A Wagga Wagga producer had experienced four deaths in a mob of 50 mixed steers purchased August 2009 and put onto excellent pasture. There was now another steer in a dam that had defied all attempts to drive it from the dam. It had bilateral pink eye and was circling. It responded poorly to sound or to movement. It was in poorer condition than most of the mob.
Neither of the Sydney Uni Interns with me that day fancied a swim. We returned to the office, did a life history on the NLIS tags from the four dead animals which revealed all four were from a line of 10 which had been grazing a river flat block near Wagga Wagga Feb-August 2009. The provisional diagnosis was now obvious. A pair of waders was purchased, the trusty .22 Brno was taken to the farm and the beast despatched by shooting from the bank (an interesting exercise with the Olympic Way behind the shooter and a steer that was very difficult to get facing the right way).
A few days later another steer from the same line developed symptoms and the two Sydney Uni interns and a CSU trainee pathologist were sent to practice their PM skills. They reported neurological signs including mental dullness and apparent blindness, the animal was also weak and in poorer condition than the rest of the mob. It was euthanised.
The first steer when pulled from the dam had bilateral white corneas. On PM it had severe liver damage, with enlargement, nodules, a pale colour and an enlarged gall bladder. The second steer had mild to moderate enlargement of the liver with rounded borders and a paler colour than normal.
Histopathology from these cases was reported:
There was a severe degree of pathological change within the liver. Severe bridging fibrosis was present diffusely throughout the parenchyma, dissecting between and isolating islands of hepatocytes. There were focal areas of nodular regeneration which were thinly encapsulated in fibrous connective tissue. Megalocytosis and karyomegaly were readily apparent, as were necrotic and degenerating hepatocytes with shrunken dark nuclei and hypereosinophilic cytoplasm. Increased amount of fibrous connective tissue were also apparent around the terminal hepatic venules.
There was a severe degree of vacuolation, most significantly at the junction of the white and grey matter within the cerebral cortex, throughout the white matter tracts within the hypothalamus and the middle cerebellar peduncles. There were occasional neurones which Alzheimer type II astrocytes were also apparent within the cerebral cortex.
Diagnosis: Severe, chronic, diffuse hepatic fibrosis Severe, acute to subacute, focal to diffuse encephalopathy. Pyrrolizidine alkaloid toxicity with secondary hepatic encephalopathy.
Comments: Changes seen within the liver were consistent with pyrrolizidine alkaloid toxicity. Reduced hepatic function leads to increased circulating ammonia levels, which leads to toxic changes within the brain.
Changes within the liver were similar to that seen in the other steer (see report 09-255) but was less severe. There was still evidence of bridging fibrosis along the sinusoidal tracts, dissecting through and separating the hepatic parenchyma. Severe fibrosis was also evidence in the areas around the central vein and portal triad. Occasional necrotic hepatocyte was also present as were proliferation of the biliaryducts. There was no evidence of nodular regeneration within the section of liver submitted.
Severe degrees of vacuolation were also present within the brain of this animal. Again significant vacuolation was noted at the junction of the white and grey matter within the cerebral cortex, throughout the white matter tracts within the hypothalamus and the middle cerebellar peduncles. Alzheimer type II astrocytes were also apparent.
Diagnosis: Severe, subacute to chronic, diffuse hepatic fibrosis .Severe, acute to subacute, focal to diffuse encephalopathy. Pyrrolizidine alkaloid toxicity with secondary hepatic encephalopathy.
Heliotrope (caterpillar weed)
Heliotropium europaeum has thrived throughout the district and especially on the Murrumbidgee river flats as a decade of poor seasons has left paddocks bare and very vulnerable to a massive growth of heliotrope (and other toxic summer weeds e.g. panics) whenever we receive summer rain. It is not very palatable and has a most unpleasant odour.
There has been a very large increase in the number of bovine heliotrope poisonings investigated and many of the losses have been severe e.g.20 cows. This is undoubtedly due both to the increased availability of the heliotrope and hungry stock grazing it. Selective control in pasture situations is not highly effective (74% with the best available herbicide mix in one set of trials) and re establishing vigorous perennial based pastures that can outcompete it difficult/impossible in a drought.
Despite the intake of heliotrope occurring in the summer and autumn invariably the losses in cattle are not seen until the following spring when green feed becomes abundant. The manifestations of the poisoning then become apparent with some cattle failing to gain weight or losing weight and showing symptoms of hepatic encephalopathy. This pattern of poisoning makes it difficult to persuade unaffected producers to take precautions and is a very real risk for the purchasers of store cattle in winter.