CHRONIC WASTING DISEASE IN UK DEER UPDATE SEAC 93-85
CHRONIC WASTING DISEASE IN UK DEER UPDATE SEAC 93-85
SEAC 93/2
CHRONIC WASTING DISEASE IN UK DEER UPDATE
2 1 MANDATE...........................................................................................................................................4 2 PREAMBLE.........................................................................................................................................4 3 CWD IN NORTH AMERICA ............................................................................................................5 3.1 HISTORICAL PERSPECTIVE OF OCCURRENCE ......................................................................5 3.1.1 CWD in captive and farmed cervidae......................................................................................5 3.1.2 CWD in free-ranging cervidae ................................................................................................6 3.2 NATURAL HOST RANGE..............................................................................................................7 3.3 EXPERIMENTAL TRANSMISSIBILITY.......................................................................................8 3.3.1 Transmissibility of CWD..........................................................................................................9 3.3.1.1 Intracerebral inoculation studies:....................................................................................................... 9 3.3.1.2 Oral and other natural exposure route studies ................................................................................. 10 3.3.2 Susceptibility of deer and elk to other TSEs ..........................................................................11 3.4 EPIDEMIOLOGY...........................................................................................................................11 3.4.1 Descriptive Epidemiological Features ..................................................................................11 3.4.1.1 Chronology of distribution in the USA ........................................................................................... 11 3.4.1.2 Chronology of distribution in CANADA ........................................................................................ 12 3.4.2 Evidence for lateral transmission ..........................................................................................13 3.4.3 The origin of CWD.................................................................................................................15 3.5 PATHOGENESIS ...........................................................................................................................16 3.5.1 Distribution of lesions / PrPCWD in clinically affected animals ..........................................17 3.5.2 Studies of PrPCWD in pre-clinically infected animals..........................................................18 3.5.2.1 Studies of PrPCWD in naturally exposed animals........................................................................... 18 3.5.2.2 Studies of PrPCWD in experimentally infected animals ................................................................. 18 3.5.3 Conclusions ...........................................................................................................................19 3.6 DIAGNOSIS ...................................................................................................................................19 3.6.1 Clinical diagnosis of CWD ....................................................................................................19 3.6.2 Laboratory Diagnosis............................................................................................................21 3.6.3 Laboratory diagnosis in live animals ....................................................................................22 Mule deer and white-tailed deer...................................................................................................................... 22 Elk................................................................................................................................................................... 22 3.7 SURVEILLANCE...........................................................................................................................23 3.7.1 Type and organisation of surveillance in free-ranging cervids .............................................23 3.7.1.1 USA................................................................................................................................................. 23 3.7.1.2 Canada............................................................................................................................................. 24 3.7.1.3 Planned surveillance on free ranging Cervidae in NA..................................................................... 24 3.7.2 Surveillance in farmed cervids ..............................................................................................25 3.7.2.1 USA................................................................................................................................................. 25 3.7.2.2 Canada............................................................................................................................................. 26 3.8 CONTROL STRATEGIES .............................................................................................................26 3.8.1 In the USA..............................................................................................................................26 3.8.2 In Canada ..............................................................................................................................28 3.8.3 Economic impact ...................................................................................................................29 4 TSE’S IN CERVIDS IN EUROPE ...................................................................................................30 4.1 THE HISTORICAL AND CURRENT SITUATION IN GREAT BRITAIN IN RELATION TO BSE 30 4.2 PAST AND CURRENT SURVEILLANCE IN EUROPE .............................................................31 5 POSSIBLE GLOBAL OCCURRENCE OF TSES IN FARMED CERVIDAE ...........................33 6 FOOD AND FEED SAFETY AND HUMAN AND ANIMAL RISK ...........................................34 6.1 FOOD SAFETY..............................................................................................................................35 6.2 FEED SAFETY AND ANIMAL HEALTH ...................................................................................36
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
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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
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• 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
10. The SEAC position statement on CWD has been revised to reflect the new data (see Annex 3). Members are requested to consider the new research published on CWD and comment on and agree the revisions to the statement.
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SEAC 93/2 ANNEX 1
A review of research on chronic wasting disease published since November 2004 SEAC Secretariat
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Restricted: Unpublished data SEAC 93/2 ANNEX 2 A summary of Food Standards Agency research on the susceptibility of UK red deer to BSE
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SEAC 93/2 ANNEX 3
Proposed revision of the SEAC position statement on chronic wasting disease in UK deer. Changes from the current statement are highlighted
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A review of the science on chronic wasting disease (October 2004) Wildlife Information Network
Position statement - Chronic wasting disease in UK deer
Introduction
1. The Food Standards Agency asked SEAC to consider the possible public and animal health implications of chronic wasting disease (CWD), in particular the level of risk posed to consumers of meat from infected animals. The committee also considered the possibility that BSE may be present in UK deer.
