INTRODUCTION.
Although polio-encephalomalacia (P.E.) of sheep has been recognised as a specific nervous disease in New Zealand for some years, it does not appear to have been similarly recognised in Australia.
P.E. IN NEW ZEALAND.
In April, 1958, Mullins et al. described an outbreak of blindness in sheep in New Zealand. The main clinical feature was a blindness commonly of a few weeks' duration. In most cases complete recovery occurred. There were some deaths and a few of these were attributed to accidents resulting from blindness.
At post-mortem examination the only abnormality detected was in the brain. Histologically there were numerous foci of non-inflammatory necrosis in the deeper layers of cerebro-cortical grey matter (polio-encephalomalacia).
Hartley and Kater (1959) reviewed a series of cases recognised by them at Wallaceville Research Station. By this time a pattern had developed. Two distinct forms of P.E. were described, a severe form and a mild form.
In the severe form, many of the affected sheep were found prostrate, lying on their sides; they usually showed nystagmus, absence of the eye preservation reflex and opisthotonus, together with intermittent clonic convulsions. Less severely affected sheep could stand with assistance, but when left alone either attempted to circle and then fell over, or adopted a "dog-sitting, star-gazing" attitude. Others showed less severe signs. The morbidity was rarely greater than 5%, the mortality, however, was almost 100%.
The mild form was characterised by the sudden appearance of partial to complete blindness. In some cases dejection and head pressing also occurred. Two outbreaks of the mild form were noted. One case occurred after shearing and the other after crutching.
PATHOLOGY
In almost all cases of severe P.E. distinct macroscopic lesions were visible. Areas of yellow, discoloured, cortical grey matter were noted. Histologically, various degrees of encephalomalacia were described.
AETIOLOGY.
The aetiology appears to remain obscure. An interesting feature was that, although the condition occurred in both sexes, there was a seasonal incidence in ewes. The condition was commonest in ewes between March and April, i.e., during pregnancy. Both entero-toxaemia vaccinated and unvaccinated sheep were affected.
CASE AT BLAYNEY.
In late July the writer was called to examine a sick, stud Merino ewe at Blayney. The ewe had been sick for at least one day when examined. Treatment appropriate for hypomagnesaemia had been given on the first day of the illness. The ewe did not respond and, when examined by the writer, was in lateral recumbency. The ewe was lying in a normal relaxed position. On being placed in a normal sitting position, the head was drawn further and further back until the animal fell on its side again. The eye preservation reflex was absent. There was no history of E.T. vaccination. The ewe was in the fourth month of pregnancy at the time.
The night after the above clinical examination the ewe died naturally. Post-mortem examination was carried out early the next morning. Nothing of significance was noted at autopsy. Urine was negative to tests for reducing sugars and acetone bodies.
However, on histopathological examination very marked lesions were seen. There was severe polio-encephalomalacia of a few days duration, particularly in the hippocampus. This was less severe in the cerebral cortex. There was accompanying extensive secondary demyelination.
P.E. IN AUSTRALIA.
This is by no means the first or the only case of P.E. in Australia. Some half dozen cases of the condition have been noted at Glenfield since June, 1963. As in New Zealand, the aetiology of the condition in Australia remains obscure.
ACKNOWLEDGEMENT.
The careful histopathology by Joan C. Kater is greatly appreciated.