During much of the 20th century, sea otter populations throughout their range were recovering from the effects of an international fur harvest that ended with the near extirpation of the species by 1900.7 Recovery rates of geographically isolated sea otter populations varied, but causes of differences are poorly understood.1 Despite large scale rapid declines in sea otter populations southwest of Cook Inlet in Alaska,4,5 populations east of Cook Inlet appear generally stable.1,2 The Southern sea otter in California has demonstrated a consistently low population growth rate and a variety of factors have been identified as contributing to the delayed recovery, including starvation, predation, mortality related to fisheries, and infectious diseases.3,8,11 Beginning in 2002, researchers in Alaska have begun to establish a network for recovering fresh-dead animals from Alaska and performing necropsies comparable to those in conducted in California. The purpose of this work is to estimate the presence and prevalence of infectious disease in sea otters in Alaska and provide a contrast of mortality patterns in the Southern sea otter.
During 2002 through January of 2005, 18 fresh-dead carcasses suitable for this protocol were recovered in Alaska. Of the 18, two were rehabilitation animals from the Alaska SeaLife Center, 14 were beach cast and two died associated with an oil spill. Eight (44%) died due to severe valvular vegetative endocarditis involving the aortic, left atrioventricular valve or both with associated extensive thromboembolic disease. Organisms isolated from 6 of these included a mixed culture of non-hemolytic Streptococcus sp. and Aeromonas sp. in one case and various strains of S. infantarius ss. coli in the other five. In the two culture negative cases, large numbers of gram-positive cocci were present in the valvular lesion histologically.
Although a relatively small number of Alaska cases have been reviewed to date, the prevalence of valvular endocarditis, was unanticipated. It is unusual to see such a clustering of this disease, unless a particularly pathogenic organism or organisms with a tropism for heart valves are involved. Typically, this is a sporadic disease secondary to chronic recurrent bacterial seeding from a primary site of infection or secondary to valvular abnormalities. A primary site could not be identified in most of these animals although in few cases, fractured teeth and in another abscessation of the laryngeal cartilages were present. Streptococcal organisms are a common cause of this disease in a wide variety of hosts. There has been one previous report of valvular endocarditis in a northern sea otter, however cultures were negative.6 Verrucous endocarditis associated with Streptococcus bovis has been described recently in mink.10 In humans, S. bovis is a major cause of valvular endocarditis and is associated with preexisting colonic pathology.9,12 In three of these sea otter cases S. infantarius ss. coli was cultured from the gastrointestinal tract; however, no associated pathology was present.
The relatively high proportion of cases of valvular endocarditis involving a member of the Strep bovis/equinus group in Alaska led to a review of the records of cases in California. In California, approximately 60 necropsies of freshly dead otters are completed each year and cases of valvular endocarditis are sporadically seen. However, in 2004, there was one case of valvular endocarditis and two cases of generalized sepsis with isolation of S. infantarius ss coli. Preliminary findings suggest that disease is a significant contributing factor to sea otter mortality in both Alaska and California, but that specific diseases may differ.
This project was supported by the US Geological Survey, Alaska Science Center, Alaska Veterinary Pathology Services, the US Fish and Wildlife Service, California Department of Fish and Game, the Minnesota Zoo Conservation Fund, and the Alaska SeaLife Center. The authors would like to thank Dr. Daniel Mulcahy (USGS) for performing necropsies and proofing the abstract, Dr. Natalie Noll (ASLC), Dr. Shawn Johnson (ASLC), Dana Jenski (USFWS) and John Haddix (USFWS) for their assistance in performing necropsies. Our thanks to the UCD protozoa laboratory including Woutrina Miller, Patricia Conrad, Andrea Packham, and Ann Melli, as well as to Dave Jessup at CDFG. We would like to thank the staff of the ASLC for their work with the rehabilitation animals and to the many people participating in the stranding network.
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