Characterization and epidemiologic investigation of apicomplexan parasites associated with meningoencephalitis in southern sea otters (Enhydra lutris nereis) and Pacific harbor seals (Phoca vitulina richardsi).

摘要

Protozoal meningoencephalitis was first recognized as a cause of mortality for southern (California) sea otters and harbor seals in 1992. My dissertation research to characterize these infections was initiated in 1998, with the specific goals to: (1) isolate and confirm the identity of these protozoal parasites; (2) investigate the relationship between protozoal parasites of otters and seals and those associated with illness of terrestrial animals and humans; (3) develop and validate serodiagnostic tests, and (4) evaluate potential risk factors for protozoal exposure. Between 1998 and 2002, 180 otters and 20 seals were necropsied, 400 otters and 100 seals were evaluated serologically and 55 protozoal isolates were obtained. Our isolates were characterized antigenically, molecularly and ultrastructurally, and were found to be indistinguishable from Toxoplasma gondii and Sarcocystis neurona. Over 36% of otters examined between 1997 and 2001 were infected with T. gondii at necropsy, while 4% were infected with S. neurona . Otter and seal sera were assessed for T. gondii and S. neurona antibodies using indirect fluorescent antibody tests (IFATs), and the otter T. gondii IFAT was validated using serum from confirmed-infected otters. Sera from California, Washington and Alaska otters were evaluated. The proportion of T. gondii-positive otters was comparable for California and (36%) and Washington (38%), whereas 0% of Alaskan otters were seropositive. An epidemiological study was performed to assess live and dead sea otter data for associations between T. gondii IFAT seropositivity and defined risk factors for T. gondii infection. Seropositivity was positively correlated with male gender, increasing age and dead versus live status. Spatial analysis revealed two clusters of T. gondii seropositive otters and one cluster of seronegative otters. Otters at one high-risk site were 9 times more likely to be seropositive to T. gondii than otters sampled at other sites. No association was found between T. gondii seropositivity and human population density or sewage exposure. Otters sampled near maximal freshwater runoff were 3 times more likely to be seropositive to T. gondii than otters sampled in areas of low flow. This study provides evidence that surface runoff is a source for T. gondii infection for southern sea otters.