Background
2. CWD has emerged as an endemic transmissible spongiform encephalopathy (TSE) in certain captive and free-ranging species of cervid (deer) in some areas of North America. The disease is characterised by weight loss and behavioural changes in infected animals, usually over a period of weeks or months leading to death. CWD has not been found in the UK or elsewhere in Europe. No definitive or suspected cases of transmission of CWD to humans have been reported.
3. SEAC considered a review of the published, and some unpublished, research on CWD, together with surveillance data on TSEs in European cervids and information on UK cervid populations (1).
Origins
4. The origins of CWD are unknown. On the basis of epidemiological data, it is highly improbable that CWD originated from the recycling of mammalian protein in processed feed. It has been suggested that CWD may have arisen from transmission and adaptation of scrapie from sheep to cervids, as a result of a spontaneous change of endogenous prion protein (PrP) to an abnormal disease-associated form, or from an unknown source.
5. Data supporting any of these possible origins of CWD are either absent or equivocal. Although CWD could have originated from scrapie, the differing properties of the two prion diseases in strain typing bioassays, whilst limited, do not support this hypothesis. Evidence for multiple strains of CWD is equivocal. It seems most 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.
Host range
6. The known natural hosts for CWD are mule deer (Odocoileus hemionus hemionus), black-tailed deer (Odocoileus hemionus columbianus), white-tailed deer (Odocoileus virginianus) and Rocky Mountain elk (Cervus elaphus nelsoni). 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.
7. There are no direct data relating to the transmissibility of CWD to UK cervid species. However, comparison of a limited number of PrP codons indicates some homology in the endogenous PrP gene of European and North American cervid species. Thus, the possibility that UK cervids may be susceptible to CWD cannot be excluded, in particular red deer (Cervus elaphus elaphus) which are closely related to elk.
8. There is no evidence to suggest that CWD is present in UK cervids. However, because surveillance in the UK is very limited, a low level prevalence of CWD cannot be ruled out. The committee endorsed the opinion of the European Food Safety Authority on CWD surveillance in the European Union (2004) .
9. Transmission studies using parenteral routes of administration to cattle, sheep and a single goat, together with data from in vitro PrP conversion experiments, suggest that a significant barrier to CWD transmission to these species may exist. No transmission has been evident so far in an on-going oral transmission study in cattle after six years. Furthermore, no signs of infection have been observed from monitoring of cattle co-habiting areas with infected cervids, or in cattle, sheep or goats in close contact with infected cervids in research facilities. Thus, although the data are limited, there is currently no evidence to suggest that CWD can be transmitted naturally to cows, sheep or goats, and it is likely that there is a strong species barrier to such transmission.
Routes of transmission
10. Epidemiological data indicate that lateral transmission between infected and susceptible cervids occurring naturally is sufficiently effective to maintain epidemics in both captive and free-living populations. There is good evidence from studies of cervids inhabiting paddocks previously inhabited by infected animals or contaminated with infected carcases, that CWD can be transmitted laterally between animals via the environment. The precise mechanism of transmission is unclear. It is possible that the infectious agent is shed in the saliva, faeces or urine or as a result of decomposition of infected carcases and transferred to other cervids grazing the contaminated areas. It is also possible that some maternal transmission occurs.
11. There have also been suggestions that the lateral transmission of CWD may be influenced by environmental factors.
Pathogenesis
12. Information on the pathogenesis of CWD is limited. The data show that, following oral challenge, PrPCWD is first detected in the oral and gut-associated lymphoid tissues before spreading more widely within the lymphoid system and then to the brain. Involvement of the retropharyngeal lymph nodes or tonsils in the pathogenesis may not occur in some elk. At the microscopic level, the nature and distribution of the tissue lesions are similar to those found for scrapie. The available data suggest the pathogenesis of CWD is similar to scrapie.
BSE in UK deer
13. Both captive and free-ranging cervids in the UK may have been exposed to contaminated feed prior to the reinforced mammalian meat and bone meal ban instituted in 1996. A study to look at the potential susceptibility of red deer to BSE has shown no signs of transmission of the disease by the oral route, but it is at a very preliminary stage. Although a theoretical possibility exists, there is no evidence from the very limited surveillance data to suggest that BSE is present in the UK cervid population.
