Progressive encephalomyelopathy and cerebellar degeneration in a captive-bred snow leopard (Uncia uncia)

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Progressive encephalomyelopathy and cerebellar degeneration in 10 captive-bred cheetahs A. C. PALMER, J. J. CALLANAN, L. A. GUERIN, B. J. SHEAHAN, N. STRONACH, R. J. M. FRANKLIN Progressive ataxia, with head tremor, developed in 10 captive-born cheetah cubs under six months of age. The condition was usually preceded by coryza and an ocular discharge. Initially the ataxia and weakness affected the hindquarters, then the forelegs, and head tremor developed later. Significant pathological changes were confined to the central nervous system. There was widespread Wallerian degeneration in the funiculi of the spinal cord (except those in the dorsal columns), in the medulla and in the cerebellum. In the cerebellum there was degeneration of Purkinje cells and of the molecular and granular cell layers. There was chromatolysis in the Purkinje cells, the ventral horn cells of the spinal cord and in the neurons of the lateral vestibular nucleus. The olivary nucleus was necrotic. There were foci of inflammatory cells in the molecular layer of the cerebellum and in the medulla. The cause of the disease remains unknown.

Veterinary Record (2001) 149, 49-54 A. C. Palmer, MA, PhD, ScD, FRCVS, R. J. M. Franklin, BSc,

BVetMed, PhD, MRCVS, Department of Clinical

Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 OES J. J. Callanan, MVB, PhD, MRCPath, MRCVS, B. J. Sheahan, MA, MVB, MSc, PhD, FRCPath,

MRCVS, Department of Veterinary Pathology, Faculty of Veterinary Medicine, University College Dublin, Dublin 4, Ireland L. A. Guerin, MRCVS, Gilabbey Veterinary Clinic, Cork, Ireland N. Stronach, BA, PhD, Fota Wildlife Park, Carrigtwohill, County Cork, Ireland

