Investigations of stranded marine mammals have led to much of the current knowledge on marine mammal diseases, as these animals provide an opportunity to study diseases in relatively inaccessible wild populations.4 Although the prevalence of disease in stranded animals is different from the prevalence in the entire population, assessing temporal trends in disease can aid in the evaluation of risk factors for disease in wild populations. In addition, tracking temporal changes in human interactions in stranding events can aid in assessing the impact of human encroachment on the habitat of pinnipeds. Two El Niño Southern Oscillation (ENSO) events have occurred in the past 10 years, a mild event from 1992-1994 and a severe event from 1997-1998.5,6 There is little information, however, on the effect of ENSO events on disease in pinniped populations. The purpose of this study was to identify the causes of stranding in two common phocid seals, northern elephant seals (Mirounga angustirostris) and Pacific harbor seals (Phoca vitulina), along the central California coast over a period of ten years (1992-2001), spanning two ENSO events.
This retrospective study was accomplished by reviewing medical records from The Marine Mammal Center (TMMC) Sausalito, California for all northern elephant seals and Pacific harbor seals that stranded live between January 1, 1992-December 31, 2001 along the central California coast. Information collected from the medical records included date and location of stranding, age class, sex, appearance at stranding, final disposition, cause of death, diseases diagnosed, and laboratory, necropsy, and histopathology results. For each seal a primary cause of stranding was determined. The primary cause of stranding was defined as the disease or condition that was the most likely cause of the animal's stranding. Up to three secondary stranding factors were also determined for each seal and these were defined as conditions that were likely contributing factors in the animal's stranding.
A total of 1277 stranded northern elephant seals were examined during the study period. The majority of these seals were preweaned pups (159), molted weanlings (901), and yearlings (206). Only six animals were subadults and five were adults. The major primary causes of stranding were malnutrition (56.5 %), Otostrongylus circumlitus infection (21.1 %), and northern elephant seal skin disease (9.8%). The most common secondary stranding causes were trauma, human interference, and ocular lesions. The prevalence of northern elephant seal skin disease was the highest in 1992 and 1994 and the highest prevalence of O. circumlitus infections occurred in 1992 and 1993. There was an increase in the number of human interactions from 1992 to 2002.
Nine hundred and forty harbor seals stranded during the study period. Of the total animals, 737 were pre-weaned pups, 161 were weanlings, 11 were yearlings, six were subadults, and 25 were adults. The most common causes of stranding were malnutrition (51.8%), respiratory disease (9.5%), trauma (8.1%), and O. circumlitus related disease (7.1 %). Common secondary stranding factors included human interference, trauma, and phocine herpesvirus-1 (PhHV-1) infection in pups and weanlings. Similar to elephant seals, the highest incidence of O. circumlitus associated disease occurred in 1992, 1993, and 1997. Between 1994 and 1998 there were a high number of strandings in which PhHV-1 was either a primary or a secondary cause of stranding. The number of human interactions in strandings varied annually during the study period, with no consistent pattern emerging.
Our data indicate that the most common cause of stranding in both elephant seals and harbor seals along the central California coast is malnutrition of young seals under a year of age. O. circumlitus related disease3 was a common cause of stranding in both species, and was more prevalent during years of moderate ENSO events (1992-1994). Potential causes of the increased prevalence during these years include increased susceptibility to infection due to poor nutritional condition,1 increased parasite load of the prey, or phocid prey shifts. The cause of the increase in prevalence of skin disease in elephant seals in 1992 and 1994 is unknown. The cause of the increased prevalence of harbor seals with PhHV-1 as a primary and secondary stranding factor between 1994-1998 is multifactoral. In all years the cases tended to be temporally clustered, which may be partially due to lateral transmission during rehabilitation.2
This study of the causes of stranding in phocid seals revealed annual variability in the prevalences of a number of diseases. Further data on factors contributing to these conditions are needed to understand these changes in prevalence, and their relationship to prevalence of disease in the population.
The authors wish to thank the staff and volunteers of The Marine Mammal Center, and the veterinary pathologists that contributed to the data presented.
1. Gershwin ME, AT Borchers, CL Keen. 2000. Phenotypic and functional considerations in the evaluation of immunity in nutritionally compromised hosts. Journal of Infectious Diseases 182(Suppl 1):S108-114.
2. Goldstein T, JAK Mazet, FMD Gulland, T Rowles, JT Harvey, SG Allen, DP King, BM Aldridge, JL Stott. 2003. (Manuscript in review). The transmission of phocine herpesvirus-1 in rehabilitating and free-ranging Pacific harbor seals (Phoca vitulina) in California. Veterinary Microbiology
3. Gulland FMD, K Beckmen, K Burek, L Lowenstine, L Werner, T Spraker, M Dailey, E Harris. 1997. Nematode (Otostrongylus circumlitus) infestation of northern elephant seals (Mirounga angustirostris) stranded along the central California coast. Marine Mammal Science 13(3):446-459.
4. Gulland FMD. 1999. Stranded seals: important sentinels. Journal of the American Veterinary Medical Association 214(8):1191-1192.
5. McPhaden MJ. 1999. Genesis and evolution of the 1997-1998 El Niño. Science 283:950-954.
6. Trenberth KE, TJ Hoar. 1996. The 1990-1995 El Nino-Southern Oscillation event: Longest on record. Geophysical Research Letters 23(1): 57-60.