EPM Update

Equine protozoal myeloencephalitis (EPM) continues to pose diagnostic and treatment challenges.
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This neurologic disease continues to pose diagnostic and treatment challenges
Bay Neurologic Horse
Horses with EPM might exhibit ataxia (incoordination), muscle atrophy (wasting), recumbency (the inability to rise), seizures, stumbling, and other neurologic signs. | Photo: Stephanie L. Church, Editor-in-Chief

Few equine conditions cause as much consternation as equine protozoal myeloencephalitis (EPM). First reported in 1968, EPM represents both amazing scientific progress and extraordinary clinical frustration. Its causative agents are widespread in the Americas, and affected horses display neurologic signs such as ataxia (incoordination) and asymmetric atrophy (muscle wasting on one side of the body). However, disease is sporadic and veterinarians cannot diagnose it definitively yet in the live horse.

So why is a disease that is one of the few treatable equine neurologic conditions and for which scientists have identified the causative organisms (now down to the genomic level) so frustrating? To address these questions, let’s first take a look at the disease and these organisms, along with EPM’s mechanisms of action, diagnosis, and treatment.

The Troublemakers

According to a 2009 Equine Research Coordination Group White Paper, a protozoon (single-celled parasite) known as Sarcocystis neurona causes an estimated 95% of EPM cases. Researchers have also identified another protozoal organism, Neospora hughesi, associated with some cases. While S. neurona and N. hughesi are “somewhat closely related,” says Daniel Howe, PhD, a molecular parasitologist at the University of Kentucky’s Gluck Equine Research Center, in Lexington, the parasites’ geographic distribution appears to be different. He says N. hughesi is “more common on the West Coast, with Neospora-positive samples seemingly pretty rare in the Midwest and East.”

Like most other parasites, S. neurona develops through several life cycle stages during which it relies on various hosts. S. neurona‘s final, or definitive, host is the opossum, which sheds the parasites when they reach their infective stages (sporocysts) in its feces. Intermediate hosts (including raccoons, armadillos, sea otters, skunks, and cats) become infected by eating food contaminated with the sporocysts. In true intermediate hosts (in which the parasite develops through several life cycle stages, as opposed to a “dead-end” host such as the horse) the sporocysts mature after several cycles to bradyzoites (another stage of maturity) that form sarcocysts in the muscle. The definitive host becomes infected by eating sarcocyst-infected muscle of one of these various intermediate hosts. The parasites reproduce in the opossum’s intestine to produce the sporulated oocysts (the “egg” stage containing the sporocysts) the opossum then excretes

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Written by:

Christy Corp-Minamiji, DVM, practices large animal medicine in Northern California, with particular interests in equine wound management and geriatric equine care. She and her husband have three children, and she writes fiction and creative nonfiction in her spare time.

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