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Bovine Spongiform Encephalopathy (BSE) in sheep

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Bovine Spongiform Encephalopathy (BSE) in sheep
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  148 Aust Vet J  Vol 80, No 3, March 2002 Scientific  EDITOR COLIN WILKS ASSOCIATE EDITOR KEITH HUGHES, EDITORIAL COMMITTEE NORMAN ANDERSON, GLENN BROWNING,COLIN CHAPMAN, ROBIN CONDRON,TREVOR FARAGHER, STEVEN HOLLOWAY,KEITH HUGHES, TONY LEPPER,JOCK M C LEAN, CARL PETERSON, ANDREW TURNER, COLIN WILKS EDITORIAL ASSISTANT ANDDESKTOP PUBLISHING ANNA GALLO The Australian Veterinary Journal welcomes srcinal contributions on all aspects ofv eterinary science. Submission of a manuscript for publicationwill be held to imply that it is a record ofunpublished srcinal work of the author(s)and, if accepted will not be publishedelsewhere in whole or part withoutpermission. The Journal reserves the rightto reject any manuscript.Send contributions to the Scientific Sectionof the AVJ to: Editor,AVA House, 272 Brunswick Road,Brunswick, Victoria 3056. Telephone: (03) 9387 2982, 9387 8808.International -61 3 9387 8808Telefax: (03) 9388 0112,International +61 3 9388 0112.Email: avjsc@ava.com.au.‘Instructions for authors’ was published inthe January,February 2002 issue. ‘ Sta tistica l guideline s for authors’ ispublish ed in this issue. Both areavailable on http://www.ava.co m.au SCIENTIFIC SECTION Australian VETERINARY  J OURNAL Bovine Spongiform Encephalopathy(BSE) in sheep? SCM AC DIARMIDMinistry of Agriculture and Forestry, POBox 2526, Wellington, New Zealand T h e spectre of BSE in sheep is worrying consumers and regulators in many countr ies . In January 2002, the Office International des Epizooties (OIE, the world organis ationfor animal health) convened a seven member Ad hocGroup on the hypotheticalpresence of BSE in sheep and goats to issue a scientific opinion on steps which should betaken to clarify the problem and manage risks. a Background The Group concluded that it is theoretically possible that BSE cases could haveoccurred in small ruminants in the field, especially in Europe. Laboratory trials haveshown that sheep and goats given oral inoculations of BSE developed clinical andpathological changes which are difficult or impossible to differentiate from scrapie bymeans of the currently available diagnostic methods. 1-3 Also there is evidence that meatand bone meal has been fed to some sheep and goats in the past. Such cases, should theyexist, are likely to be diagnosed and reported as scrapie. Currently, scrapie and BSE can only be distinguished on the basis of bioassay in mic e. 4,5 The British have been taking brains from sheep diagnosed with scrapie, inoculating theminto mice and then looking for the incubation period and lesion profile suggestive of BSE.There are, however, two problems with this approach. The first is cost. To profile a singleisolate in mice costs around £20,000. There are nearly 200 isolates under study at present.The second difficulty is time; up to 2 years to run a single lesion profile study.The OIE’s Ad hoc Group considered five aspects of the problem of BSE in sheep andgoats; risk assessment, surveillance, diagnosis, measures to protect consumers, andbreeding for resistance. Risk assessment The Group was of the opinion that the criteria described in the current BSE chapter inthe International Animal Health Code  are largely appropriate to conduct a risk assessmenton the potential presence of BSE in sheep and goats. However, because experimentalinfection of sheep and goats results in clinical signs similar to scrapie, all cases of scrapie-like disease in these species should be notified and investigated as specified in the yet to beadopted scrapie chapter of the Code  . Surveillance Surveillance for transmissible spongiform encephalopathy (TSE) in sheep and goatsshould be an ongoing process. The Group was of the opinion that with current routinediagnostic methods, it would not be possible to conclude that scrapie is the only TSEpresent in sheep and goat populations in a country where BSE risk has been identified.Therefore, such countries are encouraged to