ATAXIA in cheetah cubs (Acinonyx jubatus) was first MATERIALS AND METHODS described by Brand (1981). The cause was ascribed to copper deficiency although no biochemical analysis of patholog- Animals and clinical history ical information was provided. Similarly affected animals The affected cheetah cubs were derived from four litters were described by Zwart and others (1985); they were derived (Table 1). The first animal was referred to one of the authors from two litters and developed progressive hindlimb weak- (A. C. P.) in 1969 from Whipsnade Park Zoo, England. The ness and ataxia between 18 and 26 weeks of age. Pathological rest were born at Fota Wildlife Park, Ireland, between 1985 examination revealed Wallerian degeneration in the spinal and 1998. There were seven females and three males. cord and in one animal Wallerian degeneration of the dorsal The following comments refer to the nine animals from and ventral nerve roots and of the peripheral nerves. The con- Fota Wildlife Park. Clinical signs of ataxia developed in cubs dition was thought to be caused by copper deficiency. under six months of age, and were preceded by an ocular, A progressive form of hindlimb paralysis in adult cheetahs watery discharge which quickly became mucopurulent and was reported by Walzer and Kubber-Heiss in 1995. The animals developed into severe conjunctival swelling. Some of the aniwere from a zoo in eastern Austria, between seven and 10 years mals had a cough and a reduced appetite. At the same time of age, and developed paresis within a period of two years. One they developed a watery nasal discharge, with sneezing, and ofthem originated from the Regent's Park Zoo, London. Severe became listless. The ocular and nasal signs subsided within 'primary demyelination' was described in the spinal cord of all two weeks. Although all the cubs in an affected litter develthe animals, especially at the levels T6 to L3. The degeneration oped the ocular and nasal signs, not all of them developed was bilaterally symmetrical and affected the ventral and lat- ataxia. eral tracts towards the outer margins of the cord. Ascending The first signs of ataxia consisted of a slight swaying of the tracts 'in this section' were not completely spared. Descending trunk and incoordination of the hindlimbs, which were tracts were affected in the medulla. The animals' haematolog- abducted and protracted excessively, as if the animal had lost ical, blood chemistry and cerebrospinal fluid (CSF) values were a sense of proprioception. The tail became weak but there within normal limits. The cause ofthe condition was not deter- were no signs of urinary or faecal incontinence. In advanced mined but an hereditary factor could not be eliminated. cases there was tremor of the head. Throughout the illness, Paresis in three-week-old cheetah cubs was described by the animals remained alert and responded to visual and audiHafner and others (1996). In these animals there was bilat- tory stimuli. Their appetite did not deteriorate further, and erally symmetrical demyelination in the dorsolateral and sul- apart from a slight atrophy of the hindlimb musculature, comarginal tracts of the spinal cord but there was evidence of there was no obvious change of body condition. axonal and myelin degeneration, gliosis and remyelination. As routine, adult cheetahs were vaccinated annually The condition was thought to be a leucodystrophy and pos- against panleucopenia virus, calicivirus and rhinotracheitis sibly caused by copper deficiency. virus, using a modified live vaccine (Felocell CVR; Pfizer A further three outbreaks of paresis in cheetah cubs were Animal Health). Cheetah cubs received a similar vaccination reported by Walzer and others (1998). They were usually asso- at 10, 12 and 14 weeks of age. All the affected cubs developed ciated with a mucopurulent discharge from the eyes and nose, clinical signs of ataxia within a month of the last vaccination, pyrexia and the sudden onset of ataxia. The histopathologi- except cubs 4 and 5 (from a litter of three) which were cal changes were the same as those described by Walzer and euthanased before they were vaccinated. Kubber-Heiss (1995), with the addition of perivascular cuffDuring the illness, no significant abnormalities were ing in the rhombencephalon in four animals. A coronavirus observed during routine examinations of blood chemistry, was isolated from the brain of two cases, and feline her- haematology, CSF or urine. The concentration of copper in pesvirus 1 (FHV- 1) was isolated from another four. In a further blood remained within normal limits and copper suppletwo cases the clinical signs were reported to have resolved after ments to the diet had no effect. treatment with acyclovir and prednisolone. Antibody levels were negative to Borna disease virus, This paper describes the clinical and pathological signs Toxoplasma, feline coronavirus, FHV- 1, feline leukaemia virus, displayed by 10 young ataxic cheetahs; they are believed to feline immunodeficiency virus, and canine distemper virus be similar to those described by Walzer and others (1998). (Addie 1999). Conjunctival swabs were negative for

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Chlamydia psittaci and faeces samples were negative for Giardia species. Both the cubs and their mothers were negative for FHV. The level of antibodies to parvovirus was increased, but the increase was attributed to vaccination.

Laboratory methods The affected cubs were euthanased and postmortem examinations were carried out immediately after death. Brains and spinal cords were fixed in 10 per cent formol saline; the cerebellum was not available from cheetah 1. Other organs sampled included liver, kidney, lung, peripheral nerve, myocardium and thyroid gland. Samples of gluteal muscle were taken from cheetahs 6 to 10 indusive. Blocks ofbrain tissue were selected to include the cerebrum, diencephalon, midbrain, cerebellum, pons and medulla, and levels of the

spinal cord. Histological sections were prepared from paraffin-embedded material and stained with haematoxylin and eosin. CNS material was also osmicated and embedded in resin from which semi-thin sections were prepared for light microscopy and stained with toluidine blue; ultrathin sections were examined by transmission electron microscopy (Hitachi H-6000).

RESULTS No macroscopic changes were observed postmortem. There were pathological changes in the spinal cord and brainstem of all 10 animals, and the cerebellum was affected in eight of the nine animals from which it was available (Table 1).

