Abstract

In 1995, after a decade of growth, the southern sea otter (Enhydra lutris nereis) population began a pattern of slow decline associated with high adult mortality rates. This decline continues to date despite birth rates comparable to the Alaskan northern sea otter. As a result of these findings, research efforts were initiated to identify causes of mortality. The National Wildlife Health Center in conjunction with the U.S. Fish and Wildlife Service and the California Department of Fish and Game identified infectious diseases as a major cause of sea otter death during the period from 1992 to 1996. Multiple pathogens were implicated in these deaths. Occasionally unusual pathogens such as Coccidiodes immitis and Toxoplasma sp. were identified in the sea otter carcasses. These finding were surprising, since these are agents often cause opportunistic infections in immunosuppressed humans and domestic animals. Furthermore, animals dying with infections contained greater tissue concentrations of dibutyltin, a degradation product of tribulytin, and 1,1,1-trichloro-2,2-bis(p-chorophenyl)ethane (DDT) than animals dying of traumatic causes. Elevated concentrations of tributyltin and DDTs in the diet or body have been associated with immunologic dysfunction in other mammalian species. Together these findings raised concern regarding the immunologic health of the sea otter population and stimulated studies in our laboratory to develop immune function assays for use in this species.

To evaluate the immune system in sea otters inhabiting specific contaminated and non-contaminated sites within the Monterey Bay National Marine Sanctuary, lymphocyte function assays (proliferation and IL-2 receptor expression) were developed. Blood samples were collected from apparently healthy free-ranging southern sea otters from March 1998 through to the present. In addition to collecting CBC data, a panel of antibodies that label specific WBC subsets, such as B and T lymphocytes, were developed for use in sea otters. These reagents were used to evaluate circulating leukocyte subsets and examine their surface protein expression. These studies allowed us to develop normal ranges for the immunophenotype of circulating lymphocyte subsets and for lymphocyte function in the southern sea otter. Significant age-related changes were observed in B lymphocyte numbers and MHC II expression. The functional significance of these changes is not known. Reduced lymphocyte function was detected in a few sea otters sampled. Studies in other species suggest that these animals may be immunologically impaired.

In conclusion, our preliminary studies show that lymphocyte function assays and immunophenotyping of peripheral blood are promising tests that should be included in the minimum database to assess the health of free-ranging as well as captive southern sea otters. This data can be used to identify animals with abnormal T lymphocyte function as well as to screen the peripheral blood for phenotypic changes. These are valuable tests that can be studied in conjunction with markers of chemical exposure, behavioral studies, and tests for exposure to infectious agents. Together, this information will allow us to better understand the sea otter immune system and how environmental and anthropogenic factors may be affecting the health of the southern sea otter population.