More than 400 harbor seals, most of them immature, died along the New England coast between December 1979 and October 1980 of acute pneumonia associated with influenza virus, A/Seal/Mass/1/180 (H7N7). The virus has avian characteristics, replicates principally in mammals, and causes mild respiratory disease in experimentally infected seals. Concurrent infection with a previously undescribed mycoplasma or adverse environmental conditions may have triggered the epizootic. The similarities between this epizootic and other seal mortalities in the past suggest that these events may be linked by common biological and environmental factors.

During a 5–wk period beginning in late November, 1987, 14 humpback whales, Megaptera novaeangliae, died in Cape Cod Bay after eating Atlantic mackerel, Scomber scombrus, containing saxitoxin (STX), a dinoflagellate neurotoxin responsible for paralytic shellfish poisoning in humans. We propose a line of evidence to explain how whales, by virtue of their diving adaptations, may be particularly vulnerable to this systemic neurotoxin. Absence of STX in New England waters and shellfish during the episode suggests that the mackerel, representing the northern stock which spawns in the Gulf of St. Lawrence, accumulated the toxin there and delivered it to the Gulf of Maine and Cape Cod Bay in the fall of 1987. These findings challenge common perceptions of the manner in which planktonic toxins move through the food chain, and offer new insights into natural mortality and standings of marine mammals. It seems appropriate to search for STX and other phytotoxins when investigating marine mammal mortalities.

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The activity associated with capturing, restraining, and removing bottlenose dolphins, Tursiops truncatus, from water stimulates a stress response as reflected by circulating cortisol, aldosterone, and eosinophils. Serum cortisol increased from resting levels of about 30 to 110 nmol/L within 1 h, aldosterone rose from less than 280 pmol/L to up to 1880 pmol/L within 3 h, and circulating eosinophils were depressed to less than 40% of their initial numbers within 7 h after the animals were removed from water (calm-capture). This basic response was not enhanced when the capture procedure was prolonged for 3 h (chase-capture) or when the dolphins were given adrenocorticotropic hormone and was similar to that observed in free-ranging dolphins after they had been held in a net for up to 5 h. Eosinophil numbers appear to be a consistent and practical indicator of stress in dolphins.