Abstract
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 1900.8 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,5,6 populations east of Cook Inlet appear generally stable or increasing2,12. The southern sea otter (Enhydra lutris nereis) 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.3,4,7,10,11 In this initial pilot study, we began to establish a network for recovering fresh-dead animals from southcentral Alaska and performing necropsies comparable to those in conducted in California. Our hypothesis was that the prevalence of major infectious diseases is lower in the northern sea otter compared to the threatened southern sea otter in California. Our objective was to identify causes of mortality and compare disease prevalence rates between northern and southern sea otters.
During 2002 and 2003, we recovered eight carcasses suitable for this protocol. Of the eight, two were rehabilitation animals from the Alaska SeaLife Center, and the rest were beach cast. Two were from Kodiak, two from Homer and four from the Seward area. Seven were male, and one female. Three (38%) died due to severe valvular vegetative endocarditis with associated extensive thrombotic disease. Organisms were isolated from the heart blood of two of the three and included a nonhemolytic Streptococcus sp. and Aeromonas sp. in one case and Streptococcus bovis in the other. One animal that had been suffering from seizures and was euthanatized had an encephalocele. Two animals were emaciated and had massive colonic impactions; another died of massive trauma (boat strike); and the last was a prime condition female with a term fetus which died acutely with massive pulmonary edema, pleural effusion, and myocarditis. All cases have been negative by serology and culture for Sarcocystis neurona and Toxoplasma gondii. One animal had a T. gondii titer of 1:80; however, the significance of this finding is unknown since corresponding histologic and culture results were negative. Parasites that have been identified include the acanthocephalan Corynosoma enhydri, gastric nematodes (Anisakis sp.), a cestode (Diplogonoporus tetrapterus) and a hepatic trematode (Orthospanchnus fraterculus).
Although a very small number of cases have been reviewed to date, the emerging pattern is different from that described for the southern sea otters. In the CA animals, protozoal encephalitis, acanthocephalan-related disease, shark attack, and cardiac disease (primarily a chronic nonsuppurative myocarditis of unknown etiology) have been identified as the most common causes of death.9 Valvular endocarditis has been reported in the southern sea otters but appears to be rare. Our findings will help determine causes of the patterns observed in population trends in Alaska sea otters and may help clarify the role of infectious disease in the California population.
Acknowledgments
This project was supported by the U.S. Geological Survey, Alaska Science Center, Alaska Veterinary Pathology Services, the U.S. Fish and Wildlife Service, and the Alaska SeaLife Center. The authors would like to thank Dr. Daniel Mulcahy (USGS) for performing some necropsies and proofing the abstract, Dr. Natalie Noll (ASLC), Dr. Shawn Johnson (ASLC), and John Haddix (USFWS) for their assistance in performing necropsies. Our thanks to the UCD protozoa laboratory including Woutrina Smith, Patricia Conrad, Andrea Packham, and Ann Melli, as well as to Spencer Jang at the UCD Bacteriology laboratory and to Murray Dailey at The Marine Mammal Center in Sausalito for parasite identifications. We would like to thank the staff of the ASLC for their work with the rehabilitation animals and to the people participating in the stranding network.
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