Human health implications
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.
15. Preliminary results from transmission experiments in transgenic mice expressing human PrP suggest the presence of a significant species barrier to transmission of CWD to humans. However, these findings must be interpreted with caution as they may not accurately predict the human situation. Data from in vitro experiments on conversion of human PrP by disease-associated forms of PrP, including PrPCWD, are equivocal.
16. The committee concluded there is no evidence of transmission of CWD to humans from consumption of venison, and that there may be significant barriers to transmission. Nevertheless, as the data are extremely limited a risk cannot be ruled out should CWD enter UK herds.
Conclusions
17. There is no evidence that CWD (or BSE) is present in the UK cervid population. However, because only limited surveillance is conducted in the cervid population, a low level prevalence of CWD cannot be ruled out. It is recommended that further surveillance of TSEs in UK cervids is conducted.
18. There is no evidence of transmission of CWD to humans from consumption of meat from infected cervids. Although epidemiological and experimental data on potential transmission of CWD are extremely limited, they suggest that there may be a significant species barrier. It would be helpful if further studies were available assessing the potential species barrier for transmission to humans.
19. Although limited, there is no evidence CWD can be transmitted to cattle, sheep or goats by natural means.
20. In summary, it appears 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.
SEAC January 2005
SEAC 85/2
CHRONIC WASTING DISEASE IN UK DEER
ISSUE
1. The FSA have asked SEAC to consider the current knowledge on, and comment on the possible public and animal health implications of, CWD in UK deer.
BACKGROUND
2. Over the past few decades, chronic wasting disease (CWD) has emerged as an endemic transmissible spongiform encephalopathy (TSE) in a number of captive and free-ranging cervid species (mule and white-tailed deer and Rocky Mountain elk) in some areas of North America. To date, CWD has not been detected elsewhere in the world. CWD is naturally transmissible from infected to susceptible cervids. The primary route(s) of infection are unclear but it is possible that it may be transmitted via contaminated environments. The origins of the disease are unknown. CWD is the only known TSE to occur naturally in cervids.
3. CWD is experimentally transmissible to non-cervid species by intracerebral inoculation. Very few studies have investigated experimental transmission to non-cervid species by oral routes that may mimic the possible natural route(s) of infection. In these studies, oral transmission of CWD has only been successful to North American cervid species. Thus, it is unclear whether CWD could be naturally transmitted to other cervid and non-cervid species.
4. There is very limited epidemiological data on the possible transmission of CWD to humans as a result of consumption of infected venison. No definitive or suspected cases of transmission of CWD to humans have been reported. Thus, it is not known whether CWD can be transmitted to humans from consumption of venison.
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5. It is likely, prior to the reinforced mammalian meat and bone meal (MMBM) ban in 1996, that both captive and free-ranging deer species in the UK, and possibly elsewhere in Europe, were exposed to contaminated feed. Studies investigating experimental transmission of BSE to cervids have not been completed. Although no TSEs have been detected in deer populations in the UK (or elsewhere in Europe), surveillance data are limited. Thus, it is possible that BSE may have been transmitted to, and could be present in, UK deer. If present, deer infected with BSE could present a risk to consumers of venison.
SEAC CONSIDERATION
6. SEAC has not considered CWD previously. The committee is asked to consider the possible public and animal health implications of CWD in UK deer with a view to producing a SEAC position statement. The literature on CWD is extensive. It is therefore, envisaged that this consideration could be conducted over two consecutive meetings. The first meeting (SEAC 85) would consider the current knowledge on TSEs in deer. A list of possible areas for discussion is given at the end of the paper with a view to formulating a draft position statement and identifying key issues and questions for further discussion at the next meeting (SEAC 86). If SEAC require, it may be possible to invite an expert on CWD to SEAC 86 to provide additional expertise for consideration of the key issues identified.
7. This paper provides the following information:
• Two recent scientific reviews on CWD from the Wildlife Information Network (October 2004) and the EU Scientific Steering Committee (March 2003).
• An overview of the UK deer industry (2002).
• A summary of current TSE surveillance in deer in the UK and elsewhere in Europe as well as an EFSA opinion on TSE surveillance in deer.
• A summary of current FSA research on the susceptibility of UK red deer to BSE infection.
• Possible exposure of UK deer to TSEs as well as sources and consumption of venison in the UK.
