A producer running about 50 cows in the Lake George district rang enquiring about a 6-month-old Angus cross steer with a prolapsed rectum. Only one steer in the mob of condition score 2.5-3.0 cows was affected. The herd had been agisted on the neighbouring property that had been destocked for a number of years. That summer was a little wet and the agisted property would have been quite lush. This would have been a good environment for weed growth. Of questionable significance is the fact that the cow was agisted in southern Queensland the year before.
The steer was in store condition. The rectum while prolapsed was otherwise relatively normal. However, the liver was quite spectacular in appearance.
The liver was generally enlarged 2 to 3 times and very heavy. The surface was undulating in manner with many sunken areas. The shape was normal. Externally the liver was white with a thickened capsule. The cut surface was a browny pink colour. The liver was organised into distinct lobules grouped around bile ducts. These areas were between 1 to 4 cms across. The consistency was quite firm. The changes were confined within the liver. The morphological diagnosis was chronic generalised lobular cirrhosis of the liver.
Histopathological examination (M06-00557-F-V1) revealed marked massive bile duct proliferation with portal fibrosis and some bridging between portal areas. There was little fatty change and no bile accumulation. The nuclear size of the hepatocytes was variable but no typical megalocytes were seen. Sinusoids exhibited cellularity with small clusters of mixed mainly mononuclear cells. Some apparent extramedullary haemopoiesis was apparent. It was concluded that this was a case of toxic hepatitis.
Sporidesmin toxicity is a possibility. A few cases have been reported to the State Veterinary Laboratory Menangle over the past few years.
However, it is also possible that a toxin such as a pyrrolizidine alkaloid has been transferred to the calf either in utero or in the milk. The long-standing nature of the liver lesions supports this presumption.
The prolapsing of the rectum is interesting. Liver disease such portosystemic shunts may cause tenesmus, which may lead to a rectal prolapse. There was no evidence of this change in this animal. It has been reported that diarrhoea and straining were clinical manifestations of Senecio spp poisonings (1).