1
Mu1 tifocal symmetrical We wish to thank Dr P Harper, NSW Department of Agricul- ture. for his helpful advice and discussion. encephalomyelopathy of Simmental cattle References Harper PAW, Hartley WJ, CoverdaleORand GillJM (1989) VetRec 124: 122 Lindenberg R(1982)InHirrologyondH~o~thdogyoftheNervovrSy~~em, edited by Haymaker W and Adams RD. Charles C 'Ihomas, Springfield, (Accepted for publication 8 February 1991) Department of Agriculture, PO Box 618, Naracoorte, South Australia 527 1 JWFINNIE South East Regional Veterinary Laboratory, p 973 Department of Agriculture, Central Veterinary Laboratories, PO Box 1671, Adelaide, South Australia 5001 PH PHILLIPS A rare, possibly inherited, neurological disorder of Simmental calves less than 1 year old, designated multifocal symmetrical encephalopathy(MSE), has been described in Australia and New Zealand (Harper el al1989). The condition is manifest as hind limb, or occasionally fore limb, ataxia and paralysis, with affected animals eventually unable to rise and requiring euthanasia.Morphological changesin the brain are characterised by bilaterally symmetrical foci of malacia. This paper reports a similar disease entity in 3 Simmental calves on a property in western Victoria. Two heifers, 9 and 10-months-old,and an 11-month-old steer, presented with posterior ataxia and progressive paralysis with intermittent periods of recumbency. After a rapid cliical course of about 2 wk, the animals were unable to stand and were killed. The steer was available for necropsy. At necropsy, bilaterally symmetrical, greyish foci, 2 to 10 mm in diameter, were found in the basal ganglia, midbrain, pons, medulla oblongata, and thoracic spinal cord. No other macro- scopic changes were observed Microscopic examination of the central nervous system revealed malacic lesions in the caudate nucleus, putamen and internal capsule, adjacent to the third ventricle, anterior and posterior colliculi, substantia nigra, pon- tine and olivary nuclei, vestibular nucleus, and in the grey matter of the spinal cord, especially the dorsal portion, with some extension into the surrounding white matter. No lesions were found in the cerebral cortex, cerebellum or optic tracts, and pathological alterations were confiied to neural tissues. In the necrotic foci there was lysis and liquefaction of the neuropil and necrosis of many neurons and glial cells. Numerous axonal spheroids of varying size were evident, together with a few lipid-laden macrophages (compound granular corpuscles) in some areas of malacia. Blood vessels were virtually the only remaining elements in a few foci, and their endothelial cells were hypertrophied. The neuropil con- tiguous with necrotic areas was frequentlyvacuolated with some secondary demyelination present, especially in the spinal cord. These cerebral lesions resemble those described by Harper el al (1989) in both their nature and distribution,except for the addi- tional finding of malacia in the spinal cord in our case. We propose therefore that the condition be redesignated multifocal symmetrical encephalomyelopathy to include the extension of the lesions. The aetiology and pathogenesis of MSE is unknown, and the number of reported cases is insufficient to allow any mode of inheritancetobe determined. These3 calves,however,possessed a common ancestry, the grandsire of the steer beiig the sire of the 2 heifers, which were alsofull sisters. Bilaterally symmetrical malacicfoci, as observed in the brains of these cases, are general- ly attributed to vascular factors or inherent physicochemical properties of certainregions in the brain (Lindenberg 1982).The preservation of some neuronal and glial elements in affected areas would tend to favour the latter pathogenesis. Suspected poisoning of camels by Trema tomentosa (poison peach) Queensland Department of KFTRUEMAN Primary Industries, Animal Research Institute, Yeerongpilly, Queensland 4105 Noosa Veterinary Surgery, 15 Hilton Terrace, Tewantin, Queensland 4565 Mw POWELL Trema tomentosa (poison peach), formerly named T aspera (Hewson 1989),grows in open forest or on the edges of light rain forest in coastal and subcoastal areas of eastern and northern Australia (Everist 198l), where it is a frequent pest of cleared land. The plant contains a hepatotoxic glycoside(Oelrichs 1968). Poisoning has been recorded in cattle, sheep and goats (Mulheam 1942),horses (Hill et aZ1985) and fallow deer (McKenzie 1985). We report here the apparent susceptibility of camels to intoxicationwith poison peach. Five adult circus camels were located at a park in Noosa Heads, approximately 100kmnorthof Brisbane. They arrived there after a short road journey, and were tethered on the border of the park against a road embankment covered with a variety of shrubs. They were provided with sorghumhay, and 48 h after arrival, an adult, castrated, male camel was noticed sick. It rapidly deteriorated and became recumbent. When examined, it had a temperature of 3?C, a weak, rapid heart beat, muddy mucous membranes, rapid gut sounds and diarrhoea, and died soon after. Two other camels exhibited anorexia, sweating, epiphora and muscle fasciculation of the l i i b s and flanks. One of these was treated with liquid paraffii per 0s and both received parenteral antibiotics* and an antispasmodict. Six hours later one died, and the other was euthanased with intravenous barbiturate solution. These last 2 camels were necropsied 6 h after death. Both had subcutaneous haemorrhages over the chest and abdomen, petechial haemorrhages under the serosa of the rumen, abomasum and duodenum, and congested liver and kidneys. In the liver from one camel examinedhistologically there was acute coagulative necrosis of virtually all hepatocytes, with severe haemorrhage. On the embankment near where the camels were tethered, several lmown toxic plants were growing, namely Lun- tuna camara (lantana), Pteridium esculentum (bracken fern) and T tomentosa (poison peach). There was ample evidence that poison peach plants had been heavily grazed by the 3 affected camels, while the other 2 had beenunable toreachtheplants.Botanicalexaminationof amen sample from one affected camel did not identify any toxic species. Aquacaine UA Suspension, Commonwealth Serum Laboratories, t Buscopan Cornpositurn, Boehringer lngelheim Ply LM, Artarmon, New Parkville. Victoria South Wales Australian Veterinary Journal, Vol68, No 6. June 1991 213