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REVIEWS OF CWD
Wildlife Information Network
8. A review of available scientific literature (up to October 2004) on CWD has been prepared by the Wildlife Information Network (Annex 1). It covers current knowledge in the following areas:
• Distribution and host range
• Diagnosis and detection
• Epidemiology
• Susceptibility and routes of transmission
• Public and animal health implications
Scientific Steering Committee
9. The TSE/BSE ad hoc group of the EU Scientific Steering Committee (SSC) conducted a review of the scientific literature on CWD in March 2003 (Annex 2). The SSC concluded that: “A theoretical risk for prion transmission to humans consuming products of CWD affected-cervids of all ages in countries where CWD exists cannot be excluded. Similarly, a transmission risk of prions to domestic animals cannot be excluded. There is therefore, a scientific basis on which to exclude tissues from animals that carry a CWD risk from the human and animal feed chains.
However, the early and widespread involvement of tissues in CWD infected animals does not allow a SRM list, neither to define any lower age cut-off as has been defined for cattle in relation to BSE. Neither is there sufficient knowledge to define exclusions or amendment of any SRM rule of the basis of relative genetic resistance to infection as has been proposed for sheep and goats in the event that evidence indicates the probable natural occurrence of BSE in these species.
Although available information indicates imports of live Cervidae from North America to EU and trade in meat products from cervid species as being negligible, it is important to reach certainty that no transfer of risk takes place through trade of live cervids and its derived products.
At present, there is no scientific data that CWD is occurring in Cervidae elsewhere than in those countries from which it has previously been reported. However, systematic TSE surveillance
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of cervid populations has either been absent or has only just started in European countries. Until the results of such surveillance become available no conclusion can be drawn with regard to the occurrence of CWD or similar TSE in the cervid population of Europe.”
REPORT ON THE UK DEER INDUSTRY
10. Information on the deer industry and venison trade in the UK is limited. A 2002 report by Professor Ranald Munro (Royal (Dick) School of Veterinary Studies, Edinburgh) provides an overview of the type (wild, farmed, park or zoo), size and geographical distribution of the five main deer species in the UK (Annex 3). Information on trading and slaughter practices, routes of supply of venison into the food chain and disposal of fallen stock and byproducts is also provided. The report was commissioned by Defra and FSA to inform surveys of TSEs in UK.
11. In the report, Professor Munro makes a number of observations about the possibility of TSEs in UK deer (pages 43 and 48-50): • Although surveillance is limited, as yet, CWD has not been found in deer populations in the UK.
• Prior to the reinforced MMBM ban in 1996, deer were exposed to feed potentially contaminated with MMBM.
• Red deer, a deer species prevalent in the UK, are closely related to Rocky Mountain elk (a North American species known to be susceptible to CWD). Thus, of the five principal UK deer species (red, roe, fallow, sika and muntjac), red deer may be the UK species with the greatest potential to develop TSEs.
• Early in the BSE epidemic, cases of BSE occurred in zoological collections of a number of species (antelope, Ankole cattle, bison, eland, oryx, gemsbok, kudu and nyala) presumably from the use of feed concentrates contaminated with MMBM. Although deer in zoos were fed similar concentrates, there are no reports of BSE cases in these animals.
SURVEILLANCE OF TSEs IN EUROPEAN DEER
12. Limited surveys have been carried out for TSEs in European deer populations but, to date, these programmes have not reported
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TSE cases. A summary of TSE surveys of deer in the UK and other EU Member States is given at Annex 4.
13. The European Food Safety Authority (EFSA) recently published an opinion on proposals for an EU surveillance programme for TSEs in deer (2004) (Annex 5). The opinion is under consideration by the EU.
FSA RESEARCH ON TSEs IN DEER
14. A FSA funded study is underway to investigate if UK red deer (a species closely related to Rocky Mountain elk) are susceptible to BSE infection by oral or intracerebral challenge (Annex 6). The study is in its early stages and is due to complete in 2007. To date, there are no clinical or pathological signs of BSE in orally or intracerebrally challenged animals at 12 or 6 months postadministration, respectively. Please note that Annex 6 has not been circulated outside the committee as it contains new scientific data that has not yet been published in a scientific journal.
ANIMAL EXPOSURE AND VENISON CONSUMPTION
Potential exposure of UK deer to TSEs
CWD
15. No live cervids from North America have been imported into the EU (see Annex 2, page 38). In addition, HM Customs and Excise have no record of imports of live cervids from North America into the UK. Thus, opportunities for natural transmission of CWD from infected animals imported from North America into the UK or Europe have not been available.
