Sarcosporidiosis is an infection with a protozoal parasite of the genus Sarcocystis. These parasites have an indirect lifecycle, typically with carnivores as the definitive host and prey animals as the intermediate host.
Sarcocystis is routinely found in the carcasses of sheep across southern Australia, with prevalence estimated to range from 0.4-0.9% (Abbott 2018). Although commonly identified, sarcosporidiosis is considered to cause few animal health or production issues and is often an incidental finding at post-mortem. The predominant impact of sarcosporidiosis in Australia is at abattoirs where macroscopic cysts lead to carcass trimming and condemnations, estimated to cost the sheep industry five million dollars annually.
In this case sarcosporidiosis caused by infection with Sarcocystis tenella was identified as the cause of clinical neurological disease in approximately five percent of a large mob of Merino hoggets.
Approximately five percent of 2300 Merino hoggets were noticed to be showing signs of weakness and falling when handled. There were occasional deaths occurring around self-feeders, although it was not certain if these were related to the clinical signs.
The hoggets had been fed in confinement for an extended time due to drought conditions and the wether portion had experienced ongoing urolithiasis issues. All sheep were fed a ration of 60% barley, 40% DDG pellets with ad lib access to barley straw. They were supplemented with lime and salt throughout the feeding period and in addition the wethers ration also had added ammonium chloride. All animals received a 5-in-1 clostridial vaccination and a dose of vitamin ADE approximately two months before the onset of signs.
Affected mobs initially appeared normal, but once forced to walk for a short period some sheep at the tail of the mob showed signs of weakness, then stumbled and fell. These sheep struggled to stand immediately but were able to rise if left alone.
Affected individuals remained alert with normal mentation, mildly increased heart and respiratory rates, with temperatures up to 40.8°C. All affected sheep were ataxic, had a fine muscle tremor, reduced strength and cranial nerves were unaffected.
Five affected sheep were necropsied over three visits. The only gross pathological findings were occasional small areas of consolidation in the lung and one animal with a significant suppurative pneumonia.
Serum biochemistry showed moderate increases in glutamate dehydrogenase (GLDH), aspartate transaminase (AST) and creatinine kinase (CK) with no evidence of either hypocalcaemia or hypomagnesaemia.
Initial histological examination of a brain from an affected sheep identified two distinct and likely unrelated lesions. The first was a parasitic encephalitis caused by protozoa, morphologically consistent with Sarcocystis and the second a non-neoplastic proliferation observed in the basis of the thalamus, possibly a hamartoma. A hamartoma is a benign tumour-like nodule composed of an overgrowth of mature cells and tissues normally present in the affected part of the body, often with one element predominating (Blood & Studdert 1999).
Histological examination of subsequent submissions found significant, widespread protozoal infection. These findings included multifocal, lymphoplasmacytic encephalitis, myositis and myocarditis with intralesional protozoal cysts. PCR was used for protozoal speciation, identifying Sarcocystis tenella as the causative organism.
Treatment was not attempted as by the time a final diagnosis was made it had rained, enabling the affected mob to be released from confinement onto pasture. The producer reported that the number of clinical cases seemed to gradually decrease, although the mob was observed and handled less.
Infection of sheep with Sarcocystis sp. is relatively common in southern Australia, however, it is typically considered to cause few animal health or production issues. This outbreak was an unusual presentation of sarcosporidiosis, particularly in Australia where such events are rarely described.
It was considered that the parasitic encephalitis found in the initial investigation was insufficient to cause the clinical signs observed across the flock, but subsequent findings indicated that the signs were likely from a combination of damage to both the nervous and muscular systems.
The definitive hosts of Sarcocystis tenella (also known as S. ovicanis), include dogs and foxes. Throughout the feeding period there were deaths in the confinement area, which may have attracted these species, contributing to contamination of the area and exposing the hoggets to S. tenella. The cysts produced by S. tenella infection are not macroscopically visible and are thus not a meat quality issue unlike infection with some other Sarcocystis infections.
Treatment options for this presentation of sarcosporidiosis are limited. The coccidiostats amprolium and salinomytin are possible treatments for ovine sarcocystosis (O’Toole et al. 1993), although are only likely to be successful if given early in the disease course, which was not possible in this case.
There is no definitive explanation as to why this outbreak occurred. It is possible that a combination of high stocking density, reduced immune function and the increased presence of pest canids led to the perfect storm of conditions. Prevention of similar outbreaks should focus on reducing the exposure of sheep to infective Sarcocystis stages through reducing the access of pest and working canids to sheep carcasses, the control of pest canids and optimising sheep immune function through good nutrition and management strategies.
Histology and Microbiology and Parasitology Laboratories at Elizabeth Macarthur Agricultural Institute for their diagnostic and technical support throughout the investigation.