|Sofaly, C - OHIO STATE|
|Reed, S - OHIO STATE|
|Gordon, J - OHIO STATE|
|Oglesbee, M - OHIO STATE|
|Njoku, C - OHIO STATE|
|Grover, D - OHIO STATE|
|Saville, W.J.A. - OHIO STATE|
Submitted to: Journal of Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 30, 2002
Publication Date: December 20, 2003
Citation: Sofaly, C.S., Reed, S.M., Gordon, J.C., Dubey, J.P., Oglesbee, M.J., Njoku, C.J., Grover, D.L., Saville, W. 2003. Experimental induction of equine protozoal myeloencephalitis (epm) in the horse: effect of sarcocystis neurona sporocyst inoculation dose on the development of clinical neurologic disease. Journal of Parasitology 88:1164-1170. Interpretive Summary: Sarcocystis neurona is a single celled parasite and is the most important cause of a neurologic disease of horses, equine protozoal myeloencephalitis (EPM). Opossums are the reservoir (definitive) host for the parasite because they excrete the environmentally resistant stage (sporocyst) in the environment. Horses become infected by ingesting sporocysts. Under laboratory conditions it is difficult to induce EPM in horses hampering treatment and preventive medication evaluation. Scientists at the Beltsville Agricultural Research Center and the Ohio State University fed graded (100 to 1,000,000) sporocysts to horses and found that the highest dose produced most consistent EPM. These results will be of interests to biologists, veterinarians, parasitologists, and equine farmers.
Technical Abstract: The effect of inoculation dose of Sarcocystis neurona sporocysts on the development of clinical neurologic disease in horses was investigated. Twenty-four seronegative weanling horses were subjected to the natural stress of transport then randomly assigned to 6 treatment groups of 4 horses each. Horses were then immediately inoculated with either 102, 103, 104, 105, 106 S. neurona sporocysts or placebo via nasogastric tube and housed indoors. Weekly neurologic examinations were performed by a blinded observer. Blood was collected weekly for antibody determination by Western blot analysis. Cerebrospinal fluid was collected prior to inoculation and prior to euthanasia for S. neurona antibody determination. Horses were euthanized and necropsied between 4 and 5 wk after inoculation. Differences were detected among dose groups based on seroconversion times, severity of clinical neurologic signs, and presence of microscopic lesions. Seroconversion of challenged horses was observed as early as 14 days post infection in the 106 sporocyst dose group. Mild to moderate clinical signs of neurologic disease were produced in challenged horses from all groups with the most consistent signs seen in the 106 sporocyst dose group. Histologic lesions suggestive of S. neurona infection were detected in 4 of 20 horses fed sporocysts. Parasites were not detected in equine tissues by light microscopy, immunohistochemistry, or bioassay in interferon-gamma gene knock-out mice. Control horses remained seronegative for the duration of the study and had no histologic evidence of protozoal infection.