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Title: UTILIZATION OF STRESS IN THE DEVELOPMENT OF AN EQUINE MODEL FOR EQUINE PROTOZOAL MYELOENCEPHALITIS

Author
item SAVILLE, W - DEPT. OF VET. PREV. MED.
item STICH, R - DEPT OF VET PREV MED
item REED, S - DEPT OF CLINICAL SCIENCES
item NJOKU, C - DEPT OF VET PREV MED
item OGLESBEE, M - DEPT OF BIOLOGICAL SCI
item WUNSCHMANN, A - DEPT OF BIOLOGICAL SCI
item GROVER, D - DEPT OF VET PREV MED
item LAREW-NAUGLE, A - DEPT OF VET PREV MED
item STANEK, J - DEPT OF VET PREV MED
item Dubey, Jitender

Submitted to: Veterinary Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/1/2000
Publication Date: N/A
Citation: N/A

Interpretive Summary: Sarcocystis neurona is a single-celled parasite that causes a fatal neurological disease in horses, equine protozoal myeloencephalitis (EPM). Opossums are the reservoir hosts for S. neurona. Horses become infected by ingesting food and water contaminated with the resistant stage of the parasite (sporocyst) shed in feces of opossums. Although nearly half of the horses in the U.S. have them exposed to S. neurona, only a small proportion of infected horses develop clinical signs of EPM. Scientists at the Beltsville Agricultural Research Center and the Ohio State University report an experimental model of S. neurona in the horses using transplant as a stress. The results will be of use to veterinarians, horse owners and parasitologists.

Technical Abstract: Neurologic disease in horses caused by Sarcocysits neurona is difficult to diagnose, treat, or prevent, due to the lack of knowledge about the pathogenesis of the disease. This in turn is confounded by the lack of a reliable equine model of equine protozoal myeloenvephalitis (EPM). Epidemiologic studies have implicated stress as a risk factor for this disease, thus, the role of transport stress was evaluated for incorporatio into an equine model for EPM. Sporocysts from feral opossums were bioassayed in interferon-gamma gene knockout (KO) mice to determine minimum number of viable S. neurona sporocysts in the inoculum. A minimum of 80,000 viable S. neurona sporocysts were fed to each of the 9 horses. A total of 12 S. neurona antibody negative horses were divided into 4 groups (1 to 4). Three horses (group 1) were fed sporocysts on the day of arrival at the study site, 3 horses were fed sporocysts 14 days after acclimatization (group 2), 3 horses were given sporocysts and dexamethason 14 days after acclimatization (group 3) and 3 horses were controls (group 4). All horses fed sporocysts in the study developed antibodies to S.neurona in serum and cerebrospinal fluid (CSF) and developed clinical signs of neurologic disease. The most severe clinical signs were in horses in group 1 subjected to transport stress. The least severe neurologic signs were in horses treated with dexamethasone (group 3). Clinical signs improved in 4 horses from 2 treatment groups by the time of euthanasia (Group 1-d 44; Group 3-d 47). Post mortem examinations, and tissues that were collected for light microscopy, immunohistochemistry, tissue cultures, and bioassays in KO mice, revealed no direct evidence of S. neurona infection. However, there were lesions compatible with S. neurona