investigation. Causes of death in the other four deceased individuals were not attributed to nor associated with any degenerative neurological disorder and no signs or symptoms associated with a degenerative neurological disorder were noted for any of the remaining living participants of the feasts. It was noted that only one case of CJD had occurred among known participants at the feasts, that this case was consistent with the commonest form of sporadic CJD, that this individual had only participated in one feast and that it was unlikely that he had consumed CWDinfected venison at the feasts “because venison and other game from outside Wisconsin that was served at these feasts did not originate from known CWD-endemic areas.” Limitations of the investigations were noted to include reliance on recall of events from up to 25 years previously and the fact that not all participants in the feasts could be contacted and interviewed. However, those who were interviewed agreed in their recall of events (CDC, 2003). 221. It is important to recognise that the limited epidemiological investigations that have been carried out are not able to rule out the possibility that CWD might play a role in causing illness in humans (CDC, 2003). 222. Three further cases of prion disease in young humans in the USA have been investigated for possible links to CWD (Belay et al., 2004). The first case was a 25-year-old man who died in 2001 after about 22 months of illness. Gerstmann-Sträussler-Scheinker syndrome (GSS) was diagnosed by analysis of the prion gene, with a P102L mutation together with valine at codon 129 in the mutant allele. It was noted that the disease had occurred at an unusually young age, even for GSS, and the possibility that exposure to CWDinfected venison contributed to early onset of the disease could not be ruled out; the patient’s grandfather had regularly hunted in southeastern Wyoming, around the known CWD-endemic area, and had given venison to the patient’s family. Two other cases of prion disease occurred in individuals of 26 and 28 years of age, from adjacent counties, and with onset of illness only months apart, therefore an environmental source of infection was investigated. However, these two individuals were finally diagnosed with different prion diseases: sporadic CJD in one case and GSS in the other, indicating that a common cause was unlikely. In the first case CJD was confirmed from autopsy samples (by histopathology, immunohistochemistry and immunoblotting); the individual had no history of hunting nor of regular consumption of venison, and although he may have eaten venison originating from the Upper Peninsula of Michigan while at college CWD has never been detected in deer from Michigan. Phenotypically this individual fit the “MM2 sporadic CJD” phenotype described by Parchi et al. (1999). In the other case post mortem immunohistochemistry revealed prion deposition which was consistent with GSS and a GSS P102L mutation was detected in a blood sample from one parent (appropriate samples were not available from the affected patient); this individual may possibly have eaten venison from Michigan on one occasion at about two years of age (Belay et al., 2004). 223. A further three cases of CJD in individuals of 54 to 66 years old who were deer and elk hunters (two individuals) or ate wild-harvested venison (one individual) have been CWD Review / Dr Debra Bourne / October 2004 / For SEAC / Page 47 of 66 investigated. There was no evidence that any of these individuals had hunted in known CWDendemic areas; information available indicated hunting or eating venison from Washington State and Pennsylvania. Two individuals were V/V at codon 129 the third was M/M; they were considered to fit known subtypes of sporadic CJD (MM1, VV1 and VV2 subtypes as described by Parchi et al. (1999)). Further investigations were also made on the only two nonfamilial cases of CJD in individuals with a history of eating venison from the known CWD-endemic areas. One was reported to have eaten venison from two deer harvested in an area with endemic CWD, but both deer had been tested and not found to be CWD-positive; the patient’s illness was consistent with the CJD subtype MM1. The other individual grew up in a CWD-endemic area and ate locally-harvested venison; her disease fit the MM1 CJD phenotype and no atypical neurological features were noted (Belay et al., 2004). 224. Additional epidemiological notes are that the incidence and age distribution of CJD in Colorado and Wyoming, where CWD is thought to have been endemic for decades, are similar to those found in other areas of the USA. In Wyoming, seven cases of CJD have been reported between 1979 and 2000 with an average annual age-adjusted CJD death rate of 0.8 per million and no cases reported in humans less than 55 years old. In Colorado in the same period 67 cases of CJD have been reported, with an average annual age-adjusted CJD death rate of 1.2 per million (Belay et al., 2004). 225. In summary, there is no evidence of an increase in incidence of CJD in Colorado and Wyoming, nor have epidemiological investigations carried out so far found any evidence of a link between CWD and cases of CJD in persons in the USA (Belay et al., 2001; CDC, 2003; Belay et al., 2004). Laboratory studies 226. There is evidence from an in vitro cell-free system that there may be a considerable “species barrier” reducing the probability that CWD will affect humans. It was shown that PrPres associated with chronic wasting disease (PrPCWD) from elk, mule deer or white-tailed deer was able to readily induce substantial conversion of recombinant cervid PrPsen molecules form any of these three species to the protease-resistant state. In the same system, CWD-associated PrPres was shown to convert human PrPsen but at a much lower efficiency: more than 14-fold lower efficiency than inter-cervid conversion reactions and more than