BSE
16. There are no quantitative data that would allow an estimation of past exposure of wild, farmed or park (and zoo) deer to animal feed containing MMBM. However, it appears likely that each of these deer populations consumed MMBM to some extent (see Annex 3 page 10).
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Sources and consumption of deer and elk products in the UK 17. In the UK, much of the venison from wild deer is exported (see Annex 3, pages 29-33). However, most venison from UK farmed deer is sold in the UK (see Annex 3, pages 38-39). 18. Specific figures for imports of edible deer and elk products from North America into the EU are not available. However, figures for ‘game meat (excluding rabbits, hares and swine)’ suggest that a very limited quantity of deer and/or elk meat may have been imported from North America into the EU, including the UK, over the period 1988-2001 (see Annex 2, pages 51-52). More recent information (2001-2004) from HM Customs and Excise supports this conclusion.
19. There are few data on consumption of UK produced or imported venison. National Diet and Nutrition Surveys1,2,3 provide profiles of eating habits in the UK. An analysis of the surveys indicates that venison is rarely consumed in comparison with beef and lamb (of the combined total of 5608 consumers in the surveys, 2064 (37%) had consumed lamb, 4819 (86%) had consumed beef and 12 (0.2%) had consumed venison). Data on venison consumption from the surveys suggest a trend towards increased venison consumption (0.14% versus 0.41% of consumers ate venison in the years 1986/7 and 2000/1, respectively). However, the data are too limited to allow a quantitative assessment of venison consumption.
ADVICE SOUGHT FROM THE COMMITTEE
20. The committee is asked to consider the possible public and animal health implications of TSEs in UK deer with a view to producing a SEAC position statement. The FSA have asked that SEAC address the following question in the position statement:
• What is the level of risk posed to consumers from eating meat from a CWD infected animal?
21. To help its consideration the committee may wish to consider the following areas: 1 J Gregory, K Fisher, H Tyler & M Wiseman. Dietary and Nutritional Survey of British Adults, HMSO, 1990.
2 S Finch, W Doyle, S Lowe, C Bates, A Prentice, G Smithers & P Clarke. National Diet and Nutritional Survey; People 65 Years and Over. Volume 1: Report of the Diet and Nutrition Survey, TSO 1998.
3 L Henderson, J Gregory & G Swan. National Diet and Nutritional Survey; Adults Aged 19 to 65 years. Volume 1: Types and Quantities of Foods Consumed, TSO 2002.
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• possible origins of CWD.
• possible routes of intra- and inter-species transmission of CWD.
• potential susceptibility of UK cervid and non-cervid (livestock) species to CWD.
• likelihood of the presence of TSEs in UK deer.
• possible human and animal health risks of TSEs in UK deer.
Are members aware of any other data that can add to the information in this paper?
Would the committee wish to invite an expert on CWD to the next meeting and, if so, could members suggest a particular expert?
ANNEX 1, 2, 3, 4, 5
ANNEX 1
CWD REVIEW OCT 2004
ANNEX 2
Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT
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3.1.1 CWD in captive and farmed cervidae
The clinical syndrome of wasting and death in captive deer was first recognised in the late 1960’s in the USA in a wildlife facility in northern Colorado (Fort Collins area). Biologists working on natural history and nutritional studies with captive mule deer observed the clinical signs and called the syndrome chronic wasting disease (CWD). It was initially thought to be associated with stresses of captivity, nutritional deficiencies, or intoxication. Only after histological studies it was recognised as a spongiform
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encephalopathy (Williams and Young, 1980). It was later recognised in a similar wildlife facility in Wyoming (Sybille). The disease was also recognised in Rocky Mountain elk from both facilities (Williams and Young, 1982). CWD in farmed elk it is thought to have entered Canada with elk imported from the United States in the late 1980s. The first case of CWD in farmed elk was diagnosed in 1996. Another infected elk farm was detected in 1998. Alberta (56%) and Saskatchewan (37%) have 71,500 elk ie 93% of the farmed elk population of Canada. The two provinces also account for 77% or 826 elk farms in Canada. (A Dagenais, Pers Com 2003). In 2000-2001, 40 infected elk farms were found in the province of Saskatchewan and 2 infected farms (1 herd of elk and 1 herd of white-tailed deer) in the province of Alberta. There are no obvious linkages with the Saskatchewan focus of CWD and possible sources are still being investigated. A total of 8,300 cervids (99% elk) have been slaughtered for CWD control purposes and 231 CWD infected cervids detected by laboratory testing.
