EPM: including updated diagnostics (Proceedings)


EPM: including updated diagnostics (Proceedings)

Aug 01, 2011

Equine protozoal myeloencephalitis (EPM) is a common neurological disease of horses in the Americas. Horses with EPM most commonly have abnormalities of gait but also may present with signs of brain disease. The disease ranges in severity from mild lameness to sudden recumbency and clinical signs usually are progressive. A causative agent, Sarcocystis neurona, has been isolated from affected horses and serologic surveys suggest that upwards of 50% of horses in endemic sections of the US have been infected with this agent. EPM is considered a treatable disease although the response often is incomplete.

History and distribution

The disease was first recognized in the US in 1964 (reported in 1970), and possibly earlier in Brazil. Since 1970, EPM has been reported in horses from most of the contiguous 48 states, Panama, Canada and Brazil, and there have been unpublished reports of the occurrence of the disease in Venezuela, Colombia, Argentina, and Mexico. The majority of affected horses are 1-5 years old, but older horses commonly also are affected. Although EPM has allegedly been confirmed in a 2-month-old, the disease is almost unknown in suckling foals. Prevalence of EPM by breed and gender is close to that in the general horse population; however, Standardbreds and males were over-represented in two published surveys. EPM also has been reported in a pony.

Causative agent(s)

Protozoa may be found in any part of the CNS, usually in association with mixed inflammatory cellular response and neuronal destruction. Schizonts (a proliferating form of the organism), in various stages of maturation, or free merozoites are seen commonly in the cytoplasm of neurons or mononuclear phagocytes and rarely in other inflammatory or CNS cells. The parasite is in the order Apicomplexa, which includes the family Sarcocystidae. In 1991, protozoa from the spinal cord of a horse from New York state were isolated in continuous culture in a bovine monocyte cell line and named S. neurona. Since then, many additional isolates have been obtained in monocyte or endothelial cell culture from horses throughout the country (including UF). A few cases of EPM in the Americas have been associated with Neospora hughesi. Serologic surveys of horses have suggested an exposure rate to Neospora spp. of 10-25%.

Life cycle

Species of Sarcocystis have an obligatory prey-predator two-host life cycle. The genus is named for the terminal developmental stage (sarcocyst) found in the intermediate host. The sarcocyst is the only developmental stage that is infectious for the definitive host. Because S. neurona sarcocysts have been found in only one horse (a foal), it is assumed that the horse is usually an aberrant dead-end host. Ingestion of sarcocysts by the appropriate flesh-eating (i.e., predator or scavenger) definitive host results in invasion of the small intestinal epithelium and sexual proliferation and differentiation to produce oocysts. The oocysts of Sarcocystis each contain two sporocysts which usually are released from thin-walled oocysts before they are passed with feces. Sporocysts are immediately infectious for the intermediate host. They are quite persistent in the environment and may survive for months, even during extremes of heat and cold. Intermediate hosts are infected by ingestion of contaminated feed or water.

Opossums (Didelphis virginiana in the US) has been identified as the definitive host. Several intermediate hosts including the 9-banded armadillo (Dasypus novemcinctus), the striped skunk (Mephitis mephitis), and the raccoon (Prylon locor) have been identified. Their combined geographic range covers the area where EPM occurs. The domestic cat also can support the life cycle in nature although its importance in maintaining the life cycle is unclear. Several other hosts of dubious significance, including the Pacific Harbor seal, the California sea otter, the domestic dog, and farmed mink, have also been identified. It should be noted that S. neurona has been responsible for significant die-offs of sea otters during the last decade. By epidemiologic techniques, S. neurona has been shown to expand clonally be self-mating in opossums. The possibility also has been raised that the organism may be transmissible between carnivorous intermediate hosts, as routinely happens in the closely related Toxoplasma gondii. The hosts for N. hughesi are not known.