In the spinal cord of all the animals there was Wallerian degeneration in the funiculi, except the dorsal columns (Figs 1 to 4). The degeneration was bilaterally symmetri-

FIG 2: Cheetah 2. Ventral column in the thoracic spinal cord showing dilatation of degenerating myelin sheaths. Haematoxylin and eosin. x 72

FIG 1: Cheetah 2. Transverse section of thoracic spinal cord to show the distribution of holes in the white matter, the majority of which represent nerve fibres undergoing Wallerian degeneration. Note the relative preservation of the dorsal columns. Haematoxylin and eosin. x 16

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FIG 3: Cheetah 5. Longitudinal section through the ventral column showing dilated myelin sheaths (some containing myelophages), denoting Wallerian degeneration and gliosis. Haematoxylin and eosin. x 1 10

FIG 5: Cheetah 3. Electron micrograph of the ventral white matter showing degenerate myelin sheaths from which the axons are absent. The extracellular space is expanded (probably owing to suboptimal tissue fixation) but there are abundant astrocytic processes. These ultrastructural features are characteristic of Wallerian degeneration. Lead citrate/uranyl acetate-stained ultrathin resin section. x 3500 FIG 4: Cheetah 3. Section through the ventral column showing thinly dispersed surviving myelinated axons, separated by gliosis. Resin section, toluidine blue. x 50

of the cord there were few affected neurons. Neurons showing these changes were observed in all except cheetahs 1, 4 and 6, but their apparent absence in these three cases may have been due to incomplete histological coverage. There were no abnormalities in peripheral nerves, in their terminal branches in the gluteal muscle or in the muscle fibres themselves. In all except cheetahs 1 and 4 Wallerian degeneration was cal and accompanied by severe gliosis. The changes were traced rostrally into the cerebellum by way of the caudal ceremost severe towards the circumference of the cord, bellar peduncle. It was also found in the middle and rostral decreased centripetally, and occurred throughout its length. cerebellar peduncles except in cheetahs 1, 2, 3 and 4. A section The intensity of Wallerian degeneration varied; it was slight through the rostral cerebellar peduncle was not available from in cheetah 3 and most severe in cheetahs 6, 9 and 10. The cheetah 10. The cerebellum from cheetah 1 was not available for hisdorsal columns, on the other hand, were almost completely spared, an isolated, degenerating nerve fibre rarely being tological examination. No abnormalities were found in the cerebellum of cheetah 3, but there were severe changes in the found. Ultrastructurally, the degeneration in the white matter of cerebellum in the rest of the cases, although in cheetah 2 the the spinal cord was characterised by a marked loss of axons, changes were confined to the white matter. In the cerebellar cortex of cheetahs 4 to 10 there was a few degenerate axons, myelin figures and numerous astrocytic processes containing abundant stacks of intermediate swelling of Purkinje cell cytoplasm (similar to chromatolyfilament (Fig 5). A few macrophages were observed. These sis), shrinkage and displacement of nuclei and cell death features are characteristic of both chronic and ongoing (Figs 7, 8). The loss of Purkinje cells was accompanied by Wallerian degeneration. There was no evidence of axons from gliosis which extended into the molecular layer which itself which myelin was absent, or of axons surrounded by abnor- was often narrower than normal. There was overt loss of mally thin myelin, features characteristic of a primary granular cells in cheetahs 6, 7, 8 and 9 (Fig 9). These changes were especially evident in the declivus and tuber vermis in demyelination and subsequent remyelination, respectively. There was chromatolysis and neuronal necrosis in the grey cheetahs 6, 7 and 9. matter of the spinal cord (Fig 6). Affected neurons were present in the ventral horns, in the thoracic nucleus and in an area immediately lateral to this nucleus. In transverse sections

FIG 6: Cheetah 6. Two ventral horn cells in the grey matter of the spinal cord undergoing chromatolysis. Haematoxylin and eosin. x 270

. 4 D a>s

t

FIG 7: Cheetah 10. Purkinje cells undergoing chromatolysis. Haematoxylin and eosin. x 1 10

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FIG 9: Cheetah 6. Loss of Purkinje cells, a cluster of hypertrophied

astrocytes (boxed area)

and a thinning of the granular cell layer. Haematoxylin and eosin. x 160

FIG 8: Cheetah 4. Cerebellar cortex, showing a reduced number of Purkinje cells and an increase of Bergmann astrocytes. Haematoxylin and eosin. x 110

