Angiostrongylosis in dogs in Sydney Department of Veterinary Patblogy, University of Sydney, New South Wales 2006 Department of Veterinary Clinical Sciences, University of Sydney New South Wales 2006 vineyard V e t e r G clinic, 102Windsor Road, Vineyard, New South Wales 2765
GH COLLINS TLW ROTHWELL
RMALIK DB cHuR(sH MKDOWDEN
Angwstrongylus cantonensisChen 1935, commonly known as theratlungwoqhas longbeenrecognisedas acauseof parasitic meningitis in man and other animals (Alicata and Jindrak 1970; Chin-Yun 1976;Masonetall976 McKenzieetal1978; Soulsby 1982; Chan et al1987; Wright et all991). A cantonensis is widely distributed in Southeast Asia, the Pacific islands and Northern Australia. The clinical manifestations of neural angiostrongylosis in dogs have been documented comprehensively in the field (Mason et al 1976; Mason 1987, 1989)andthelaboratory(Jindrak and Alicata 1970).In Australia, casesindogs (Masonetal1976;Mason 1987,1989)andinhorses (Wright et al1991) have been restricted to Queensland. The Me cycle ofA cantonensis was first describedby Mackerras and Sandars (1955). Adult nematodes normally live in the pulmonary arteries and right ventricle of various rat species. First stage larvae passed in the faeces of infected rats are ingested by an intermediate host (various species of slugs and snails), and develop to third stage infectivelarvae. Severalgroups of animals, including crustaceans, land planarians and fish, can serve as paratenic hosts (Alicataand Jindrak 1970). Rats acquire infection by ingesting infected intermediate or paratenic hosts. Larvae migrate through the spinal cord to the brain, where they develop into immature adults before becoming established in the pulmonary arteries. Animals other than rats can be infected with third stage larvae and support development to the immature adult stage (Alicata and Jidrak 1970). The migration of larvae and immature adults in the spinal cord and brain of these abnormal hosts may give rise to variable neurological sequelae. InJune 1989,a9-weeks-oldmaleBullTerriercross-bredpuppy waspresented withhind limbweakness and urinary incontinence, and subsequently referred to Sydney University Veterinary Teaching Hospital (SUVTH) for evaluation Neurological examination demonstrated non-ambulatory paraparesis with decreased muscle tone in the pelvic limbs. Tendon jerks, withdrawal reflexes, pain sensation and radiographs of the vertebral column were within normal limits. The owners declined further investigation for financial reasons, and the puppy was euthanased. Cerebrospinal fluid (CSF) was collected from the cistema magna before necropsy. CSF analysis demonstrated increased protein concentration (0.54 g/l) and marked eosinophilic pleocytosis (886 x 1$ cells/l). Histologically, there was severe meningoencephalomyelitis with eosinophil-rich inflammatory foci throughout the brain and cord. A nematode profile was seen in sections from the cerebellum. The puppy had been bred in Strathfield, purchased at 6 weeks of age and kennelled in a suburban backyard in the same district. In April 1991, two 12-weeks-oldGerman Shepherd pups were presented with hind limb weakness and generalised hyperaesthesia. One was unable to stand, the other had difficulty in rising. Other litter-mates were apparently unaffected. Spinal reflexes appeared normal, although severe pain, elicited by handliig, complicated the neurological assessment. In the previous year, a similar case from the same kennel improved after 170
treatment with calcium. The initial treatment was therefore with intravenous calcium glubionate*. However, both puppies were presented again the next day with diarrhoea and pyrexia; the hyperaesthesia had not improved. Treatment was changed to flunixin, ttimethoprid sulphadiazine and an anti-diarrhoeal mixture. Five days later,bothpuppies were near normal, although subtle hind limb ataxia persisted. Three weeks later a 5-weeks-old male German Shepherdpuppy from the same premises was presented with diarrhoea, generalised hyperaesthesia, muscle wastage and neurological disease. The puppy died within 48 h of presentation. A further male puppy from the same litter was presented several days later with similar signs. Haematology demonstrated neutrophilia and eosinopenia, while an extensive panel of biochemical tests were within the normal range. The diarrhoea improved with symptomatictreatment, but the neurologicalsigns persisted. The animal was referred to SUVTH for evaluation. Non-ambulatory tetraparesis associated with marked, generalised muscle atrophy and urinary incontinence were eVident on physical examination. Patella jerks were diminished slightly, withdrawal reflexes were weak and proprioceptive deficits were observed, particularly in the pelvic limbs. Tactile sensation and nociception were considered normal. Fasciculations were observed in the muscles of the tongue. These findings were indicative of severe diffuse lower