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This article was published in 1983
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Ataxia in Sheep
H.C. Grant-Frost, B.V.Sc., Veterinary Inspector, MUDGEE
INTRODUCTION
Interest in gait abnormalities in sheep has increased in recent years, especially since the severe outbreak of Tribulus Ataxia seen in central western areas of NSW since March, 1981. Apart from well-defined ataxias such as Phalaris and Ryegrass Staggers in sheep other ataxias have in previous years occurred in the Upper Hunter, Yass and warialda areas of NSW.
HISTORY
As far back as 1962 an unusual gait abnormality was described in merinos on two Mudgee properties. It is of interest to note that one of these properties was a stud, and the other had purchased rams from this flock on a regular basis for some years. Affected sheep on the stud property included at least three rams. One ram was sent to VRS Glenfield in 1964 for detailed investigation.
For the past five to six years a specific gait abnormality has occurred in one flock about 30 km south of Mudgee. The property is situated in hilly country with pasture consisting of clover/natural grasses and small areas sown to Phalaris grass. Tribulus sp. has never been seen on the property. Each year, up to 25 ataxic sheep are seen amongst 1-2 year old Merino ewes. Few wethers are run on the property. Clinical signs are not related to season, pregnancy, grazing of Phalaris or sheep running in any particular paddocks.
CLINICAL SIGNS
These develop over a period of at least two months. In the early stages abnormality of gait occurs only after the sheep have been driven for a considerable distance, when a slight dragging of the hind limbs is seen. Over a period of weeks this becomes progressive hind limb ataxia leading to flaccid paralysis. The front legs are never affected and, in the advanced stage of ataxia, hindquarters are dragged forward and/or sideways by the normal locomotion of the front limbs. The crab-like gait of Tribulus Ataxis is absent. In the final stages of the disease the sheep go down, rest for a period and then may struggle up again. Affected sheep remain bright and alert and retain their appetite. They would die of thirst, starvation or misadventure if they were not euthanased. About three years ago the owner sold some young sheep to a neighbour. Three months later about six animals in the purchased group developed ataxia. No other cases had been seen before or have occurred since in this flock.
HISTOPATHOLOGY
Brain and spinal cord were examined at the Regional Veterinary Laboratory, Orange. In the brain severe diffuse status spongiosis involving the white matter tracts of the cerebral cortex, the cerebellum and brain stem were seen. There was localised non-suppurative inflammatory response (perivascular cuffing) in the corpora quadrigamina.
In the spinal cord sections of thoracic and lumbar cord showed severe active Wallerian degeneration of all white matter tracts, and degeneration and necrosis of neurones of the grey matter, more severe in the lumbar card. No significant findings occurred in Heart, Liver, Lung, Kidney and Spleen.
BIOCHEMISTRY
Liver copper and kidney selenium levels were within normal limits.
DISCUSSION
Histopathological sections were referred to Dr. W. Hartley in New Zealand for his comments. He states that the lesions were almost certainly those that he described as Murrurundi disease some years ago. The aetiology of course is obscure but either a slow virus disease or genetic origin have been considered. The genetic theory is favoured by Dr. Hartley and staff at the Regional Veterinary Laboratory in Orange. In support of such a theory is the fact that replacement rams in the affected flock have for many years been introduced from a single Merino Stud and that the owner has bred some of his own flock rams using the same bloodline.
Retrospective examination of records of the 1962/64 cases bear strong similarities to the independent assessment of the cord and brain pathology in two sheep examined at the Orange Regional Veterinary Laboratory. As mentioned previously, there was circumstantial evidence of a genetic factor in the early cases.
Concerning clinical signs, the ataxias in these flocks appear to be identical. The 1962/64 case also involved a progressive flaccid paralysis of the hind limbs with no front limb involvement. Illness in the early cases similarly all progressed to total recumbency and death caused by starvation, thirst or misadventure. In each instance, sheep of identical age were affected, i.e., two tooths.
In the past 45 years there have been other reports of ataxic sheep in Mudgee District, but in many cases detailed investigations were not carried out. On three properties, however, Tribulus ataxia was diagnosed.
It appears that the best way to investigate the problem, and any genetic involvement, would be to breed from affected ewes and rams and see how their progeny develop. The limiting factor here would be the rams ability to mate successfully; the use of A.I. could be considered.
SUMMARY
Ataxia in Merino sheep in the Mudgee District is described. There is evidence that recent cases on one property are similar to ataxia seen in two other flocks in 1962/64, and similar to an ataxia named 'Murrurundi disease' by Dr. W. Hartley.
ACKNOWLEDGEMENTS
The assistance and interest by Chris Bourke and Mark Carigan, V.R.0.'s, Regional Veterinary Laboratory, Orange, is gratefully acknowledged, as is the interest shown by Dr. W. Hartley, New Zealand.