implement and maintain an adequatesurveillance system and to store isolates for future differential testing.Appropriate diagnostic methods should be used to enable characterisation of isolates.This will enable ‘new or unusual’ isolates to be recognised and subjected to furthercharacterisation, possibly by bioassay, to confirm the presence of BSE.The surveillance scheme for the detection of BSE in sheep and goats must take intoconsideration the composition and distribution of the national sheep and goat populations Editorial a The Members of the OIE Ad Hoc Group on the Hypothetical Presence of Bovine Spongiform Encephalopathyin Sheep and Goats were; Professor A Shimshony (Israel), Professor M Savey (France), Dr L Detwiler (USA),Dr D Heim, (Switzerland), Dr D Matthews (UK), Dr BEC Schreuder (the Netherlands) and Dr SC MacDiarmid(New Zealand).  Aust Vet J  Vol 80, No 3, March 2002149 Scientific  Codon171 is the focus of attention in breeding programs thataim to increase resistance to infection with scrapie (and possiblyBSE). Although the frequency of occurrence of this genotype israre, if not absent, in some breeds, such breeding programs haveto be seen as potential long-term solutions. Whereashomozygosity for arginine at codon171 is the long term goal of such programs, heterozygosity (QR) is likely to reduce the risk of horizontal transmission of disease, and protect public health byreducing the range of infectious tissues in the body of an infectedsheep. In other sheep populations the genetic make-up may bedifferent and strains of scrapie to which they are exposed mayalso differ. Consequently, the approach outlined above may notbe applicable to all situations.There is clear evidence that breeding for genetic resistance toscrapie can reduce or eliminate clinical disease from affectedflocks. The same would probably apply should BSE be found insheep. Therefore, it is possible that breeding for genetic resistanceto scrapie may also contribute to controlling potential animaland public health problems arising from BSE in sheep and goats. However, because the interrelationship between genotype andresistance is still unclear, especially with respect to the possibleexistence of a carrier state, the Ad hoc Group was unable to makespecific recommendations with respect to trade. Researchcurrently in progress may allow recommendations to be made inthe foreseeable future. Implications for Australia and New Zealand Australia and New Zealand are both widely recognised asbeing free from scrapie 8 and BSE. Both countries were given themost favourable rating, Level I, in the European Commission’srecent Geographical BSE Risk Assessment. It might be thought that the detection of BSE in Europeansheep would be to Australia’s and New Zealand’s advantage.However, such a development would probably not benefit oursheepmeat exports. Consumer fears would probably result in adecline in demand for all lamb, regardless of srcin. Evenwithout proof that BSE is present in European sheep flocks, EUmember countries are implementing greatly increasedsurveillance for scrapie-like diseases in their sheep populations. Itis almost inevitable that, to allay consumer concerns and retainaccess to markets, Australia and New Zealand will also have tosignificantly increase surveillance for scrapie, going well beyondwhat is currently in place. If BSE is found in European sheep,nobody will benefit. References 1. Foster JD, Parnham DW, Hunter N, Bruce M. Distribution of the prion protein insheep terminally affected with BSE following experimental oral transmission. J Gen Virol  2001;82:2319-2326.2. Foster JD, Parnham DW, Chong A, Goldmann W, Hunter N. Clinical signs,histopathology and genetics of experimental transmission of BSE and naturalscrapie to sheep and goats. Vet Rec  2001;148:165-171.3. Bradley R. Bovine spongiform encephalopathy and its relationship to the newvariant form of Creutzfeldt-Jakob disease. In: Rabenau H, Cinatl J, Doerr H,editors. Prions: A Challenge for Science, Medicine and Public Health System  ,Karger, Basel. 