motor neurone disease. Electrodiagnostic testing was performed under halothane/nitrous-oxide anaesthesia before euthanasia and necropsy. Denervation potentials were detected in limb muscles during needle electromyography. Although motor nerve conductionvelocitiesof the tibia1 andulnarnerve were withinthenormal range, evoked compound muscle action potentials were reduced in amplitude (cf Sims and Redding 1980). Necropsy and histopathologyrevealed severewsinophilic granulomatousmeningoencephalomyelitis, and an inflammatory focus in the meninges contained a degenerate nematode. Severe wsinophilic enteritis and patchy interstitial pneumonia were observed, while muscle sections showed only neurogenic atrophy. Several large nematodes were subsequently dissected from under the cere bellar meninges, and later identified as A cantonemis. In retrospect, it seems liiely that the hyperaesthesia and ascending paraparesisobserved in the other threeGerman Shepherdpuppies were also referable to neural angiostronglyosis. A visit was made to the property where the puppies were born and reared. Dogs were housed outdoors in the rear garden of a house in Baulkham Hills. The garden was largely untended and contained a large amount of rubbish, mainly wood, bricks and decaying vegetation. There were at least 20 dogs, and several ducks, turkeys and peacocks. The food for the animals was kept in an open shed. The owner stated that rats had been common on the property, but that he had recently tried to reduce their numbers. Several puppies had been observed eating slugs. Slugs, Limax maximus, and snails, Helix aspersa and Strangesta capillacea, were common, and 5 specimensof each were collectedfor laboratory examination. No infective larvae were found. Clearly, neural angiostonglyosis must be considered in the differential diagnosis of ascending paralysis in young dogs born and reared outside of Queensland,particularly when paraparesis is accompanied by hyperaesthesia. A tentative diagnosis is suggestedby the presenceof largenumbersof eosinophils in the CSF (Mason 1989). The occurrence of A cantonensis in one suburb, and the probable presence of the parasite elsewhere in Sydney, raises questions about the present distribution of this important parasite within Australia, and whether rats infected with A cantonemis living in suburban areas constitute a public health risk. The first question could be addressed by a country-wide survey
Calcium-Sandoz, Sandoz Australia Pty Ltd, New South Wales
Australian VeterinaryJournal, Vol69, No 7, July 1992
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)
171
GH COLLINS TLW ROTHWELL
RMALIK DB cHuR(sH MKDOWDEN
Angwstrongylus cantonensisChen 1935, commonly known as theratlungwoqhas longbeenrecognisedas acauseof parasitic meningitis in man and other animals (Alicata and Jindrak 1970; Chin-Yun 1976;Masonetall976 McKenzieetal1978; Soulsby 1982; Chan et al1987; Wright et all991). A cantonensis is widely distributed in Southeast Asia, the Pacific islands and Northern Australia. The clinical manifestations of neural angiostrongylosis in dogs have been documented comprehensively in the field (Mason et al 1976; Mason 1987, 1989)andthelaboratory(Jindrak and Alicata 1970).In Australia, casesindogs (Masonetal1976;Mason 1987,1989)andinhorses (Wright et al1991) have been restricted to Queensland. The Me cycle ofA cantonensis was first describedby Mackerras and Sandars (1955). Adult nematodes normally live in the pulmonary arteries and right ventricle of various rat species. First stage larvae passed in the faeces of infected rats are ingested by an intermediate host (various species of slugs and snails), and develop to third stage infectivelarvae. Severalgroups of animals, including crustaceans, land planarians and fish, can serve as paratenic hosts (Alicataand Jindrak 1970). Rats acquire infection by ingesting infected intermediate or paratenic hosts. Larvae migrate through the spinal cord to the brain, where they develop into immature adults before becoming established in the pulmonary arteries. Animals other than rats can be infected with third stage larvae and support development to the immature adult stage (Alicata and Jidrak 1970). The migration of larvae and immature adults in the spinal cord and brain of these abnormal hosts may give rise to variable neurological sequelae. InJune 1989,a9-weeks-oldmaleBullTerriercross-bredpuppy waspresented withhind limbweakness and urinary incontinence, and subsequently referred to Sydney University Veterinary Teaching Hospital (SUVTH) for evaluation Neurological examination demonstrated non-ambulatory paraparesis with decreased muscle tone in the pelvic limbs. Tendon jerks, withdrawal reflexes, pain sensation and radiographs of the vertebral column were within normal limits. The owners declined further investigation for financial reasons, and the puppy was euthanased. Cerebrospinal fluid (CSF) was collected from the cistema