ROB FAIRLEY
Each year our laboratories see cases of acorn poisoning in the autumn and mainly in calves. It often occurs because of either a shortage of feed or the use of calves to clean up laneways or small oak plantations besides driveways or railway lines.
An important clinical aspect is that calves do not become sick immediately and by the time they are sick they may have been out of the affected areas for many days. Hence, acorn poisoning may not come to mind initially. Clinically, calves may just be anorexic, dull and depressed but some will have blood in their faeces and the latter should raise a suspicion.
If you are called to investigate an episode of sick calves this autumn and at post-mortem you find pale, enlarged kidneys with perirenal edema acorn poisoning should be your prime differential. There may be red staining of the edema fluid. Some of the calves may have excess, clear, colourless to pale yellow abdominal and thoracic fluid.
Amarathus (redroot) can also cause similar post-mortem findings and Leptospira copenhageni can also produce similar lesions – to date cases of this infection in calves have been seen in South Auckland, Waikato, and the Thames Valley.
If you only have sick calves and suspect acorn toxicity take serum to measure BUN and creatinine. Both will be very high in acorn poisoning. At post-mortem a variety of tissues should be collected and on examination of the kidney the pathologist will be able to tell if there are changes of toxic tubular damage present. Such changes are not specific to acorns but when combined with a history of grazing an area with acorns the diagnosis is appropriate.