of rats for the presence of lungworms,perhaps with the assistance of pest controllers. The second question is more difficult to answer, as most human infections are thought to be acquired through the ingestion of uncooked infected paratenic hosts, such as prawns, crabs or fish. However, infection may also occur through ingesting planarians OT slugs on salad vegetables, and there is some evidence that infected slugs and snails occasionally release infective larvae (Alicata and Jin&ak 1970). The possibility exists, therefore, that people living in suburban areas could become infected by eating contaminated produce from their gardens. Before the public health risk can be assessed there is an urgent need for more comprehensive information on the distribution of A cmfonensis in Australia. The assistance of Dr David Spratt in c o n f i i g the identity of the parasites is much appreciated. Ms J Phillips assisted in collecting samples from the Baulkham Hills property, while the earlier case was referred by Enfield Veterinary Hospital.

References Alicata JE and Jindrak K (1970) Angidrongylosis in the Pacific and Southeusthh, Charles C Ihomas. USA, p 105 chaaSW, Chan KW, Lam K. FarringtonM, Wong HW and Yuen P (1987) Trans Roy SOCTrop Med Hyg 81:808 chin-Yun Y (1976) Am J Trop Med Hyg 2 5 233 JindrakKandAficaralFJ (1970)AmJVetRes31:449 Mackems MJ and Sandars DF (1955) Ausf JZool3:l Mason KV (1987)Ausf Vet J64:u)l Mason KV (1989)Ausi Vet J a 1 5 2 Mason KV, Prescott CW. Kelly WR and Waddell AH (1976) Aust VefJ 52:295 McKenzieRA, Green PE and W d AD (1978)Awt Vet J 5 4 8 6 Sims MH and Redding WR (1980) Am J VefRes 41: 1247. Soulsby En.(1982) Helminths, Arthropodr and Protozm of Domesticated Animals, 7th edn, Bailliere. Tindall, London, p 280 Wright JD.Kelly WR.Waddell AH and Hamilton J (1991) Aurt Vet 5 6 8 5 8

(Acceptedfor publication30 March 1992)

Spongiform encephalopathy in an imported cheetah (Acinonyxjubatus) RL PEET

Department of Agriculture, Animal Health Laboratories, Baron-Hay Court, South Perth, Western Australia 6151 Department of Agriculture, Broome, Western Australia 6725

JM CURRAN

DuringDexxmber1991,a5Syroldmalecheetahat theBroome

Zoo was observed to be ataxic and apparently disoriented. The keeper had noticed a change in gait some 2 weeks previously, but its appetite was good. The animal was treated empirically with amoxycillinand clavulanic acid by a veterinary practitioner, and a sample of blood collected. This showed a strong positive titre to toxoplasmosisand a tentative diagnosis was made. However, the animal continued to deteriorate, and 2 weeks later exhibited severe ataxia, falling, locomotory weakness, disorientation and distress. A decision was made to euthanase the animal. It was tranquilised, eufhanased,and necropsied, within 30 minutes of death, at the veterinary clinic in the zoo grounds. Necropsy revealed no visible lesions, and samples were collectedfor laboratory analysis.These included fresh and bufferedfarmalin fixed sagittal halves of the brain,the entire fixed spinal

Australian VeterinaryJowml, Vol69, No 7, July 1992

cord to the distal lumbar area,fixed samplesof liver, kidney, lung, spleen, heart and a range of skeletal muscles. Fresh liver, kidney, blood and urine were also submitted to Animal Health Laboratories(AHL). Histopathology revealed widespread axonal degeneration and demyeliiation of all tracts in the spinal cord with macrophages visible in some empty cylinders. This extended up the pyramidal tracts in the medulla and into the white matter tracts of the brainstem as far as the internal capsule area. Severe spongiform change was visible in the grey matter of the neuroaxis, especially in the corpus striatum, midbrain and thalamic areas. This was characterised by small ovoid spaces (variable in size) in the neuropil and vacuolation within the perikarya of some neurons similar to that described by Wyatt et ul (1991). Spongiform change and/or vacuolated neurons were not seen in the grey matter of the spinal cord. The liver appeared congested and oedematous, .but there were no visible lesions and hepatic encephalopathy was considered unlikely. There were no significant lesions in any of the organs and a diagnosis of probable spongiform encephalopathy was made on the basis of the neuropathology. Other differential diagnoses (Wyatt et ul199 1) were considered but were not applicable. Because of the neuropathological findings, a quarantine order was placed on the zoo and the previously buried carcase disinterred and incinerated. The fresh and fixed nervous tissue, haematoxylineosin stained histological slides and a blood sample were despatched as a category 3 (high level of suspicion of exotic disease) submission to Australian Animal Health Laboratory (AAHL) at Geelong. They were unable to confirm the diagnosisbut agreed to forward the specimens to the reference laboratory (Central Veterinary Laboratory, Weybridge, UK). This laboratory confiied the presence of fibrils by electron microscopy and verified the diagnosis of spongiform encephalopathy after examining our stained histological slides. The cheetah was born at Marwell Zoo in Hampshire, England on 16June 1986. It and 2 litter mates (one male, one female) were imported into Perth, Western Australia, on 9 May 1989. The f i t case of bovine spongiform encephalopathyin an exotic ruminant occurred in 1986 in a 33-months-old hand-reared nyala (Trugeluphusungasi> at Marwell Zoo (Jeffrey and Wells 1988). The second case was confiied 1year later, again at the Marwell Zoo in a 36-months-old gemsbok (Oryx gazellu) by the same authors. Some zoos, including this one, practised a ‘feeding in‘ of culled carcases to other zoo animals, particularly canids and felids (cunningham 1991). The cheetah probably ingested the infective agent at this zoo and the clinicaldiseasedid not become apparentuntil December 1991at Broome. This is consistent with suggested incubation periods of other animal spongiform encephalopathies (Collee 1991). The cheetah is considered a ‘dead end’ host to this disease and should not represent a threat to Australian domestic livestock. To our knowledge, this is the fist diagnosis of spongiform encephalopathy in a cheetah (Acinonyx jubutus) and of spongiform encephalopathy in a zoo animal outside the UK. We thank Drs D Morrell and A Woods for referring the case and assisting in the necropsy, staff at AHL for rapid processing of tissues, Mr GAH Wells and staff at Weybridgefor confirming our diagnosis, and AAHL for forwarding the material to Weybridge.

References Collee JG (1991) Med krb Sci 48: 296 Cunningham AA (1991)JZoo WiZdife Med22: 304 Jeffrey M and Wells GAH (1988) Vet Pathol 25: 398 Wyatt JM,Peanon GR. Smerdon Th’,Gruffydd-Jones TJ. Wells GAH and Wilesmith Nv (1991) Vet Rec 129 233

(Acceptedfor publication13 April 1992)

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