Artificial induction of red gut in sheep.

Eight out of 10 lambs died within six to 11 hours after occlusion of the cranial mesenteric blood vessels by a snare placed around both the artery and vein. Death resulted from shock and was accompanied by post mortem findings identical to those seen in red gut. It is suggested that the cause of death in the naturally occurring disease is from arrested mesenteric blood flow following intestinal torsion.

Suspected lysosomal storage disease in kangaroos.

A probable neurovisceral lysosomal storage disease is reported, for the first time, in immature red and grey kangaroos (Macropus rufus and M. giganteus). Foamy, pale eosinophilic, periodic acid-Schiff positive, intracytoplasmic material was stored in the liver, lymphoid tissue, kidney, adrenal gland, stomach, blood vessels and central nervous system. Extensive Wallerian-type degeneration was present in the central nervous system. Electron microscopic study of one animal revealed electron dense, cytoplasmic lamellar bodies in neurons and foamy visceral cells. The disease differs from other reported storage diseases in the distribution and nature of the lesions.

Redgut in sheep: a disease with a twist.

Redgut is a condition of sheep characterised by sudden death. Post-mortem findings are reddened small and large intestines, which are usually displaced. Sheep are predisposed to the condition by a combination of circumstances, including a small rumenoreticulum because of the nature of the feed (usually highly digestible forage), and increased large intestinal size and function. To accommodate this, and because there is not a large rumenoreticulum to stabilise the gut position, the intestinal mass moves to an unstable position in the peritoneal cavity. Some unknown event precipitates a further change in intestinal position, resulting in accidental torsion of the intestinal mass, with resultant obstruction of the mesenteric blood vessels and death from shock. The condition can be prevented by careful attention to feeding regimes that prevent development of the predisposing feature of small forestomachs and an oversized large intestine, resulting in a displaced intestinal mass. This is achieved by intermittent grazing of dangerous pastures.

Secondary phosphorus poisoning in dogs.

Subsequent to a possum (Trichosurus vulpecula) poisoning operation purportedly using 1% phosphorus baits, six dogs with access to poisoned possums died of phosphorus poisoning. Two dogs survived, following treatment with oral copper sulphate and parenteral vitamin K. Clinical signs included depression, jaundice, vomiting and bloody diarrhoea. Post-mortem lesions included large areas of subcutaneous, interstitial and intermuscular haemorrhage, subserosal haemorrhage and liver degeneration. Free phosphorus was detected in the ingesta of three of the dogs which died up to 7 days after the last of the poison was laid. Analysis of two batches of baits used showed P levels of 1.17% and 1.24%.

Tactical control of ovine Campylobacter abortion outbreaks with a bacterin.

Abortions due to Campylobacter fetus fetus (C. fetus fetus) were diagnosed in three Canterbury ewe flocks 6 weeks prior to lambing. In two of the flocks, two inoculations of a C. fetus fetus bacterin, 10 days apart, reduced the incidence of abortions in the treated ewes to about one third and one half respectively of the level in the control ewes in the same flock. The treatment had no effect in a third flock where an outbreak had been in progress for 2 weeks before investigations started. The results confirm earlier Scottish work where pregnant sheep were inoculated with a C. fetus fetus vaccine following artificial challenge with C. fetus fetus. This inoculation significantly reduced the number of C. fetus fetus abortions. The results also indicate that treatment must start very early in an outbreak.