CWD in a mule deer in Canada was first reported at the Toronto Zoo in Ontario in 1976. This animal was probably one of a group transferred from the Colorado Division of Wildlife to the Denver Zoo. CWD was not formally diagnosed at the Denver Zoo though clinical signs shown by some deer there were highly suggestive of CWD
3.1.2 CWD in free-ranging cervidae
The first case of CWD in a free-ranging cervid was found in 1981 in a Rocky Mountain elk in Rocky Mountain National Park, Colorado, USA. The first affected mule deer diagnosed in a wild population was found in 1984 about 1 mile west of the Colorado Division of Wildlife deer pens where CDW was first observed. (Spraker et al., 1997). In the late 1980s, the disease was diagnosed more frequently (Williams and Young, 1992). Surveillance of wildlife in Canada has detected 7 cases of CWD in wild deer (6 mule deer and 1 white tailed deer and all in the province of Saskatchewan) in the course of testing 16,495 wild cervids in Saskatchewan, Alberta and Manitoba. These cases may have occurred due to interaction of wild deer with farmed elk. It is also possible that there is a reservoir of infection in free-living deer. However, the prevalence of infection appears to be very low, based on wildlife surveillance to date. Further surveillance is undertaken to accurately estimate the prevalence of CWD in wild deer.
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Reviews of CWD should be consulted for additional information on the emergence of the disease and other information on all aspects of the disease (Willams and Young 1992, Williams and Miller 2002, Williams et al. 2002).
3.2 NATURAL HOST RANGE
Only three species of cervidae are known to be naturally susceptible to CWD: mule deer, white–tailed deer and Rocky Mountain elk. One case was originally reported in black tailed deer (Odocoileus hemionus columbianus) (Williams and Young 1980), a subspecies of mule deer. Hybrid mule deer X white-tailed deer have also been affected. Other non domestic ruminants, including moose (Alces alces), pronghorn antelope (Antilocapra americana), Rocky Mountain bighorn sheep (Ovis canadensis canadensis), mouflon (Ovis musimon), mountain goats (Oreamnos americanus), and a blackbuck (Antilope cervicapra) have been in contact with CWD-affected deer and elk or have resided in premises in which CWD had occurred and have not developed the disease (Williams and Young, 1992). Cattle, sheep and goats that have resided in research facilities together with CWD-affected animals for prolonged periods or under field conditions did not develop the disease. These observations of apparent cross-species resistance are supported by molecular studies of Raymond et al. (2000)1 and in vivo studies of Miller et al. (2000). However, the in vitro conversion experiments are not necessarily informative about the species barrier in vivo and should therefore be interpreted with caution.
Assuming a single (parental) strain of agent, susceptibility of cervids depends on the interaction of this agent with host PrP and other undefined host factors. It may depend also on the ability of the CWD agent to mutate to a version to which the new host is more susceptible (i.e. with a shorter incubation period etc.). The efficiency of interspecies transmission of the TSE’s (the species barrier) is considered by some to be dependent on the compatibility of the PrP between donor and recipient. The basis of this ‘species barrier’ is incompletely understood, but interspecies differences in the amino acid 1 An important factor controlling interspecies TSE susceptibility is prion protein (PrP) homology between the source and recipient species/genotypes. Raymond et al show that the CWD-associated PrP-res (PrPCWD) of cervids readily induces in vitro the conversion of recombinant PrP-sen molecules to the protease-resistant state in accordance with the known transmissibility of CWD between cervids. In contrast, PrPCWD –induced conversions of human and bovine PrP-sen were less efficient, and ovine PrP-sen was
8
sequence of the prion protein and the strain of prions involved play crucial roles (Bosque, 2002). Genetic homology between species confers similarities and divergence in the spatial configuration of the respective protein is an important element of the structural basis of the species barrier (Billeter et al. 1997). Sequences of the prion protein gene are very similar between certain cervid species (Kaluz et al. 1997, O’Rourke et al. 1998, Cervenakova et al. 1997). In term of prion protein sequences relative to phylogeny, reindeer have convergence with whitetailed and mule deer, whereas in non-cervid ruminants there is divergence from the cervids, particularly so in the case of bovines (Wopfner et al., 1999)2 . Another phylogenetic analysis suggests that cattle and mule deer have converged with great apes including humans in key areas of their prion protein (Krakauer et al. 1996). It is difficult to draw specific inferences from these data but such studies provide indications as to species in which the PrP gene should be examined in more detail. Polymorphisms of the PrP gene influence susceptibility to infection and disease phenotype. In Rocky Mountain elk, sequence analysis of the PrP gene showed only a single polymorphism; one amino acid change (Met to Leu) at codon 1323 . In over 43 Rocky Mountain elk (genotyped and postive for CWD) it was found that elk, homozygous for PrP codon 132-Met (M/M) were over-represented in both free-ranging and farm-raised CWD-affected animals when compared to unaffected control groups. In the same group several heterozygous M/L were positive. Positive elk with the homozygous codon 132 L/L were not found (O’Rourke et al, 1999 and Belanchandran personal comm.). Research is continuing into the influence of genetics on susceptibility; there may be an association between PrP genotype and resistance in elk but this has not been recognised (O’Rourke 1999 and unpublished data) .