In areas of Purkinje cell loss there were occasional accumulations of small numbers of lymphocytes, evidence of capillary hyperplasia and aggregation of microglia (microglial 'stars') (Fig 10). The intensity of these inflammatory changes was greatest in cheetahs 4, 6, 7 and 9. There was Wallerian degeneration in the deep cerebellar white matter of all except cases 3 and 4. The degeneration affected groups of nerve fibres, extended into the white matter of individual folia, and was often accompanied by a prolific astrocytosis (Fig 1). Chromatolysis and neuronal necrosis were also found in other regions of the brain, including the lateral vestibular nucleus in cheetahs 5, 6, 7 and 10, but not in cheetahs 2 and 8 (Fig 12). Sections through this nucleus were not available from cheetahs 1, 3, 4 and 9. Chromatolysis was also observed in the red nucleus of cheetahs 2, 6 and 7, but this nucleus was not available in sections from the other animals. Elsewhere, in the brainstem, perivascular cuffing with lymphocytes occurred in the spinal nucleus of the trigeminal nerve in cheetahs 2 and 3 (Fig 13) where it was distributed bilaterally. In cheetah 2, cuffing was also present in the red nucleus, adjacent to neurons which were undergoing chromatolysis. There was necrosis and neuronal loss in the olivary nucleus from cheetahs 1, 2, 4, 6, 9 and 10 (Fig 14). In cheetahs 2 and 10 these changes were accompanied by oedema, vascular proliferation and aggregation of lymphocytes. There was also chromatolysis, necrosis of neurons and abundant macrophages. In cheetahs 1 and 4 there was a loss of nerve cells and gliosis. Wallerian degeneration was also observed to a variable extent in the tectospinal tract and occasionally the rubro-

spinal tract, the medial longitudinal fasciculus, the spinothalamic tract and the lateral lemniscus. DISCUSSION

The striking pathological change common to all the 10 cheetahs was the Wallerian degeneration in the spinal cord. It affected all parts of the white matter except the dorsal columns and was bilaterally symmetrical. This pattern is similar to that described by Walzer and Kubber-Heiss (1995) and Walzer and others (1998) and there is little doubt that it is caused by the same disease, although Walzer and KubberHeiss did not describe changes in the cerebellum. However, cheetahs 2 and 3 also showed no cortical lesions in the cerebellum. In the spinal cord, the Wallerian degeneration was accompanied by a gliosis, the severity of which appeared to be related to the duration of the clinical signs. Both the gliosis and the myelin degeneration were more intense in the peripheral parts of the cord. The preservation of the dorsal columns may provide a clue to the origin of the pathological process. The nature of the myelin in the dorsal columns is similar both structurally and biochemically to that in other spinal tract systems, but their cells of origin are quite different; those of the dorsal columns reside outside the CNS, in the dorsal root ganglia, whereas those of the rest of the tracts stem from neuronal cell bodies located within the CNS. The trigeminal tract of the medulla was also spared, and this tract has a similar relationship to the peripherally situated trigeminal ganglion as the dorsal column has to the dorsal root ganglion. Wallerian degeneration in the inferior and superior cerebellar peduncles was probably due to the degeneration of the afferent spinocerebellar tracts in the cord, as was the chromatolysis in the neurons of the thoracic nucleus. Similarly, the

FIG 11: Cheetah 9.

Pathological astrocytes (gliosis) in an area of Wallerian degeneration in the roof of the cerebellum. Haematoxylin and eosin. x 270

FIG 10: Cheetah 4. Proliferation of rod cells (microglia) in the molecular layer of the cerebellum. Haematoxylin and eosin. x 1 10