fivefold lower than conversion of human PrPsen by PrPres from the brains of humans with CJD (Raymond et al., 2000). While encouraging, interpretation of this study is complicated by the fact that conversion of human PrPC by PrPBSE and PrPSc from sheep were of similar efficacy, both being more than 10-fold less efficient compared with corresponding homologous conversions) and one of these appears to be orally transmissible to humans (BSE) while the other (scrapie) appears not to be (Raymond et al., 2000). In previous experiments PrPBSE had showed 10-fold greater conversion efficacy for bovine PrPsen than for human codon 129-M (methionine) PrPsen and 30-fold greater conversion efficacy than for human codon 129-V (valine) PrPsen, while ovine PrPSc showed five-fold greater conversion efficacy for ovine PrPsen than for human 129-M PrPsen and eight-fold greater conversion than for human 129- V PrPsen (Raymond et al., 1997). 227. Results of recent work in transgenic mice expressing human PrP (see paragraph 71), in which transmission of CWD from elk by intracerebral inoculation failed, was considered to “strongly suggest” a species barrier to transmission of elk CWD to humans (Kong et al., 2004). CWD Review / Dr Debra Bourne / October 2004 / For SEAC / Page 48 of 66 Potential risk from consuming cervid products Velvet antler 228. Limited studies to date indicate risk from this product may be very low. No CWDspecific PrP accumulation was detected in a sample of velvet from an elk stag which developed clinical CWD about three months later; there were severe brain lesions and extensive CWD-specific PrP staining in both the brain and peripheral lymphoid tissue of the stag (Kahn et al., 2004). Consumption of venison and other parts of the animal 229. PrPCWD has not been detected in muscle tissue from infected cervids (Spraker et al., 2002c). However, it has been recommended by the World Health Organisation that no parts or products of any animal know to be CWD-positive should be consumed (WHO, 2000). Public health authorities in the USA and Canada have indicated agreement with this (Canadian Food Inspection Agency, 2003; Chronic Wasting Disease Alliance, 2004). It has been suggested that if a harvested cervid is being tested for CWD, the test results should be awaited before the meat is eaten (Wisconsin Department of Agriculture, Trade and Consumer Protection, 2002). Authorities in North America have widely advised that (a) tissues likely to contain the greatest amount of CWD agent in infected cervids, including the brain, spinal cord, lymph nodes, spleen, tonsils and eyes, should not be consumed from any harvested deer; (b) meat should be boned out and fat and connective tissue removed (which would also remove lymph nodes); and (c) hunters should avoid eating meat from deer or elk which look sick or which test positive for CWD (Buege, 2002; Chronic Wasting Disease Alliance, 2004; Williams et al., 2002; Wisconsin Department of Agriculture, Trade and Consumer Protection, 2002; Belay et al., 2004). Potential risk from handling and processing cervids 230. In order to minimise any potential risk from exposure to the agent of CWD, hunters, meat processors and taxidermists handling cervid carcasses are advised to wear latex or rubber gloves when handling or dressing cervids from CWD-endemic areas, to minimise handling of brain and spinal cord, and to thoroughly wash knives and other implements after use on deer or elk carcasses (Belay, 2004; Williams et al., 2002). It has been suggested that the risk of “build-up” of infectious CWD agent in a venison processing plant would be unlikely (Buege, 2002). Potential risk from disposal of carcasses and subsequent contamination of ground/water/air 231. In 2002, a risk analysis was produced on disposal of deer from Wisconsin in municipal solid landfills. It was noted that it is not known how much infected material a human (or animal) must consume or be exposed to in order to be infected with CWD. The report took into account the probable species barrier for transmission to humans (Raymond et al., 2000). It was noted that the CWD agent is hydrophobic and likely to adhere to organic materials within a landfill, taking several months to move through the landfill, and that any infectivity exiting the landfill would be captured in the landfill effluent. If effluent was transferred to a wastewater plant (rather than recirculated in the landfill) the agent would be expected to partition with the sludge fraction, which would be diluted greatly with other solids and mixed with nine inches (22.5 cm) of topsoil, providing “an extremely large dilution factor.” It was concluded that there was no significant risk to human health from disposing of deer infected with CWD in properly constructed landfill sites (Olander, 2002). Page 1 of 43 © Defra 2006 EVALUATION OF ANIMAL FEED USE AND SUPPLY ROUTES IN THE UNITED KINGDOM AND THEIR VULNERABILITY TO CROSSCONTAMINATION DECONTAMINATION TECHNOLOGIES This research project aims to determine whether BSE can be transmitted to UK red deer by including infected material in their feed. http://www.food.gov.uk/science/research/researchinfo/bseresearch/tseresearch/m03programme/m03projilist/m03024/ Last Year Cost £ This Year Cost £ http://www.mrc.ac.uk/index/current-research/current-tse_portfolio_search/current-tse_search_results/current-tse_project_details.htm?PID=M03024 This study will determine in the first instance whether the BSE agent can actually be transmitted to red deer. If this is possible the study will also provide a description of any resultant clinical disease, pathological changes and positive control tissue material all of which would aid surveillance for BSE in deer within the UK . Site last updated: 22 Jun 2006 http://www.mri.sari.ac.uk/vir-dagleish-proj2.asp #################### https://lists.aegee.org/bse-l.html ####################
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