3.3 EXPERIMENTAL TRANSMISSIBILITY snip...
3.4 EPIDEMIOLOGY
3.4.1 Descriptive Epidemiological Features
3.4.1.1 Chronology of distribution in the USA
The occurrence of CWD was, for several years after its discovery, noted only in two wildlife research facilities in Colorado and Wyoming. Mule deer supplied to two other research facilities from the Colorado wildlife facility developed CWD. In captive
12
deer and elk prevalence varies from <1% to nearly 100% depending on the herd size, location, and the origin of animals. It is highest in the captive facilities where CWD has been present for many years. Between June 1986 and May 1997, CWD was the only reported natural cause of adult mortality among Rocky mountain elk held at the wildlife research facility near Fort Collins (Colorado). Of 23 elk that remained in this herd >15 months old, four developed CWD.
In the early 1980’s, CWD was recognised in free-ranging cervids (Spraker et al., 1997). Between March 1981 and June 1995, CWD was diagnosed in 49 free-ranging cervids from north central Colorado. Mule deer were the primary species affected and accounted for 41 of the 49 cases, but six Rocky Mountain elk and two white-tailed deer were also affected. Within the free-ranging cervids, pre clinical prevalence (based on the detection of PrPCWD by IHC) is higher in mule deer (<1-15%) than elk (<1%) (Miller et al., 2000). Overall, in free-ranging deer in the historic enzootic area’s in Colorado/Wyoming, prevalence among hunter killed animals is <10% (Williams and Miller, 2002). During the 2002 hunting season a rapid screening test (BioRad ELISA) was applied on a volunteer basis to screen more than 25,000 specimens from Colorado harvested elk and deer. The IHC was used as a confirmatory test for those samples indicated positive screen test results and findings from this survey will be available soon.
3.4.1.2 Chronology of distribution in CANADA CWD is thought to have entered Canada with elk imported from the United States in the late 1980s. Investigations have shown that a farm (later referred to as the ‘source farm’) established in Saskatchewan in 1987 spread infection via elk sales to 21 other farms, which in turn infected 17 more farms in the same province. The source farm held 63 elk imported from the United States, including from at least one farm that was subsequently confirmed as CWD-infected. The Canadian elk herd was expanding rapidly in the late 1980s and foundation herds that had imported elk from the United States traded animals throughout Saskatchewan and Alberta. At this time, Manitoba and British
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Columbia did not allow elk farming and, from 1988, Provincial authorities prohibited the entry of cervids into Alberta.
Due to concern about the entry of bovine tuberculosis, the Canadian government prohibited the import of cervids from 1990 to 1999. From 1999, cervids could again be imported from the United States, under conditions designed to prevent the introduction of CWD. Some Provinces conducted testing for CWD but there was no official control program for CWD until 2000. In 2001, CWD was made reportable at the federal level. Movement of live elk was key to the spread of CWD in Saskatchewan. According to the Canadian Food Inspection Agency’s investigations, the source farm sold 864 elk in the 1990s. A total of 274 elk that had been sold within 36 months of quarantine being imposed in 2000 were traced, slaughtered and tested to reveal 21 CWD-infected animals (prevalence 8%). Depopulation and testing of the remaining 403 animals in the source herd revealed a within-herd prevalence of 11%. The CFIA investigated all herds that had received cervids from the source herd. The last reported case of CWD in farmed elk was in March 2002.
As said earlier, CWD in a mule deer in Canada was first reported at the Toronto Zoo in Ontario in 1976.
