Epidemiology of Sarcosystis neurona in a coastal marine mammal: clues to understanding land to sea disease transmission

Sarcocystis neurona, the principal cause of equine protozoal myeloencephalitis, was recognized as an important cause of mortality in sea otters (Enhydra lutris) after a large outbreak was observed in April 2004 coincident with... [ view full abstract ]

Sarcocystis neurona, the principal cause of equine protozoal myeloencephalitis, was recognized as an important cause of mortality in sea otters (Enhydra lutris) after a large outbreak was observed in April 2004 coincident with a major rainfall event. In recent years, this parasite has been detected in a wide range of marine mammal species in the Northeast pacific region. The definitive host of this parasite is the Virginia opossum (Didelphis virginiana), an adaptable generalist species that has been expanding its range in western North America. Risk of S. neurona infection in sea otters has been associated with consumption of clams and soft-sediment prey types and a temporal association with large runoff events has been observed. Hypothesizing that infection risk would be greater in association with watersheds with greater opossum density and human hydrological disturbance, we examined the spatial distribution of S. neurona antibody levels based on serum indirect fluorescent antibody test and assessed risk factors for exposure to S. neurona in sea otters from California, Washington, British Columbia and Alaska. Significant spatial clustering of cases was observed, with higher prevalence in California and Washington, compared with British Columbia and Alaska. Older, male animals were at greatest seroprevalence risk and strong associations were observed with particular land cover types, in particular wetlands, cropping land and areas of high human housing unit density. Sea otter habitat containing soft sediment was associated with greater risk than hard substrates or areas with high kelp cover and consumption of a diet rich in clams was associated with increased S. neurona seroprevalence. These findings suggest a transmission pathway analogous to, but distinct from that described for Toxoplasma gondii, with infectious stages reaching susceptible hosts through freshwater runoff and being concentrated in specific locations by the action of ocean physical processes, marine habitat features and potentially, invertebrate bioconcentration.