The effects of the Ikeda strain of Theileria have been well documented in the past few years outlining the most susceptible classes of cattle and the likely clinical signs (ref/s). This case highlights that symptoms are not always classic and cases may present as neurological in appearance. It illustrates that theileria must always be considered as a possible diagnosis when investigating deaths in mature cows.
The manager of a moderate sized property on the southern outskirts of Narrabri reported the deaths of a number of cows in October 2013. The property was running a Hereford herd and was not self-replacing, with all replacement females being purchased from various areas including the local region and the northern tablelands. Pasture conditions on the property were deteriorating due to lack of rainfall but this property was well managed and had maintained adequate feed for the stocking rate.
The initial phone call indicated that there was a freshly dead cow and at least two others that were unwell. An autopsy was conducted on the dead cow, an approximately 6 year old Hereford cow that was non-pregnant and non-lactating. The autopsy revealed an enlarged liver (X times enlarged) and grossly enlarged spleen (three times normal size) with yellowing of the fat tissue but no gross appearance of anemia (Figure 1). Anthrax was immediately ruled out with a carcass-side ICT Anthrax test kit. A full set of samples were taken for laboratory work-up. Despite the tell-tale post-mortem findings, theileria was initially ruled out on the basis of the cow not being pregnant or in high energy demand, and the fact that live cases were demonstrating signs of neurological disease. Other differential diagnoses included toxic plants and urea poisoning.
Two live animals were examined in the paddock. One had symptoms of weakness and moved slowly. It had a calf at foot, estimated to be about xx months old. The other cow was not lactating and exhibited signs of aggression (charging), ataxia, head tremor, and falling.
Laboratory results indicated elevations in both liver and kidney enzymes in serum and a PCV of 0.15. Blood ammonia concentration was also markedly increased and urea poisoning was considered. Histopathology indicated centrilobular hepatic necrosis due to anoxia (anaemia) or a hepatotoxin, along with less significant findings in other organs. Transmissible spongiform encephalopathy was also ruled out.
A paddock inspection for toxic plants was undertaken and another live animal showing similar clinical signs was examined. This time a cow was observed in the paddock showing signs of trembling and aggression (charging). It also had periods of recumbency.
A second and then a third autopsy were conducted in the following days, with both of these showing varying levels of jaundice and enlargement of the spleen. At this point the laboratory was contacted to examine smears for Theileria and tick fever.
A blood sample and smears were taken from one cow showing moderate signs of disease (briefly describe signs in this cow, to show consistent with prior observations -i.e. was she also showing neuro signs? -i.e. what do moderate signs look like?) that was able to be yarded and placed in the crush.
The laboratory was able to confirm the presence of the Ikeda strain (by PCR technique) of Theileria in blood cells with a prevalence of less than 1%. This cow had a PCV of 0.16. Smears were negative for Babesia and Anaplasma.
The author acknowledges that errors in judgment were made when initially diagnosing this case. Post-mortem evidence of enlargement of the liver and spleen and the presence of jaundice should have ticked most of the boxes required to take appropriate samples to test for the presence of Theileria. A few factors played a part in initially ruling this out as a possibility:
It has also been observed in past cases of theileria that it is not uncommon to find only small percentages of affected blood cells. This case confirms that levels of less than 1% infected red blood cells can be associated with cases that show clinical signs and hence theileria should always be considered a possibility in cases where anemia can be confirmed, especially where the Ikeda strain is identified by PCR.
Finally the author notes that observed clinical signs of theileria can be vague and are generally subjective, especially when exhibited in a paddock situation. In this case the differential diagnoses list should have been extrapolated more from the autopsies conducted than from observed behavior in live animals.
The author would like to acknowledge former District Veterinarian Libby Guest from Narrabri who conducted one of the autopsies and re-iterated the strong possibility of Theileria.
Senior District Veterinarian at Kempsey, Dr Ian Poe, also provided invaluable information on clinical signs of affected animals.