EDITORIAL

Bovine spongiform encephalopathy and Australia The incidence of bovine spongiform encephalopathy (BSE) intheUnitedKingdom is expected to peak during 1992before a gradual decline to near zero incidence by the turn of the century. Since 1986some 30 000 cases have occurred on about 10 000 farms (about 5% of UK farms), mostly dairy farms in Southern England As many as 1200 cases have o c c u ~ ~ eind a single month creating a considerableproblem in carcasedisposal. It is believed that the seeds of the present epidemic were sown in 1981-82 At this mid point in the epidemic in what has been a testing time for disease control authorities in the UK, it may be worthwhile to summarise some of what is now known of the emergence of this hitherto unknown disease and to remind ourselves of a set of circumstances that can wreak such havoc on our clients’ livestock property and a nation’s wealth. BSE is a scrapie-likedisease. The first cases were identifiedby pathologists at the Central veterinary Laboratory, Weybridge, in November 1986 after histopathological examination of brains from two cows independently submitted from the Veterinary Investigation Centres in Kent and Devon. The diagnosis of BSE, like scrapie, is in the first instance a clinical diagnosis. Confirmation of the clinical diagnosis is based on histopathological findings particularly of characteristic vacuolation of neurones. Two important refinements to diagnosis were introduced as the epidemic continued to rise (Taylor 1991): (a) By distinguishing between “suspicion” and “conviction” to allow observationon the development of cliical disease, the accuracy of the cliical diagnosis was improved at the time the decision to slaughter was taka, (b) Histopathological confiiation of the cliical diagnosis has been reduced to examination of a single brain stem, paraffin-embdded section obtained via the foramen magnum, obviating the need to open the cranial cavity and create aerosols when sawing through the skull. In 1988 the accuracy of the clinical diagnosis confiied by histopathology was 94%, which declined to 86% by 1991 (Taylor 1991). The accuracy of the clinical diagnosisis significantlyworse in the spring, presumably reflecting difficulty in differentiating BSE from somemetabolic and paresis&aralysis syndromes associated with calving. There is no confirmatory live-animal test, and this has been identified as a high research priority by one of several committees (the Tyrrell Committee) set up to advise on BSE. The development of a live-animal test, possibly based on the detection of BSE associated fibrils in lymph node biopsy samples by electron microscopy or immunological methods (Ikegami ef a2 1991), would be a useful adjunct to diagnosis particularly as the epidemic nears its end At that time, the need to verify freedom rather than wait out an incubationperiod of several years will be important.although any such test is likely to be difficult to apply and imperfect in outcome. The origins of the epidemic appear now to be reasonably well understood although important details are still missing (Wilesmith ef af 1991). Around 1981-82 changes in the rendering of offal, described as changes from a high temperature, batch-to-batch process with solvent extraction of fats to a continuous flow, low temperature process without solvent extraction of fats, were introduced in some plants. These changes were introduced apparentlyfor reasons of efficiency and improvednutritionalvalue of the m e a w n e meal end-product of the rendering process. It is believed that these changes favoured retention and/or noriinactivationof the sheep scrapie agent in the AustralianVeterinaryJournal Vol69, No 7, July 1992

final product. The scrapie agent is extremely resistant to heat, disinfectants and conventional autoclaving procedures. Some strains are not inactivated by the application of 160OC dry heat for an hour. Rendering plants in northern VK, where the incidence has been relatively low, did not make these changes. Scrapie of sheep persists in the UK as a not well-defined, low incidence, endemic disease. The extent of contamination of calf feed pellets, in which up to 10% meat/bone meal was incorporated, was probably augmented further, before the ban on the use of meatbone meal in animal feeds in 1988,by the incorporation of offal frompreclinical,perhaps also clinicalcases, in cattle. Lymphoid tissue and thymus carry high concenations of the agent early in the come of the disease and before the onset of clinical signs. The case/farm rate is curiously low (average 3/farm) presumably reflecting a low level of contaminationof the feed or a varying susceptibility among the exposed cattle. There is apparently no particular breed susceptibility. The incubation period of BSE, like scrapie, is minimally 2.5 years and may be as long as three or four years. There has been no signifcant horizontal spread of BSE. Each diagnosed case is considered an index case in what is considered an extended common source epidemic. Progeny born to infected dams are beiig closely monitoredfor evidence of verticaltransmission. Cases in other countries have been in cattle imported from the UK or fed feed imported from that country. Scrapie is the prototype of the spongiform encephalopathy group of diseases, which in addition to BSE includes transmissible mink encephalopathy, chronic wasting disease of deer and elk, and kuru, Gerstmann-Straussler-Scheinkerand CreutzfeldtJackob diseases of man. Despite considerable research effort during the past several decades the nature of the scrapie agent remains enigmatic. Its properties are highly unusual and three theories have been advanced. Either it is a virus for which the nucleic acid has yet to be demonstrated (virus thwry),or it is a new class of agent in which the nucleic acid is unusually small and probably does not code for any protein (virino theory), or thirdly and most heretical the “infectious” agent is solely a protein for which the prion protein (for proteinaceous infectious particle) is considered the prime candidate (prion theory). There is a normal cellular gene that codes for the prion protein and presumably the normal protein fulfils a normal function in the cell. Either a mutation in the gene or the introduction of the protein from an heterologous source leads to a kind of polymerisation of the prion protein to form fibrils described in some diseases as amyloid-like. These fibrils, which are called scrapie-associatedfibrils in the case of scrapie, are presumably linked to the degeneration of the neurones. Kuru was almost certainly transmitted by ingestion of human brain tissue, and mink encephalopathy was believed to be transmitted by ingestionof scrapie-infectedsheep carcases. With such past experiences it might have been predicted that the entry of the scrapie agent in the UK into the food chain and the emergence of a disease such as BSE could occur. This is unfair judgement. Responses to disease control must always be based on real rather than imagined risk, although what is real or imagined in risk assessment will be debated. Such risk assessment and what to do about the present low level endemicity of scrapie, and presumably BSE some time around the turn of the century, is a major legacy of the BSE experience and a major stimulus for research. 153

