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Populations of sea otters, seals and sea lions have collapsed across much of southwest Alaska over the past several decades. The sea otter decline set off a trophic cascade in which the coastal marine ecosystem underwent a phase shift from kelp forests to deforested sea urchin barrens. This interaction in turn affected the distribution, abundance and productivity of numerous other species. Ecological consequences of the pinniped declines are largely unknown. Increased predation by transient (marine mammal-eating) killer whales probably caused the sea otter declines and may have caused the pinniped declines as well. Springer et al. proposed that killer whales, which purportedly fed extensively on great whales, expanded their diets to include a higher percentage of sea otters and pinnipeds following a sharp reduction in great whale numbers from post World War II industrial whaling. Critics of this hypothesis claim that great whales are not now and probably never were an important nutritional resource for killer whales. We used demographic/energetic analyses to evaluate whether or not a predator-prey system involving killer whales and the smaller marine mammals would be sustainable without some nutritional contribution from the great whales. Our results indicate that while such a system is possible, it could only exist under a narrow range of extreme conditions and is therefore highly unlikely.

Elevated mortality appears to be the main reason for both sluggish growth and periods of decline in the threatened California sea otter population. We assessed causes of mortality from salvage records of 3,105 beach‐cast carcasses recovered from 1968 through 1999, contrasting two periods of growth with two periods of decline. Overall, an estimated 40%‐60% of the deaths were not recovered and 70% of the recovered carcasses died from unknown causes. Nonetheless, several common patterns were evident in the salvage records during the periods of population decline. These included greater percentages of (1) prime age animals (3–10 yr), (2) carcasses killed by great white shark attacks, (3) carcasses recovered in spring and summer, and (4) carcasses for which the cause of death was unknown. Neither sex composition nor the proportion of carcasses dying of infectious disease varied consistently between periods of population increase and decline. The population decline from 1976 to 1984 was likely due to incidental mortality in a set‐net fishery, and the decline from 1995 to 1999 may be related to a developing live‐fish fishery. Long‐term trends unrelated to periods of growth and decline included a decrease in per capita pup production and mass/length ratios of adult carcasses over the 31‐yr study. The generally high proportion of deaths from infectious disease suggests that this factor has contributed to the chronically sluggish growth rate of the California sea otter population.

An indirect fluorescent antibody test (IFAT) for detection of Toxoplasma gondii infection was validated using serum from 77 necropsied southern sea otters (Enhydra lutris nereis) whose T. gondii infection status was determined through immunohistochemistry and parasite isolation in cell culture. Twenty-eight otters (36%) were positive for T. gondii by immunohistochemistry or parasite isolation or both, whereas 49 (64%) were negative by both tests. At a cutoff of 1:320, combined values for IFAT sensitivity and specificity were maximized at 96.4 and 67.3%, respectively. The area under the receiver-operating characteristic curve for the IFAT was 0.84. A titer of 1:320 was used as cutoff when screening serum collected from live-sampled sea otters from California (n = 80), Washington (n = 21), and Alaska (n = 65) for T. gondii infection. Thirty-six percent (29 out of 80) of California sea otters (E. lutris nereis) and 38% (8 out of 21) of Washington sea otters (E. lutris kenyoni) were seropositive for T. gondii, compared with 0% (0 out of 65) of Alaskan sea otters (E. lutris kenyoni).

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During diving, marine mammals initiate a series of cardiovascular changes that include bradycardia and decreased peripheral circulation. Because heat transfer from thermal windows located in peripheral sites of these mammals depends on blood flow, such adjustments may limit their thermoregulatory capabilities during submergence. Here, we demonstrate how the thermoregulatory responses of bottlenose dolphins (Tursiops truncatus) are coordinated with the diving response. Heart rate, skin temperature and heat transfer from the dorsal fin and flank were measured while dolphins rested on the water surface, stationed 5–50 m under water and floated at the surface immediately following a dive. The results showed that heat flow ranged from 42.9+/−7.3 to 126.2+/−23.1 W m(−)(2) and varied with anatomical site and diving activity. Upon submergence, heat flow declined by 35 % from the dorsal fin and by 24 % from the flank. An immediate increase in heat flow to levels exceeding pre-dive values occurred at both sites upon resurfacing. Changes in heart rate during diving paralleled the thermoregulatory responses. Mean pre-dive heart rate (102.0+/−2.6 beats min(−)(1), N=26) decreased by 63.4 % during dives to 50 m and immediately returned to near resting levels upon resurfacing. These studies indicate that heat dissipation by dolphins is attenuated during diving. Rather than challenge the diving response, heat transfer is delayed until post-dive periods when the need for oxygen conservation is reduced.