On the 28th December, 1977 I investigated a condition resulting in some mortality in merino wethers. The owner suspected that 1080 rabbit poison, which had been used in the paddock since the previous rain, must be responsible but had been confident no bait material had remained.
The condition described by him was that when the mob was moved some sheep lagged behind, appeared to cramp and shortly went down, trembling and showing difficulty in breathing. If left the sheep moved off again later, but once affected, they usually tucked up and died on the camp after several days.
post-mortem examination of a wether which died that morning revealed very severe congestion in all viscera. The lungs were full of sanguineous frothy fluid. Myocardial ecchymoses were present.
A live animal was taken to the Regional Veterinary Laboratory for examination. He could be stood up but this resulted in almost doubling of the heart rate from 70/minute to 130/minute. A twisted neck suggestive of a cow with milk fever and muscular tremors were pronounced and copious clear watery urine was passed, this giving a positive acetest reaction.
Post-mortem examination of this (animal) revealed no marked congestion, although some was noted in the kidneys. The liver was fatty. Histopathology did reveal congestion and polymorphonuclear cell infiltration in liver and kidney haemorrhage and early nephritis, and congestion in lungs. A Haematological examination showed P.C.V. of 45% and total R.B. cell count of 18.21 x 106 - both suggestive of haemoconcentration.
An attempt was made to discover a description of Fluoroacetate poisoning in sheep.
Jubb and Kennedy - Pathology of Domestic Animals, Vol. 1., discuss the clinical entity in ruminants particularly with reference to Acacia georginae (Gidyea), poisoning in sheep and cattle. 'Sheep may collapse suddenly and die within a few minutes and those less severely affected may develop cardiorespiratory distress and weakness if driven and shortly die. Showing these signs, some, if left undisturbed, may recover to appear normal until again forced to exercise ... death occurring with cardiac failure, fibrillation, cyanosis, dyspnoea and terminal convulsions ....'
'The post-mortem findings are referable to myocardial injury...'
Diagnosis can be confirmed to some degree only on the histological myocardial lesions.
Blood and Henderson 'Veterinary Medicine (3rd edition) referring to Gidgee poisoning mentions tachycardia (to 300/minute) 'dyspnoea, cyanosis, convulsions and death. Cardiac irregularity, moderate bloat and frequent micturition are also observed in some cases ... At necropsy there is congestion of the alimentary mucosa, flabbiness of the myocardium and ... haemorrhage. There may be oedema and congestion of the lungs'.
At this stage, as most of the above agreed with the clinical condition seen, and history of possible access existed, a chronic fluoroacetate poisoning was suspected.
On 4.1.1978, the owner again wanted to know how long the poison lasted as the sheep had been off poisoned country for over a week and were still dying.
A further visit revealed that dead sheep still showed the same congestion but also the rumen had shrunk to about 1 litre of desiccated fibrous material and intestinal contents were also completely desiccated. An examination of two affected sheep in the mob revealed that they moved off when disturbed with heads carried very low. The gait progressively became shorter with increasing humping of the back. After about 50 metres the sheep stopped and just collapsed in sternal recumbency. Muscle trembling and gasping shallow respiration were noticeable after this exertion.
Botulism was then suspected and subsequently a search through the inspissated ruminal contents revealed a large portion of animal tissue - probably rabbit skin.
A common behavioural trait seen in Botulism in sheep is a rather constant waggling of the tail as if fly struck. This was not very noticeable in this outbreak, only being seen occasionally in three affected wethers. In a previous outbreak which followed rotting of vegetation under summer floodwater this behaviour was very common.
Several points are of interest in this outbreak.
Firstly, depraved appetite which resulted in the condition was completely unsuspected in the area. Numerous neighbouring properties would have a heavy cover of rabbit carcases but no problems occur.
Secondly, death from congestive heart failure would be expected with chronic 1080 poisoning but has not been described in Botulism. Seddon (1965) states 'one of the characteristic features of classical botulism is the absence of gross post-mortem changes. In this outbreak there was not much pathology to note in animals destroyed, but in animals which died naturally the converse was the case. I have rarely seen more severe pulmonary congestion.
Thirdly, a follow up enquiry to the owner revealed some interesting details. Eight sheep were in a hospital pen when the condition was diagnosed. He started dosing them with water, 2 gallon twice a day, using a drenching bottle and about 500 mm of stomach tube. All 8 survived, one paralysed wether taking over 2 weeks to be able to walk and drink of his own accord. This wether has now joined other paddocked sheep. The owner had no difficulty passing a small diameter tube, only a few times encountering a cough which necessitated a second attempt.
Most of the sheep were drinking within a week, others being given another 'drench' when they looked hollow.
This outbreak of Botulism deserves consideration for two reasons - both just mentioned and which may be of importance - namely that a very marked pathological picture may be present when dead animals rather than moribund ones are examined, and that water deprivation may be the main cause of death in affected sheep, particularly in the course of the disease. This latter fact may be of importance in other species. Horses are said to mouth water at the trough but be unable to swallow.
Sheep are said to survive Botulism more commonly than other species, and they are also known to be highly resistant to water deprivation.