Multifocal symmetrical encephalomyelopathy of Simmental cattle

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Mu1 tifocal symmetrical We wish to thank Dr P Harper, NSW Department of Agricul- ture. for his helpful advice and discussion.

encephalomyelopathy of Simmental cattle References

Harper PAW, Hartley WJ, CoverdaleORand GillJM (1989) Vet Rec 124: 122 Lindenberg R(1982)InHirrologyondH~o~thdogyoftheNervovrSy~~em,

edited by Haymaker W and Adams RD. Charles C 'Ihomas, Springfield,

(Accepted for publication 8 February 1991)

Department of Agriculture,

PO Box 618, Naracoorte, South Australia 527 1

J W F I N N I E South East Regional Veterinary Laboratory, p 973

Department of Agriculture, Central Veterinary Laboratories, PO Box 1671, Adelaide, South Australia 5001

PH PHILLIPS

A rare, possibly inherited, neurological disorder of Simmental calves less than 1 year old, designated multifocal symmetrical encephalopathy (MSE), has been described in Australia and New Zealand (Harper el al1989). The condition is manifest as hind limb, or occasionally fore limb, ataxia and paralysis, with affected animals eventually unable to rise and requiring euthanasia. Morphological changes in the brain are characterised by bilaterally symmetrical foci of malacia. This paper reports a similar disease entity in 3 Simmental calves on a property in western Victoria.

Two heifers, 9 and 10-months-old, and an 11-month-old steer, presented with posterior ataxia and progressive paralysis with intermittent periods of recumbency. After a rapid cliical course of about 2 wk, the animals were unable to stand and were killed. The steer was available for necropsy.

At necropsy, bilaterally symmetrical, greyish foci, 2 to 10 mm in diameter, were found in the basal ganglia, midbrain, pons, medulla oblongata, and thoracic spinal cord. No other macro- scopic changes were observed Microscopic examination of the central nervous system revealed malacic lesions in the caudate nucleus, putamen and internal capsule, adjacent to the third ventricle, anterior and posterior colliculi, substantia nigra, pon- tine and olivary nuclei, vestibular nucleus, and in the grey matter of the spinal cord, especially the dorsal portion, with some extension into the surrounding white matter. No lesions were found in the cerebral cortex, cerebellum or optic tracts, and pathological alterations were confiied to neural tissues. In the necrotic foci there was lysis and liquefaction of the neuropil and necrosis of many neurons and glial cells.