2001:105-144.4. Bruce M. Strain typing studies of scrapie and BSE. In: Baker H, Ridley RM,editors. Methods in Molecular Medicine: Prion Diseases  . Humana Press, NewJersey, 1996:223-236.5. Bruce M, Will RG, Ironside JW et al. Transmissions to mice indicate that ‘newvariant’ CJD is caused by the BSE agent. Nature  1997.389:498-501.6. Collinge J, Sidle KCL, Meads J et al. Molecular analysis of prion strain variationand the aetiology of ‘new variant’ CJD. Nature  , 1996.383:685-690.7. Hunter N. Genotyping and susceptibilty of sheep to scrapie. In: Baker H, RidleyRM, editors. Methods in Molecular Medicine: Prion Diseases  . Humana Press,New Jersey, 1996:211-221.8. MacDiarmid SC. Scrapie: the risk of its introduction and effects on trade. Aust Vet J  1996;73:161-164. as well as husbandry and feeding practices. For example, dairybreeds are more likely to have received concentrate feedspotentially contaminated with meat and bone meal. Diagnosis of BSE in sheep and goats The differential diagnosis of scrapie and BSE in sheepcurrently presents major technical difficulties. Lesion profilinghas been mentioned already. Another promising approach is byexamining the glycoform patterns of TSE isolates on westernblots of brain tissue. 3,6 However, to date, such glycotyping insheep has not been consistent or reproducible in the hands of different researchers. Recognising the difficulties, the Grouprecommended an approach to be implemented to check whethera suspicious case in a sheep or a goat is due to either a scrapiestrain or BSE. First, the laboratory should confirm that the casemeets the criteria to be diagnosed as a TSE. The isolate shouldthen be tested by molecular methods such as western blot orELISA. to determine whether it meets the criteria to beconsidered as a ‘typical scrapie strain’. Should the isolate not meetthe criteria of ‘typical scrapie’, investigation should progress tothe mouse bioassay system. Specified risk material (SRM) Another aspect to the problem is what can be done to protectthe consumer if BSE is shown to be present in sheep?In cattle,BSE infectivity is largely confined to the central nervous system(CNS), which can easily be removed. 3 CNS tissues, and a rangeof others that might be considered contaminated under certaincircumstances, are known as SRM. In the case of BSE in sheep,there is evidence that infectivity is distributed more widely, rightthrough the peripheral lymph nodes. 1,3 That is, trimming cannotrender sheep meat safe to the same extent that it can with beef.The International Animal Health Code  chapter on BSE describeswhich tissues should be removed from cattle. However, theGroup considered that these recommendations are not sufficientto address the issue of the potential presence of BSE infectivity invarious tissues of sheep and goats because the distribution inthose species is more widespread than in cattle, more closelyresembling the distribution of scrapie infectivity. Because of the widespread distribution of infectivity in at leastsome sheep infected with BSE, and because of the effects of ageand genotype, the Group was not able to make simplerecommendations on which tissues should be excluded from foodchains. When assessing the potential BSE infectivity in carcases of sheep and goats, the following organs have to be considered: skullsincluding brains, ganglia, eyes and tonsils, vertebral column including ganglia and spinal cord, thymus, spleen, ad renal gland,pancreas, liver, the entire gastro-intestinal tract and the largelymph nodes. The inclusion of each of these organs in a list of SRM would depend on age and genotype of the animals. Control of TSE through genetic selection Sheep are not universally susceptible to scrapie. The genotypeof the sheep, and specifically codons136,154 and171of the PrPgene, play a part in conferring susceptibility or resistance toinfection. 7 Susceptibility appears to depend also on the strain of scrapie agent to which a sheep is exposed.Codon171 encodes for arginine (R), glutamine (Q) or, morerarely, histidine (H). Published data suggest that sheep that arehomozygous for arginine at codon171 (RR) are not susceptibleto infection with scrapie. It seems probable, from preliminaryexperimental data, that this may also confer resistance toinfection with BSE. 2
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