In summary, since 1996, CWD has been diagnosed in 42 elk farms and one whitetailed deer farm in Canada (Saskatchewan and Alberta). 95% Of infected elk herds had only a few (1-3) infected animals as diagnosed by IHC on the brain and most (91%) elk diagnosed with CWD were at a pre-clinical stage. Approximately 65% of infected herds in Saskatchewan had a prevalence of infection less than 5%. While animals less than 12 months of age have been diagnosed with pre-clinical infection by IHC, the youngest elk diagnosed with clinical CWD was 17 months old. With elk, as with deer, animals of all ages and both sexes have been found infected with CWD and no bias has been evident.
3.4.2 Evidence for lateral transmission
snip...
3.5.3 Conclusions
In deer and elk, PrPCWD has a very wide and early tissue distribution, which resembles the distribution of scrapie and BSE agents in tissues in TSE-susceptible sheep and is different to that seen in BSE in cattle. However, tissue distribution is not identical for deer4 and elk. In the latter species it accumulates later in the incubation period into detectable levels. This widespread distribution of PrPCWD early in the incubation period presents significant, if not insurmountable, difficulty with respect to the potential for decisions on the removal of specified risk materials (SRM) in CWD.
snip... SEE MORE;
ANNEX 3
Report on the Deer Industry in Great Britain, 2002
http://web.archive.org/web/20050301193321/http://www.seac.gov.uk/papers/munrodeerrptannex3.pdf
ANNEX 4
TSE SURVEILLANCE IN DEER
ANNEX 5
The EFSA Journal (2004) 70, 1-7, Opinion on a surveillance programme for Chronic Wasting Disease in the European Union
http://www.efsa.eu.int 1 of 7
Opinion of the European Food Safety Authority on a surveillance programme for Chronic Wasting Disease in the European Union
Question N° EFSA-Q-2003-088
Adopted on 3rd June 2004
SUMMARY OF OPINION
The European Commission (EC) requested the European Food Safety Authority (EFSA) and its Scientific Panel on Biological Hazards for an opinion on a surveillance program for Chronic Wasting Disease (CWD) in the European Union (EU). The European population of cervids consists of several million free-living cervids and hundreds of thousands of captive cervids. It is theoretically possible for European cervids to be infected by PrPCWD, PrPBSE, PrPScrapie or even an unknown TSE strain; however, it is unknown how the phenotype of such a TSE in European cervids would look like. Currently, only a few European countries conduct surveillance programs on TSE in free-living or captive cervids and only a few experimental research studies are conducted to obtain data on the susceptibility of European cervids for TSE.
During the assessment, opportunities and difficulties were discussed and several problems when considering surveillance for CWD in European cervids emerged influencing the implementation of such a surveillance program. These include the existence of various species and sub-species of cervids, and variation in the cervid population distribution and density in the different EU countries. Different diagnostic methods and currently used tests for TSEs in EU and North America were evaluated and discussed. Sensibility and specificity of the test as presented was evaluated as well as their potential for discriminating different TSEs (CWD – BSE – scrapie) if they occur in cervids.
Evaluation of data submitted for six tests suggest that these rapid tests would appear able to detect a case of TSE in European cervids in a properly defined surveillance program. However, since these tests have not been validated for European cervids it is not possible to recommend specific test(s). In addition, Immunohistochemistry (IHC) and Western blotting tests should be used to confirm a diagnosis of CWD. As there might be differences in sensitivity and specificity between brain and lymph node samples and differences in deposition of PrP as observed in different species of cervids infected with CWD, both retropharyngeal lymph node and the obex of the brain (with intact dorsal motor nuclei of the vagus) should be included in the testing.
At present, biological strain typing by transmission to laboratory rodents is the only definite method allowing differentiation between CWD and BSE/scrapie. Current molecular and IHC methods show potential to differentiate these diseases.
The EFSA Journal (2004) 70, 1-7, Opinion on a surveillance programme for Chronic Wasting Disease in the European Union http://www.efsa.eu.int 2 of 7
It is recommended to initiate as soon as possible an EU-wide experimental screening on TSE using a rapid test and confirmatory methods and targeting at-risk groups of animals, i.e. farmed deer and fallen stock cervid species in Europe older than 18 months. Experimental studies are essential to understand the pathogenesis, tissue distribution of PrP and to ascertain tissue infectivity of TSEs in European cervids before large scale surveillance could be expected to give reliable results. Such experimental studies should start in parallel with any planned surveillance.
It is also recommended to further support and/or initiate research on molecular methods to differentiate between CWD and BSE/scrapie. Even though human TSE-exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. The Working Group thus recognises a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as central nervous system (CNS) and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products for humans are available.
Key words: TSE, CWD, Cervids, Elk, Deer, rapid tests, surveillance
snip,,,see full text;
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
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