Numerous axonal spheroids of varying size were evident, together with a few lipid-laden macrophages (compound granular corpuscles) in some areas of malacia. Blood vessels were virtually the only remaining elements in a few foci, and their endothelial cells were hypertrophied. The neuropil con- tiguous with necrotic areas was frequently vacuolated with some secondary demyelination present, especially in the spinal cord. These cerebral lesions resemble those described by Harper el al (1989) in both their nature and distribution, except for the addi- tional finding of malacia in the spinal cord in our case. We propose therefore that the condition be redesignated multifocal symmetrical encephalomyelopathy to include the extension of the lesions.

The aetiology and pathogenesis of MSE is unknown, and the number of reported cases is insufficient to allow any mode of inheritance tobe determined. These 3 calves, however,possessed a common ancestry, the grandsire of the steer beiig the sire of the 2 heifers, which were also full sisters. Bilaterally symmetrical malacic foci, as observed in the brains of these cases, are general- ly attributed to vascular factors or inherent physicochemical properties of certain regions in the brain (Lindenberg 1982). The preservation of some neuronal and glial elements in affected areas would tend to favour the latter pathogenesis.

Suspected poisoning of camels by Trema tomentosa (poison peach)

Queensland Department of KFTRUEMAN Primary Industries, Animal Research Institute, Yeerongpilly, Queensland 4105

Noosa Veterinary Surgery, 15 Hilton Terrace, Tewantin, Queensland 4565

Mw POWELL

Trema tomentosa (poison peach), formerly named T aspera (Hewson 1989), grows in open forest or on the edges of light rain forest in coastal and subcoastal areas of eastern and northern Australia (Everist 198l), where it is a frequent pest of cleared land. The plant contains a hepatotoxic glycoside (Oelrichs 1968). Poisoning has been recorded in cattle, sheep and goats (Mulheam 1942), horses (Hill et aZ1985) and fallow deer (McKenzie 1985). We report here the apparent susceptibility of camels to intoxication with poison peach.

Five adult circus camels were located at a park in Noosa Heads, approximately 100kmnorthof Brisbane. They arrived there after a short road journey, and were tethered on the border of the park against a road embankment covered with a variety of shrubs. They were provided with sorghum hay, and 48 h after arrival, an adult, castrated, male camel was noticed sick. It rapidly deteriorated and became recumbent. When examined, it had a temperature of 3?C, a weak, rapid heart beat, muddy mucous membranes, rapid gut sounds and diarrhoea, and died soon after.

Two other camels exhibited anorexia, sweating, epiphora and muscle fasciculation of the l i ibs and flanks. One of these was treated with liquid paraffii per 0s and both received parenteral antibiotics* and an antispasmodict. Six hours later one died, and the other was euthanased with intravenous barbiturate solution.

These last 2 camels were necropsied 6 h after death. Both had subcutaneous haemorrhages over the chest and abdomen, petechial haemorrhages under the serosa of the rumen, abomasum and duodenum, and congested liver and kidneys. In the liver from one camel examinedhistologically there was acute coagulative necrosis of virtually all hepatocytes, with severe haemorrhage. On the embankment near where the camels were tethered, several lmown toxic plants were growing, namely Lun- tuna camara (lantana), Pteridium esculentum (bracken fern) and T tomentosa (poison peach).

There was ample evidence that poison peach plants had been heavily grazed by the 3 affected camels, while the other 2 had beenunable toreachtheplants.Botanicalexaminationof a m e n sample from one affected camel did not identify any toxic species.

Aquacaine UA Suspension, Commonwealth Serum Laboratories, t Buscopan Cornpositurn, Boehringer lngelheim Ply LM, Artarmon, New

Parkville. Victoria

South Wales

Australian Veterinary Journal, Vol68, No 6. June 1991 213