ABSTRACT

Results of serology studies conducted from 1975-1996 on Alaskan populations of Steller sea lions (Eumetopias jubatus) were synthesized and supplemented with analyses of archived sera to assess the chronological and spatial patterns of exposure to disease agents and the role that infectious disease may have played in the decline of Steller sea lions in the Gulf of Alaska and Aleutian Islands. Serum samples were obtained during three periods (1970s, 1980s and 1990s) and were tested for exposure to Leptospira interrogans, caliciviruses, Chlamydophila psittaci, Brucella sp, morbilliviruses, influenza A, Toxoplasma gondii, phocid herpesviruses and canine parvovirus. Testing for these agents and canine adenoviruses 1 and 2 continued through 2000. In most cases, conclusions cannot be drawn about chronological changes in the prevalence of disease agents during the decline of Steller sea lions because the samples were not collected from all regions in each time period, nor from sufficient numbers of animals in each age class. In addition, samples were not all analyzed by the same laboratories, were not stored under controlled conditions, were not tested for the same disease agents, and assays were not validated for Steller sea lions.

There is no convincing evidence of significant exposure to influenza A, morbilliviruses, Brucella abortus, canine parvovirus and Leptospira sp. However, there is evidence of exposure to a herpesvirus, C. psittaci, caliciviruses, T. gondii and canine adenovirus in regions of both increasing and decreasing sea lion abundance. As these agents are either present throughout the areas examined, or were not evident in all of the animals examined, it is unlikely that these disease agents caused the population decline of sea lions by epidemic mortality. However, as the number of samples tested for morbillivirus is low, and the assays used have not been validated for Steller sea lions, exposure to a morbillivirus during the peak of the decline cannot be completely ruled out from the data available.

Some pathogens become endemic and interact with malnutrition or predation to decrease survival or reproduction therefore preventing recovery of depleted populations. In other species, C. psittaci, herpesviruses, adenoviruses, and T. gondii are more readily expressed as clinical diseases when individuals are stressed. It is possible that these agents could be contributing to the lack of recovery by causing undetected mortality and morbidity, or by reducing fecundity and juvenile survival rates. A systematic disease agent monitoring protocol should therefore be initiated to adequately test for disease agents in different time periods and regions.

Serological studies are limited in that they only assess immunological response following exposure to infectious agents. They do not give information on the prevalence of disease agents, or on presence of clinical disease. Further studies should be aimed at detecting infectious agents directly, and determining their association with morbidity and mortality, as well as changes in host population dynamics.

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