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FIG 12: Cheetah 7. Chromatolysis, loss of neurons and gliosis in the lateral vestibular nucleus. Haematoxylin and eosin. x 1 10

chromatolysis in the lateral vestibular nucleus is likely to have been related to the degeneration of the vestibulospinal tract, and the chromatolysis in the red nucleus was probably related to similar changes in the rubrospinal tract. In the absence of degeneration in the peripheral nerves and of neurogenic muscle atrophy, the chromatolysis in the ventral horn cells is more difficult to explain. It is possible that such affected cells do not supply voluntary muscle but are concerned with internal relays. In the cerebellum, the pathological changes appear to have involved a number of different processes. The end result was a loss of Purkinje cells, either singly, in a series or in complete rows. Neurons in all folia appeared to be susceptible, although the most severe changes were in the declivus and tuber vermis. Sick Purkinje cells initially showed swelling of the cytoplasm which became amorphous and eosinophilic (chromatolysis) and may be an axonal response related to the Wallerian degeneration in the deep cerebellar white matter. The Wallerian degeneration in this region of the cerebellum usually paralleled that observed in the cerebellar peduncles and it was accompanied by a severe astrogliosis, similar to that in the spinal cord. In addition to these changes in the cerebellum, which could be termed long term, there was evidence of more acute changes, usually related to an inflammatory process, in both the cerebellum and the brainstem. Focal accumulations of microglia were frequently observed in the molecular layer of the cerebellum. This type of microglial cell accumulation occurs in viral encephalitides, such as canine distemper and ovine louping ill. Local vascular hyperplasia and perivascular cuffing, sometimes extending to meningeal vessels, were other indicators of an acute inflammatory process. There was also perivascular cuffing in the brainstem of cheetahs 2 and 3, affecting the nucleus of the spinal tract of the trigeminal nerve and, in the case of cheetah 2, there was

FIG 14: Cheetah 6. Inferior olive showing oedema, capillary

hyperplasia, macrophages and neuronal loss.

Haematoxylin and eosin. x 1 10

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FIG 13: Cheetah 3. Perivascular cuffing and proliferation of microglia in the region of the nucleus and tract of the spinal trigeminal nerve. Haematoxylin and eosin. x 1 10

cuffing with lymphocytes and plasma cells in the region of the red nucleus. Walzer and others (1998) also reported perivascular cuffing in the rhombencephalon (hindbrain) in four cheetahs. Degeneration of nerve cells in the nucleus of the olivary nucleus was observed in six of the cheetahs. The nature of the damage was both acute and chronic. In some cases there were early changes of local oedema, vascular hyperplasia and the presence of macrophages. Adjacent neurons were undergoing chromatolysis. In other cases there was an overt loss of nerve cells and gliosis. A comparable degeneration in the olivary nucleus was described by Montgomery and Storts ( 1983) in an hereditary form of striantonigral and cerebello-olivary degeneration in the Kerry blue terrier which they regarded as a form of transsynaptic retrograde degeneration, perhaps due to changes in the transmitter systems. A similar lesion developed in the inferior olive of dogs treated experimentally with monoamine oxidase inhibitors (Palmer and Noel 1963). It is uncertain how these various neuropathological processes in the cheetahs can be reconciled with a single aeti-

ology. It appears that although the disease may have an acute onset it eventually enters a chronic stage of progressive deterioration. The cause of the condition is still unknown. The possibility of a genetic basis was considered by Bradley ( 1999) who concluded that although there may be a genetic predisposition the pattern of incidence does not indicate a major genetic factor. On the other hand, the condition may be caused by a viral infection, or even be related to vaccination with a modified live vaccine. However, the latter possibility is unlikely because cheetahs 4 and 5 had not been vaccinated. There is, however, morphological evidence suggesting viral involvement - perivascular cuffing in the cerebellum and brainstem and nests of microglial rod cells in the molecular layer of the cerebellum. But it is difficult to understand how a virus could be responsible for such a bilaterally symmetrical distribution of tract degeneration in the spinal cord, with preservation of the dorsal column, unless, as has already been suggested, the targets of infection are neurons located within the CNS. A bilateral and symmetrical distribution of lesions in the CNS is often associated with neurotoxicity, but in the present circumstances it is difficult to imagine a toxic agent which is so widely distributed geographically and historically. A symmetrical distribution of lesions in the CNS also occurs in nutritional deficiencies, for example in thiamine deficiency in the cat and in copper deficiency in the lamb, but the cheetahs' diets have been varied and have not be incriminated.

