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Equine Protozoal Myeloencephalitis (view source)
Revision as of 23:36, 8 July 2010
, 23:36, 8 July 2010→Aetiology and Epidemiology
====Aetiology and Epidemiology====
====Aetiology and Epidemiology====
The average incidence of EPM according ot the United Sattes Department of Agroiculture is around 14 cases per 10,000 horses per year. The true incidecne is porbbaly underestimated due to the complexity of the clincial dx and difficulty in finding conclusive CNS lesions. Racing and showing animals have been shown to be at higher risk than beeding and pleasure horses. EPM is a disease of the Western Hemisphere, with cases outside of the Americas havign spendt time in endemic regions. The diseas ehas been reporetd in England among horses imported from the Eastern US an din an Arbaian horse in South Africa imported from the US. The cases demonstarte the porbbaility of persitent, subcliicsal, latent infections. But a few reports exist of neurological horses with consistent cx, positivew immunoblot test results and no hx of travel in the American continent. This may be due to cross-reactign Ags. TBs, SBs and Quarterhorses are most commonly affected across the US and Canada. this may refelct managemetn, env or use of these breeds rather than an innate breed charcterisitic.
Most cases of EPM are caused by an Apicomplexan protozoan, [[Sarcocystis|Sarcocystis neurona]] . Horses are infected by ingestion of S neurona sporocysts in contaminated feed or water. The organism is assumed to undergo early asexual multiplication (schizogony) in extraneural tissues before parasitizing the CNS. Because infectious sarcocysts are not formed, the horse is considered an aberrant, dead-end host for S neurona . All Sarcocystis spp have an obligate predator-prey life cycle. The definitive (predator) host for S neurona is believed to be the opossum ( Didelphis virginiana ). Opossums are infected by eating sarcocyst-containing muscle tissue from an infected intermediate (prey) host and, after a brief prepatent period (probably 2−4 ωκ), infectious sporocysts are passed in the feces. Nine-banded armadillos, striped skunks, raccoons, sea otters, Pacific harbor seals, and domestic cats have all been implicated as intermediate hosts; however, the importance in nature of each of these species is unknown. A few cases of EPM, both in the Americas and Europe, are associated with Neospora hughesi , an organism that is closely related to S neurona . The natural host(s) of this organism have not yet been identified.
Most cases of EPM are caused by an Apicomplexan protozoan, [[Sarcocystis|Sarcocystis neurona]] . Horses are infected by ingestion of S neurona sporocysts in contaminated feed or water. The organism is assumed to undergo early asexual multiplication (schizogony) in extraneural tissues before parasitizing the CNS. Because infectious sarcocysts are not formed, the horse is considered an aberrant, dead-end host for S neurona . All Sarcocystis spp have an obligate predator-prey life cycle. The definitive (predator) host for S neurona is believed to be the opossum ( Didelphis virginiana ). Opossums are infected by eating sarcocyst-containing muscle tissue from an infected intermediate (prey) host and, after a brief prepatent period (probably 2−4 ωκ), infectious sporocysts are passed in the feces. Nine-banded armadillos, striped skunks, raccoons, sea otters, Pacific harbor seals, and domestic cats have all been implicated as intermediate hosts; however, the importance in nature of each of these species is unknown. A few cases of EPM, both in the Americas and Europe, are associated with Neospora hughesi , an organism that is closely related to S neurona . The natural host(s) of this organism have not yet been identified.