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ARS Home » Research » Publications at this Location » Publication #192835
Title: EQUINE PROTOZOAL MYCLOENCEPHALITIS

Author
item SELLON, DEBRA - WASHINGTON STATE U
item Dubey, Jitender

Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 4/28/2006
Publication Date: 1/1/2007
Citation: Sellon, D.C. and J.P. Dubey. 2007. Equine protozoal myeloencephalitis. In: Sellon, D.C. and Long, M.T., editors. Equine Infectious Diseases. St. Louis, MO:Elsevier Inc. p. 453-464.

Interpretive Summary: Sarcocystis neurona is a single-celled parasite. It causes a fatal disease in horses called Equine Protozoal Myeloencephalitis (EPM). EPM also occurs in other animals. Opossums are the definitive host for this parasite, and the main reservoir of infection. Opossums become infected by consuming the encysted stage of the parasite (sarcocyst) in infected animal tissue and they excrete millions of the resistant stage (oocysts) in their feces. Horses become infected by ingesting food and water contaminated with oocysts. Scientists at the Beltsville Agricultural Research Center and Washington State Univ. review EPM in horses..This paper will be of interest to biologists, parasitologists, and veterinarians.

Technical Abstract: In 1970, Rooney et al reported 52 cases of focal myelitis-encephalitis in horses from Kentucky and Pennsylvania, with highest incidence in young Standardbreds.1 Horses were presented for evaluation of progressive spinal ataxia of one or more limbs. At necropsy, focal lesions of vascular damage, hemorrhage, mononuclear cuffing, gliosis and neuronal and axonal degeneration were observed in one or more segments of the spinal cord. This report is now thought to be the first published description of equine protozoal myeloencephalitis (EPM). In 1974, separate reports by Beech et al2,3, Dubey et al4 and Cusick et al5 described 14 horses in the United States with focal malacia and hemorrhage in the white and gray matter of the brain and spinal cord. Protozoal organisms observed in the central nervous system (CNS) tissues of each horse resembled Toxoplasma gondii, but differed in several respects, including an absence of T. gondii antibody responses in affected horses. A subsequent serosurvey of horses revealed that 20% of 1,294 serum samples tested by microtitration indirect hemagglutinin test were positive for antibodies to T. gondii.6 Attempts to induce disease in healthy ponies by oral administration of infective T. gondii oocysts with concomitant corticosteroid injections were unsuccessful7,8 and the etiologic agent of EPM remained a mystery for almost 20 years.