Improving the Knowledge of EPM

Equine protozoal Myeloencephalitis (EPM) is a neurologic disease in horses predominantly caused by the protozoa Sarcocystis neurona. Carried by the North American opossum, Didelphis virginiana, horses are exposed to S. neurona when eating or drinking food or water contaminated with opossum feces. While exposure to the protozoa is high, only around 1% of horses develop clinical disease. While the mechanism by which S. neurona causes central nervous system damage is still unknown, this dissertation examines the histopathologic damage and potential persistence of S. neurona after anti-protozoal treatment between groups of horses with acute and chronic disease. This dissertation also examines the ability of two diagnostic techniques, immunohistochemistry (IHC) and polymerase chain reaction (PCR), to detect S. neurona. Horses were grouped based on duration of clinical signs; acutely affected horses exhibited clinical signs <6 months, while chronically affected horses exhibited clinical signs >6 months, including those previously treated for EPM. A comparison of necropsy reports revealed that chronically affected horses with EPM had more degenerative changes compared to acutely affected horses with EPM. However, when histologic changes were quantified, acutely affected horses had similar degenerative changes compared to chronically affected horses. When IHC and PCR were compared, IHC detected S. neurona presence (9/9 horses with EPM) significantly more often than PCR 4/9 horses with EPM). Our studies also show that S. neurona can be persistent in horses, as evidenced by the detection of S. neurona in the CNS of horses previously treated for EPM. Four horses had previously been treated for EPM, and all four had S. neurona present in their CNS even after anti-protozoal treatment, suggesting the ability for S. neurona to persist. In addition, this dissertation examines the possibility of using soluble CD14 (sCD14) as a supplemental assay for differentiating neurologic diseases such as EPM and cervical vertebral stenotic myelopathy (CVSM). When sCD14 levels were assessed in control EPM, CVSM, and EPM+CVSM horses, sCD14 concentrations in the cerebral spinal fluid (CSF) were significantly different between control and EPM horses and EPM horses and CVSM horses. With this information, clinicians and researchers may use sCD14 as a supplemental assay for differentiating between healthy, EPM, and CVSM horses. Finally, future directions include preliminary data that may lead to a potential for a peptide vaccine protecting horses from EPM clinical disease. Further insight into the persistence of S. neurona after anti-protozoal treatment is needed, the classification of acutely and chronically affected horses and the ability of sCD14 detection as a supplemental assay will be required; this this dissertation allows for the continuation of knowledge in combating the elusive protozoa, S. neurona.