The host range of scrapie/BSE has become an important issue. One of ten experimentally infected pigs developed disease following experimental inoculation of BSE-infected brain tissue (Taylor 1991). and a case of an apparently new spongifom encephalopathy in a cat was described with no agent or source of an agent identified (Leggett et ul 1990). Seven additional cases of feline spongiform encephalopathy, confirmed by detection of characteristicfibrils by electron microscopy and by showing the presence of a modified prion protein by immUnoblotting, have been reported (Pearsonet d 1991). Reported elsewhere in this issue (Peet and Cirran 1992) is the first case of a spongiformencephalopathyin anexotic cat, namely a 5.5 years old male cheetah,one of three cheetahs, imported into the Broome Zoo, Western Australia from Marwell Zoo,UK in 1986. The first cases of BSE in exotic ruminants were also recognisedinMarwellZooaround 1986, andtheremustbeahigh level of suspicion that the affected cheetah was fed BSE-infected feed from one of several possible sources. It will be important to define the source(s)of infectionfor feline species. Other infected cats may have been or could be imported into Australia. It is most unlikely that cats would be other than a dead end host for BSE. Reports of possible transmission of BSE to other species resulted in considerablemedia hysteria in the UK with “mad cow disease” the catchcry. A working party chaired by Sir Richard Southwood made an interim recommendation in June 1988 that, although there was no known hazard to human health, it would be a sensible precaution to exclude suspect cattle from the food chain. This recommendation, which remains in force, had the effect of shifting attention from animal to public health issues. Historically Australia has at least two interesting connections to the world of spongifom encephalopathies.Scrapie was diagnosed in 1952in 4 of 10 Suffok sheep imported from the UK to a Victorian property in 1951 The episode was dealt with by

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immediate slaughter and quarantine of the property, (Bull and Murnane 1958). The discovery and transmissibility of kuru among the Fore people of Papua New Guinea was the work of CarletonGajdusek, who left the Walter and Eliza Hall Institute in Melbourne about 1956toreturn toUnitedStatesbutpausedinNew Guineatostudy kuru, which subsequently became a major theme of his work. In defining the nature of kuru, Gajdusek was profoundly innuenced by the work of Hadlow (1959) on scrapie. As the enormity and significance of the BSE epidemic in the UK gradually dawned on an unsuspecting world, the Australian response through AQIS/Bureau of Rural Resources was timely and appropriate. Imports of cattle, cattle semen and cattle embryos were suspended in May 1988 and a formal ban imposed in November 1988. Trace-back work failed to find any evidence of BSE- infected cattle in Australia. Vigilance, particularly by field veterinarians, will remain the price we should be more than willing to pay for remaining free of both scrapie and BSE.

Michael J Studdert School of Veterinary Science The University of Melbourne References BullLBandMumaneD(1958)Au.st VetJ34:213 Hadlow WJ (1959)Loncef 2: 289 Ikegami Y,It0 M, Iscinura H, Momotani E, Sasaki K et a1 (1991) Vet Rec 128 271 Leggett MM. Dukes J and Pine HM (1990) Veer Rec 127 586 PeetRLandCurranJM(1992)Aut VetJ69 171 Peanon GR, Gruffydd-Jones TJ. Wyatt JM,Hope J, Chong A el a1 (1991) Vet Rec 128 532 Taylor KC (1991) Vet Rec 129 522 Wilesmith JW, Ryan JBM and Atkinson MJ (1991) Vet Rec 128 199

Australian Veterinary Journal Vol69, No 7,July 1992

Bovine spongiform encephalopathy and Australia.

EDITORIAL Bovine spongiform encephalopathy and Australia The incidence of bovine spongiform encephalopathy (BSE) intheUnitedKingdom is expected to pe...
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