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This article was published in 1952
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K.V. BYRNE, B.V.Sc., Inspector of Stock, Young.

In February and March, 1952, widespread losses took place in the Young Pastures Protection Board District from Botulism in livestock. Most of these occurred in sheep although there was a little mortality in cattle also. The circumstances surrounding all these losses were similar; particularly in that the animals had been observed eating rabbit carcases, and that the pastures, although adequate in quantity, were very deficient in quality, consisting of old dry feed only.

At that particular time there was a general mortality in rabbits from myxomatosis; while a considerable amount of poisoning with strychnine also was occurring. In some cases the rabbits suspected of being the source of the Botulism toxin had been poisoned and in others they had died from myxomatosis. In the majority of mortalities the latter had been the case but this is not considered significant as losses from the rabbit disease were much more widespread than those from poisoning.

Losses took place in all classes of sheep but were most severe in ewes, especially in ewes in lamb. To give an indication of their severity the following figures for five properties are quoted:—

Number Type of Sheep Deaths
(1) 1000 Ewes and Wethers 179 ewes, 15 wethers
(2) 712 Aged Ewes 232
2450 Young Ewes 200
(3) 938 Ewes 85
400 Wethers 55
355 Weaners 20
(4) 700 Wethers 30
1200 Ewes 20
(5) 300 Ewes 65

The most helpful guide in determining whether or not Botulism was the cause of a mortality was the symptoms. The general picture presented was that the affected animal stood around in a dopey condition, slobbered from the mouth, showed nervous muscular spasms and wriggling of the tail after the manner of a fly-blown sheep. The last was found to be the most constant and striking symptom.

Symptoms as described by various owners of affected sheep were as follows:—

(1) Fluid coming from mouth, wagging of tail, wobble in hind quarters when walking, neck very stiff and carrying head very low.
(2) General listlessness. Would run a short distance with head down and wagging their tails, then stop and either lie down or fall over. Usually died in a week or so.
(3) Sheep listless and mainly away from mob. Would run for a few yards with head on one side. Would then stop and walk backwards, stamping hind feet as if fly-blown.
(4) In early stages sheep hung back while moving a mob. Later they seemed to lose control of their hind legs. This became worse until death. Affected sheep also seemed humped up, and there was a clear saliva coming from the mouth.
(5) Wagging of tail, trying to pass urine, head lowered to ground, frothing at mouth, breathing very quickly. These symptoms lasted from two to thirty hours.
(6) Staggery gait, twitching of tail, head extended. Showed some nervous symptoms. Death occurred in from a few hours to two days. Sbme sheep lay down and made no attempt to get up.
(7) Frothing of mouth, tucked up and twitching of tail. A weakness shown in legs after driving, which made sheep lie down.

Another owner not quoted above also stated that he had seen the sheep walking backwards.

Post-mortem examination of a sheep destroyed for the purpose or carried out soon after death usually showed nothing of significance except that fragments of rabbit carcases were frequently present in the rumen. However, the latter was not always the case. Where a post-mortem was delayed until 10 to 12 hours after death, decomposition was far advanced; the carcase being very distended and showing the dark green discolouration commonly seen in sheep dead from Entero-toxaemia. When the post-mortem examination was conducted the similarity to this latter disease continued and the general post-mortem picture was such that in the absence of a knowledge of the symptoms and history a diagnosis of Entero-toxaemia could easily be given. This actually occurred with the writer with the first case investigated, and, acting on that advice, the owner concerned inoculated with a Cl. welchii vaccine. This was followed by a cessation of the mortality, but subsequently (after 1 to 2 weeks) the losses recommenced.

Eventually, laboratory examination of specimens failed to support the diagnosis of Entero-toxaemia, but because of the similarity of the post-mortem picture to that disease, material for examination for its presence was sent from all further mortalities investigated. Examination for toxin was negative in all cases except one, in which a weak toxin was demonstrated.

In no case was the laboratory able to isolate the organism of Botulism from rabbit carcases obtained in these mortalities, but on previous experience of the disease in this State it was considered most likely that the type of organism responsible would have been type "B". As no toxoid was available for that type, no vaccination procedure could be adopted and the basis of control was an attempt to prevent stock eating the rabbit carcases. Because of the widespread mortality taking place in the latter it frequently was found impracticable either to place the stock in a paddock where no carcases were to be found or to gather up carcases.

The reason for the ingestion of the carrion was the failure of the pasture, owing to a long dry spell, to provide an adequate supply of nutriments. The principal method of control, therefore, was the giving of sufficient supplementary feed to remedy the deficiency. From the attempts made by various stock owners to do this it would appear that unimproved pasture in this district at the end of a long dry summer has very little food value, however bulky it may be. This conclusion was drawn from the fact that a maintenance ration had to be supplied before any worthwhile improvement took place. On several occasions stock-owners provided less than a full ration; hoping that the pasture, which had plenty of bulk, would provide the balance, but the sheep continued to eat the rabbits and losses did not decrease.

When a full ration was supplied losses ceased or fell to a very low level, whether rabbit carcases were picked up or not. The mortalities eventually ceased altogether as soon as the green shoot appeared following the March break in the weather.

In the above feeding methods it was not found necessary to supply any unusual type of foodstuff, such as meatmeal, in an attempt to remedy the protein deficiency, although food stuffs of a higher protein value, such as lucerne hay, appeared to be more valuable than cereal products. This was apparently the opinion of the sheep also, as if a combination of a cereal grain and a foodstuff such as clover hay was put out the latter was eaten first. Some owners supplied mineral licks but others did not and their use did not appear to be essential.

One significant feature observed was that losses were much more severe on unimproved pasture than on improved pasture. No general attempt was made to treat sick animals, but one owner reported that out of 8 sick ewes dosed with linseed oil, 4 recovered; whilst another stated that he saved 3 wethers by giving them a dose of 2 ozs. of castor oil.

Conclusion:—That losses in sheep from Botulism resulting from the eating of carrion can be prevented or reduced to a tolerable level, without denying access to the carrion, by feeding a ration which is adequate in quantity and quality of the usual type of stock foodstuffs. It would appear also that prevention of losses from Botulism is another sound reason for urging landholders to give attention to pasture improvement.

Acknowledgement: It is mentioned that after the losses ceased questionnaires were sent to those stock owners who had serious loss. All were good enough to reply and their answers were very helpful in preparing this article. They also confirmed the opinions formed by the writer during the course of the mortalities.


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