Steller sea lion research >Other Hypothesis >Disease

Disease and the decline of Steller sea lions

It is unclear whether infectious diseases, which can degrade the health, reproductive capacity, and survival of individuals, have played a role in the decline of Steller sea lion populations. Dr. Kathy Burek headed up a team of researchers to review all information collected to date about the incidence of disease among Steller sea lions.

Results to date suggest diseases are not a primary cause of the decline because they are either not present, or are present in both declining and thriving populations. However, endemic agents may be more pathogenic in stressed animals. Further research is necessary to compare the immune responses of different populations to pathogens that are present.

Last updated 23 June 2006

Infectious disease and the decline of Steller sea lions (Eumetopias jubatus) in Alaska: insights from serology data. Burek, K.A., F.M.D. Gulland, G. Sheffield, K.B. Beckman, E. Keyes, T.R. Spraker, A.W. Smith, D.E. Skilling, J.E. Evermann, J.L. Stott, J.T. Saliki and A.W. Trites. 2005. Journal of Wildlife Diseases 41(3):512-524. abstract Serology data were examined to determine whether infectious disease may have played a role in the decline of Steller sea lions (Eumetopias jubatus) in the Gulf of Alaska and Aleutian Islands. Available published data, historical unpublished data, and recent collections (1997-2000) were compared and reviewed. Data was stratified by geography in order to compare the declining western Alaska population in the Aleutian Islands regions through eastern Prince William Sound to the increasing population in Southeast Alaska.  Prevalences of antibodies from the 1970s to early 1990s were noted for Leptospira interrogans, Chlamydophila psittaci, Brucella spp., phocid herpesvirus 1, and canine parvovirus.  Serum samples collected and analyzed from 1997?2000 were tested for antibodies to these agents as well as to caliciviruses, marine mammal morbilliviruses, and canine adenoviruses 1 and 2.  Conclusions could not be drawn about changes in the prevalence of exposure to disease agents during the decline of Steller sea lions because data were not comparable either because of inconsistencies in test techniques, or because the samples were either not collected in all decades from all regions or were not tested for antibodies to the same disease agents in different decades.  Despite these shortcomings, the available data contained no convincing evidence of significant exposure of Steller sea lions to morbilliviruses, B. spp., canine parvovirus or L. interrogans.  Steller sea lions have been exposed to a phocid herpesvirus, caliciviruses, canine adenovirus, and C. psittaci or to cross reactive organisms in regions of both increasing and decreasing sea lion abundance.  These disease agents are not likely to have been the primary cause of the decline because they are found at comparable levels in both the increasing and the decreasing populations.  However they may have contributed to the decline or impeded recovery of the Steller sea lion population due to undetected mortality and morbidity, or reduction of fecundity and body condition in animals under other stresses.  Systematic monitoring for disease agents and their effects is needed to determine whether infectious disease is currently playing a role in the decline and lack of recovery of Steller sea lions.
Disease agents in Steller sea lions in Alaska: A review and analysis of serology data from 1975-2000. Burek, K.A., F.M.D. Gulland, G. Sheffield, D. Calkins, E. Keyes, T.R. Spraker, A.W. Smith, D.E. Skilling, J. Evermann, J.L. Stott and A.W. Trites. 2003. Fisheries Centre Reports Vol 11(4) pp. 26 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 sittaci, Brucella sp, morbilliviruses, influenza A, oxoplasma 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 sstudies should be aimed at detecting infectious agents directly, and determining their association with morbidity and mortality, as well as changes in host population dynamics.