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This article was published in 1942
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
AN ATYPICAL ENTEROTOXAEMIA
By J. G. JOHNSTON. Inspector of Stock. Albury.
Enterotoxaemia of sheep is a commonly known disease to sheepmen in New South Wales and other states. For some time it was considered to be a disease of lambs and only associated with flush seasons. It is now known, however, that losses occur in grown sheep and not always in flush seasons. Investigations were conducted into the cause of mortalities in the Albury District in grown sheep in 1937, 1939 and 1941.The outbreak in 1937 occurred in 550 corriedale wethers, three years old, in fat condition. Three days after changing from one pad-dock to another, eight were found dead and seven others sick. In all, 40 died over a period of ten weeks from February to May. The grazing land was of poor quality, hilly and light, carrying one sheep to 2½ acres. Pasture consisted of mixed grasses and some wattle scrub.
In 1939 (August) out of 40 fat crossbred wethers, two years old, three died in three days. The pasture consisted of clover capeweed, patterson's curse and mixed grasses. This year was about the wettest on record and there was abundant growth.
In April, 1941, 500 corriedale cross ewes were changed from one paddock to another, two days later 14 were found dead and others were sick. The ewes were dry and wet, in fat condition, deaths occurred in both types. Some had lambs several weeks old. The pasturage was, chiefly subterranean clover growing on rich Murray river frontage land. In all, 32 died. No lambs died.
Symptoms: Sick animals stand with head down, arched back or would lie normally. No interest was taken in surroundings. When disturbed they walked with a stiff staggering gait. Temperature in some cases was up to 107. There was evidence of blood discharge from the anus. If the sick animal was handled it would tremble violently. Death occurred quietly. In most carcases there was a dark tarry like discharge from the anus.
Post-mortem: Post-mortem examination presented features not usually seen in the more common types of enterotoxaemia. The mucosa of the large bowel, from caecum to anus, is intensely congested and the bowel contained blood. The mucosa of small bowel has patchy congested areas and the ingesta is blood stained. A varying quantity of straw-coloured pleural effusion may be found, up to one quart in extent. The ingesta of abomasum (mostly fluid) is brown coloured. The heart is intensely congested, the pericardial fluid bloodstained. In some cases the whole of the fatty tissue is slightly icteric and that around the kidneys oedematous.
In the 1937 outbreak, toxin tests were not undertaken but gram negative types, resembling Pasteurallae, were seen in smears from the bowel walls. Owing to delay in bacteriological examination they probably died out and did not appear in cultures.
In the 1939 outbreak a weak toxin was recovered from the bowel contents. B Coli was recovered from the kidneys and large numbers of this organism were found to be almost exclusively growing in the intestine.
In 1941 outbreak a toxin was demonstrated in the filtrate of duodenal contents which proved to be extremely toxic to small animals at Glenfield Veterinary Research Station.
Conclusion: These three mortalities had such a close resemblance in anti and post-mortem appearances it is concluded they were identical. The tests conducted in the 1941 outbreak at Glenfield Veterinary Research Station provides conclusive evidence that enterotoxaemia of an atypical form caused that mortality.