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In 1995, Palmer and Cavanagh described a similar condition in 19 cats. The cats, aged between three and 16 months, developed neurological signs which included paraplegia, headshaking, nystagmus, defective vision and reduced proprioception. Most of them had been bred in cat colonies and were derived from pathogen-free stock, but one was a domestic cat, referred from a private veterinary practice. In one outbreak, the incidence was 63 per cent of litters born, of which 65 per cent had all the kittens affected. In the spinal cord there was Wallerian degeneration, with sparing of the dorsal columns; Wallerian degeneration also affected cerebral myelin and sometimes the optic nerve. In some cases there was a focal loss of Purkinje cells. Although no virus was isolated, the clinical pattern and pathological changes suggested a viral aetiology and this possibility is supported by other reports in the literature (Palmer and Cavanagh 1995). The similarities between the diseases in the cats and the cheetahs appear to be more than coincidental. Both groups of animals were bred in isolated communities and may have been immunologically compromised. The cats were derived from pathogen-free stock and the cheetahs were bred from a limited stock, which may have compromised their immunological competence. Munson (1993) suggested that in the cheetah there has been a loss of genetic polymorphism, as a result of a reduction in the breeding population, which may have led to a loss of variation in the immune system and a relative inability to combat infectious processes. Spencer and Burroughs (1992) also showed that the level of maternally derived antibodies decreased in cheetah cubs between four and 12 weeks of age. Cheetahs do not thrive in captivity. Progressive myelopathy and cerebellar degeneration is not the only neurological disease recorded in the cheetah. A spongiform encephalopathy was described in four cheetahs by Kirkwood and Cunningham (1994). Munson and others (1999) reported a form of leucodystrophy in adult animals in both the USA and the UK which was associated with blindness, a lack of response to the environment and sometimes with incoordination and convulsions. Pathologically there was bilaterally symmetrical necrosis of cerebral white matter, accompanied by astrocytosis. The cause has not been established. Vitamin A deficiency has also been incriminated as the cause of ataxia in two adult cheetahs which had shown neurological signs from six months of age (Palmer and Franklin 1999). Pathologically there was evidence of coning of the cerebellum and ischaemic necrosis of the spinal cord. Progressive ataxia affected 18 9 per cent of litters of cheetahs born in Fota Wildlife Park between 1984 and 1999 (Guerin 1999) and is therefore a major problem in the preservation of this rare species. At present the cause is unknown. ACKNOWLEDGEMENTS The authors gratefully acknowledge the technical assistance of Mr Brian Cloak, Mr Mike Peacock, Ms Sheila Worrell, the staff of the Cork Regional Veterinary Laboratory and the wardens of Fota Wildlife Park. They also wish to thank the staff of the Regional Veterinary Laboratory for their assistance and Dr C. Walzer for advice.

References ADDIE, D. D. (1999) The Feline Virus Unit report on cheetah investigations. In Report of Workshop on Ataxia in Cheetah Cubs. Eds J. J. Callanan, L. Munson, N. Stronach. University College, Dublin, June 1999. pp 10- 11 BRADLEY, D. (1999) A genetic basis for ataxia in cheetahs? In Report of Workshop on Ataxia in Cheetah Cubs. Eds J. J. Callanan, L. Munson, N. Stronach. University College, Dublin, June 1999. pp 23-24 BRAND, D. J. (1981) Captive propagation at the National Zoological Gardens of South Africa, Pretoria. International Zoo Yearbook 21, 107-112

