In August 2006 the owner of a small beef cattle property on the mid north coast of NSW sought advice after the second of seven Hereford-cross 18-24 month old steers died. The steers were grazing a typical winter kikuyu-based pasture, with adequate but not plentiful feed.
The remaining five steers were in good body condition. One appeared lethargic and somewhat depressed but with no other clinical signs. This animal and a normal cohort were blood sampled. The sick steer died 2 days later (before lab results were available from the original submissions).
The paddocks were clean with minimal weed invasion and an initial inspection found no toxic plants along that part of the 600-metre creek frontage that was accessible, although cattle had been eating privet and other weeds.
On a second inspection (after lab results came back) some poison peach (Trema aspera) was found through the fence on a neighbouring property but with no signs that it had been grazed. Numerous cycad palms were found on a very steep creek bank that the owner said had never been previously accessed by the cattle. Many had been grazed by the cattle. There were no fruit even on the ungrazed plants so it is likely that only leaves were eaten.
In Australia there are several species of cycads and zamias including Cycas, Macrozamia, Lepidozamia and Bowenia, and on growth habit and appearance it is likely that the species involved was Macrozamia, but no botanical identification was done in this case.
Gross pathology of the first autopsy showed widespread petechial and ecchymotic haemorrhages throughout the carcass, some haemorrhage into the small intestine, and a tan /ochre coloured liver with apparent pinpoint necrosis of the parenchyma. Autopsy of the steer that died two days later showed a striking hepatopathy with apparent portal fibrosis and pin point necrosis, with a background tan colour indicating fatty change.
The differential diagnoses based on autopsy findings included bracken fern, green cestrum, pyrrolizidine alkaloidosis and poison peach toxicity.
|Normal range||Sick steer||Normal steer|
Case 1: The pathology report described moderately acute periacinar necrosis with replacement haemorrhage. Macrovesicular fatty change was evident in surviving hepatocyctes.
Case 2: Extensive acute haemorrhagic periacinar necrosis was reported. Many of the remnant hepatocytes had undergone macrovesicular fatty change. The portal tracts were oedematous and moderately fibrotic.
In this district common bracken (Pteridium esculentum), fireweed (Senecio madagascariensis) and green cestrum (Cestrum parqui) commonly intoxicate stock. The pathology was not consistent with either bracken or pyrrolizidine alkaloidosis from fireweed. Green cestrum poisoning is normally clinically more acute and animals die before fatty change occurs in the remaining hepatocytes. Cycad toxicity is occasionally reported in coastal NSW, usually associated with lesions in the spinal cord resulting in ataxia and staggers.
Cycads are commonly called ‘Burrawang Palms’, and owners refer to the condition as ‘rickets’ or Burrawang staggers. However, this case and others subsequently reported by nearby private practitioners, illustrates that cycads can cause acute liver necrosis with no signs of spinal cord pathology.
Lesions in the corticospinal and spinocerebellar tracts are associated with more long term exposure, as are the megalocytic-type hepatopathies attributed to methylazoxymethanol. However the toxin is activated by biotransformation, and it is undoubtedly a multifactorial occurrence involving stage of growth, plant genetics, concentration of toxin, amount eaten, rate of ingestion and rate of biotransformation. Biotransformation rate is influenced by ruminal flora and activity of enzymes such as Cytochrome P450. A big dose of toxin presented to the hepatocytes results in an acute lesion as in this case, while smaller doses result in spinal cord lesions or more chronic liver changes.