EPM’s Lesser-Known Cause: N. hughesi

Researchers are studying the epidemiology of Neospora hughesi in horses with equine protozoal myeloencephalitis (EPM).

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Photo: Courtesy University of California
Equine protozoal myeloencephalitis (EPM) is a frequently diagnosed neurologic disease of horses in North America. Researchers point to the protozoan parasite Sarcocystis neurona as the most common cause, but they have identified another closely related protozoon, Neospora hughesi, in affected horses’ central nervous systems.

S. neurona’s life cycle has been well-characterized (see TheHorse.com/28383). The epidemiology of N. hughesi, on the other hand, is poorly understood, and reports of infection are sparse. N. hughesi-infected horses can be asymptomatic (showing no signs), or they can exhibit clinical signs of EPM indistinguishable from those caused by S. neurona. In addition, N. hughesi has been reported to cause abortions and neosporosis (neuromuscular disease). 

Despite scientists knowing little about N. hughesi’s behavior in horses, they have drawn many biological comparisons to N. caninum, the causative agent of a neuromuscular disease that causes paralysis in dogs and abortion in cattle. N. caninum’s definitive hosts, the domestic dog and the coyote, shed oocysts in feces that can infect intermediate hosts such as cattle. Other infection sources among cattle include exposure to infected animals’ colostrum, milk, placenta, and fetal fluids. Transplacental transmission to calves also appears to be an important way N. caninum spreads. 

Researchers recently reported a similar transmission route in horses, documenting transplacental infection from two persistently N. hughesi-infected broodmares to their nine offspring over six years. Only one of those foals developed neurologic signs of EPM during the first year of life. The true clinical impact in N. hughesi-infected horses, beyond the sporadic development of central nervous infection, remains to be determined. It is likely that horses not showing signs of active disease might be at a higher risk of developing clinical disease following an immunosuppressive event such as concurrent illness

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Written by:

Nicola Pusterla, DVM, PhD, Dipl. ACVIM, is currently an associate professor of equine internal medicine at the University of California, Davis, School of Veterinary Medicine, as well as chief of large animal medicine and section head of equine medicine and dentistry. Pusterla’s research focuses on selected aspects of equine infectious diseases with an emphasis on epidemiology, clinical disease understanding, diagnostics, prevention, and treatment.

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