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GUERIN, L. A. (1999) juvenile ataxia in captive bred cheetahs at Fota Wildlife Park. In Report of Workshop on Ataxia in Cheetah Cubs. Eds J. J. Callanan, L. Munson, N. Stronach. University College, Dublin, June 1999. pp 6-9 HAFNER, A., SCHMIDT, P., HANICHEN, T. & SCHMAHL, W. (1996) Degenerative myelopathie bei geparden (Acinonyx jubatus). Berliner und Munchener Tierarztliche Wochenschrift 109,403 KIRKWOOD, J. K. & CUNNINGHAM, A. A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record 135, 296-303 MONTGOMERY, D. L. & STORTS, R. W. (1983) Hereditary striatonigral and cerebello-olivary degeneration of the Kerry blue terrier. Veterinary Pathology 20, 143-159 MUNSON, L. (1993) Inbreeding and disease in captive wild animals. In Zoo and Wild Animal Medicine. Current Therapy 3. Ed M. E. Fowler. Philadelphia, W. B. Saunders. pp 77-79 MUNSON, L., DE LAHUNTA, A., CITINO, S., RADCLIFFE, R., NEIFFER, D., MONTALI, R. J. & STALIS, I. (1999) Leukoencephalopathy in cheetahs (Acinonyxjubatus). In Report of Workshop on Ataxia in Cheetah Cubs. Eds J. J. Callanan, L. Munson, N. Stronach. University College, Dublin, June 1999. pp 20-22 PALMER, A. C. & CAVANAGH, J. B. (1995) Encephalomyelopathy in young cats. Journal of Small Animal Practice 36, 57-64 PALMER, A. C. & FRANKLIN, R. J. M. (1999) Review of neuropathological material from ataxic cheetah cubs at Fota Wildlife Park. In Report of Workshop on Ataxia in Cheetah Cubs. Eds J. J. Callanan, L. Munson, N. Stronach. University College, Dublin, June 1999. pp 13-15 PALMER, A. C. & NOEL, P. R. (1963) Neuropathological effects of prolonged administration of some hydrazine monoamine oxidase inhibitors in dogs.

Journal of Pathology and Bacteriology 86,463-476 SPENCER, J. A. & BURROUGHS, R. (1992) Decline in maternal immunity and antibody response to vaccine in captive cheetah (Acinonyx jubatus) cubs. Journal of Wildlife Diseases 28, 102-104 WALZER, C. & KUBBER-HEISS, A. (1995) Progressive hind limb paralysis in adult cheetahs (Acinonyx jubatus). Journal of Zoo and Wildlife Medicine 26, 430-435 WALZER, C., KUBBER-HEISS, A., GELBMANN, W., SUCHY, A., BAUDER, B. & WEISSENBOCK, H. (1998) Acute hind limb paresis in cheetah (Acinonyx jubatus) cubs. Proceedings of the Second Meeting of the European Association of Zoo and Wildlife Veterinarians. pp 267-273 ZWART, P., VON DER HAGE, M., SCHOTMAN, A. J. H., DORRESTEIN, G. M. & RENS, 1. (1985) Copper deficiency in cheetah (Acinonyx jubatus). Verhandlungen des Berliner 27. Internationalen Symposiums fur Erkrankungen der Zootiere, St Vincent. pp 253-257

_~ABSTRACT Fluoroscopy as an aid to the removal of oesophageal foreign bodies from dogs BETWEEN August 1993 and August 1998, 65 dogs were treated for an oesophageal foreign body. In 61 cases the attempt to remove the body was made with forceps under fluoroscopic guidance, and it was successful in 51 of them. Three dogs died or were euthanased in hospital, and two others died within two weeks of being discharged. The surviving dogs were followed up for at least four months and for a median period of two years. Forty-two of them were reported to be normal, one had a voice change and two develped a cough. The removal of oesophageal foreign bodies under fluoroscopic guidance appears to be an effective method for treatment with few complications. HOTSTON MOORE, A. (2001) Removal of oesophageal foreign bodies in dogs: use of the fluoroscopic method and outcome. Journal of Small Animal Practice 42, 227-230

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Progressive encephalomyelopathy and cerebellar degeneration in 10 captive-bred cheetahs A. C. Palmer, J. J. Callanan, L. A. Guerin, et al. Veterinary Record 2001 149: 49-54

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