|Thomas, N - MADISON, WI|
|Lindsay, D - BLACKSBURG, VA|
|Cole, R - MADISON, WI|
|Meteyer, C - MADISON, WI|
Submitted to: Journal of Comparative Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 1, 2006
Publication Date: November 1, 2007
Citation: Thomas, N.J., Dubey, J.P., Lindsay, D.S., Cole, R.A., Meteyer, C.U. 2007.Protozoal meningoencephalitis in sea otters (Enhydra lutris): a histopathological and immunohistochemical study of naturally-occurring cases. Jrnl of Comp. Path. 137:102-121. Interpretive Summary: Sarcocystis neurona is a single-celled parasite. It causes a fatal disease in horses called Equine Protozoal Myeloencephalitis (EPM). EPM also occurs in other animals. Opossums are the definitive host for this parasite, and the main reservoir of infection. Opossums become infected by consuming the encysted stage of the parasite (sarcocyst) in infected animal tissue and they excrete millions of the resistant stage (oocysts) in their feces. Horses become infected by ingesting food and water contaminated with oocysts.Toxoplasma gondii is a related parasite that causes infections in many hosts including humans.Scientists at the Beltsville Agricultural Research Center and US Geological Survey, Madison, Wisconsin report toxoplasmosis and EPM in sea otters. The results will be of interest to biologists, parasitologists, and veterinarians.
Technical Abstract: Protozoal meningoencephalitis is considered to be an important mortality factor in the California sea otter (Enhydra lutris) population. Of 344 California (CA) and Washington state (WA) sea otters examined from 1985-2004 39 (11.3%) had histopathological evidence of significant protozoal meningoencephalitis. The etiologic agents and histological lesions associated with these protozoal infections are described. Morphology of the organisms’ actively multiplicative life stages (tachyzoites for Toxoplasma gondii and merozoites for Sarcocystis neurona) and immunohistochemical stain affinity were used to identify 22/39 (56.4%) cases due to S. neurona, 5/39 (12.8%) due to T. gondii, and 12/39 (30.8%) cases with dual infections. In all dual infections active S. neurona was present, while only latent T. gondii was present in most. In S. neurona meningoencephalitis, multifocal to diffuse gliosis was widespread in gray matter and consistently present in the cerebellar molecular layer. In T. gondii meningoencephalitis discrete foci of gliosis and malacia were more widely separated, sometimes incorporated pigment-laden macrophages and mineral, and were found predominantly in the cerebral cortex, relatively sparing the cerebellar molecular layer. Quiescent tissue cysts of T. gondii were often incidental and not considered to be the cause of clinical disease and mortality. Protozoal meningoencephalitis was diagnosed more frequently in the growing population of WA sea otters (10/31, 32.3%) than in the declining CA population (29/313, 9.3%). Among sea otters with protozoal meningoencephalitis, those that had displayed neurologic signs prior to death had active S. neurona encephalitis, supporting the conclusion that S. neurona is the most significant protozoal pathogen in the central nervous system of sea otters.