Sea Otter an EPM Intermediate Host

Researchers recently identified the sea otter as a natural intermediate host for Sarcocystis neurona, the one-celled protozoan parasite that causes equine protozoal Myeloencephalitis (EPM). Muscle from a naturally-infected sea otter used in the study was used to induce sporocyst shedding in laboratory-raised opossums. How sea otters in their natural habitat become infected with S. neurona is unknown.

"Although our understanding of the epizootiology of S. neurona in terrestrial vertebrates has recently expanded, the appearance of this parasite in a marine mammal was unexpected," stated researchers in the study that appeared in a recent issue of The Journal of Parasitology. The research team consisted of individuals from the United States Department of Agriculture, Virginia-Maryland Regional College of Veterinary Medicine, the U.S. Geological Survey's National Wildlife Health Center, and The Ohio State University's (OSU) College of Veterinary Medicine. 

S. neurona sarcocysts had been isolated from the muscle of a sea otter in a previous study. "We had the (laboratory-raised) opossums for performing the research," said The Ohio State's William Saville, DVM, PhD, Dipl. ACVIM, "and we wanted to know if we could complete the life cycle because we knew the sarcocysts were there." 

Sporocysts were shed by the opossums that were fed sea otter muscle. Then the  sporocysts were given to knockout (KO) mice (genetically altered, immunocompromised mice), which developed neurological symptoms characteristic of S. neurona infection. The parasite was found in the tissues and sera of the KO mice. Scientists also examined the structure and DNA of the parasite found in the sea otter and compared it to that of previous experiments to confirm its identification as S. neurona.

According to Saville, the ability of the sea otter to complete the life cycle of S. neurona probably does not have a significant impact on the geographical spread of EPM in the horse population. S. neurona sporocysts have to be transported to sea otters either from the opossum (the only known host capable of completing the S. neurona life cycle and shedding sporocysts) or from some other unidentified host. Then, the remains of a naturally-infected sea otter would have to be consumed by an opossum or eaten by a natural predator of sea otters that excretes S. neurona sporocysts. In turn, the opossum or unknown natural predator would have to shed sporocysts in an area where they could be ingested by horses. 

This might not seem like the most efficient way for EPM to work its way into your horse's pasture, but this discovery will help experts better examine the epidemiology of EPM and new means of treating and preventing it.

For more on EPM, visit http://www.TheHorse.com/epm.

About the Author

Stephanie L. Church, Editor-in-Chief

Stephanie L. Church, Editor-in-Chief, received a B.A. in Journalism and Equestrian Studies from Averett College in Danville, Virginia. A Pony Club and 4-H graduate, her background is in eventing, and she is schooling her recently retired Thoroughbred racehorse, Happy, toward a career in that discipline. She also enjoys traveling, photography, cycling, and cooking in her free time.

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