magna before necropsy. CSF analysis demonstrated increased protein concentration (0.54 g/l) and marked eosinophilic pleocytosis (886 x 1$ cells/l). Histologically, there was severe meningoencephalomyelitis with eosinophil-rich inflammatory foci throughout the brain and cord. A nematode profile was seen in sections from the cerebellum. The puppy had been bred in Strathfield, purchased at 6 weeks of age and kennelled in a suburban backyard in the same district. In April 1991, two 12-weeks-oldGerman Shepherd pups were presented with hind limb weakness and generalised hyperaesthesia. One was unable to stand, the other had difficulty in rising. Other litter-mates were apparently unaffected. Spinal reflexes appeared normal, although severe pain, elicited by handliig, complicated the neurological assessment. In the previous year, a similar case from the same kennel improved after 170
treatment with calcium. The initial treatment was therefore with intravenous calcium glubionate*. However, both puppies were presented again the next day with diarrhoea and pyrexia; the hyperaesthesia had not improved. Treatment was changed to flunixin, ttimethoprid sulphadiazine and an anti-diarrhoeal mixture. Five days later,bothpuppies were near normal, although subtle hind limb ataxia persisted. Three weeks later a 5-weeks-old male German Shepherdpuppy from the same premises was presented with diarrhoea, generalised hyperaesthesia, muscle wastage and neurological disease. The puppy died within 48 h of presentation. A further male puppy from the same litter was presented several days later with similar signs. Haematology demonstrated neutrophilia and eosinopenia, while an extensive panel of biochemical tests were within the normal range. The diarrhoea improved with symptomatictreatment, but the neurologicalsigns persisted. The animal was referred to SUVTH for evaluation. Non-ambulatory tetraparesis associated with marked, generalised muscle atrophy and urinary incontinence were eVident on physical examination. Patella jerks were diminished slightly, withdrawal reflexes were weak and proprioceptive deficits were observed, particularly in the pelvic limbs. Tactile sensation and nociception were considered normal. Fasciculations were observed in the muscles of the tongue. These findings were indicative of severe diffuse lower motor neurone disease. Electrodiagnostic testing was performed under halothane/nitrous-oxide anaesthesia before euthanasia and necropsy. Denervation potentials were detected in limb muscles during needle electromyography. Although motor nerve conductionvelocitiesof the tibia1 andulnarnerve were withinthenormal range, evoked compound muscle action potentials were reduced in amplitude (cf Sims and Redding 1980). Necropsy and histopathologyrevealed severewsinophilic granulomatousmeningoencephalomyelitis, and an inflammatory focus in the meninges contained a degenerate nematode. Severe wsinophilic enteritis and patchy interstitial pneumonia were observed, while muscle sections showed only neurogenic atrophy. Several large nematodes were subsequently dissected from under the cere bellar meninges, and later identified as A cantonemis. In retrospect, it seems liiely that the hyperaesthesia and ascending paraparesisobserved in the other threeGerman Shepherdpuppies were also referable to neural angiostronglyosis. A visit was made to the property where the puppies were born and reared. Dogs were housed outdoors in the rear garden of a house in Baulkham Hills. The garden was largely untended and contained a large amount of rubbish, mainly wood, bricks and decaying vegetation. There were at least 20 dogs, and several ducks, turkeys and peacocks. The food for the animals was kept in an open shed. The owner stated that rats had been common on the property, but that he had recently tried to reduce their numbers. Several puppies had been observed eating slugs. Slugs, Limax maximus, and snails, Helix aspersa and Strangesta capillacea, were common, and 5 specimensof each were collectedfor laboratory examination. No infective larvae were found. Clearly, neural angiostonglyosis must be considered in the differential diagnosis of ascending paralysis in young dogs born and reared outside of Queensland,particularly when paraparesis is accompanied by hyperaesthesia. A tentative diagnosis is suggestedby the presenceof largenumbersof eosinophils in the CSF (Mason 1989). The occurrence of A cantonensis in one suburb, and the probable presence of the parasite elsewhere in Sydney, raises questions about the present distribution of this important parasite within Australia, and whether rats infected with A cantonemis living in suburban areas constitute a public health risk. The first question could be addressed by a country-wide survey
Calcium-Sandoz, Sandoz Australia Pty Ltd, New South Wales
Australian VeterinaryJournal, Vol69, No 7, July 1992
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)
171
