Pathology of domoic acid toxicity in California sea lions (Zalophus californianus).

Over 100 free-ranging adult California sea lions (Zalophus californianus) and one Northern fur seal (Callorhinus ursinus), predominantly adult females, were intoxicated by domoic acid (DA) during three harmful algal blooms between 1998 and 2000 in central and northern California coastal waters. The vector prey item was Northern anchovy (Engraulis mordax) and the primary DA-producing algal diatom was Psuedonitzschia australis. Postmortem examination revealed gross and histologic findings that were distinctive and aided in diagnosis. A total of 109 sea lions were examined, dying between 1 day and 10 months after admission to a marine mammal rehabilitation center. Persistent seizures with obtundation were the main clinical findings. Frequent gross findings in animals dying acutely consisted of piriform lobe malacia, myocardial pallor, bronchopneumonia, and complications related to pregnancy. Gross findings in animals dying months after intoxication included bilateral hippocampal atrophy. Histologic observations implicated limbic system seizure injury consistent with excitotoxin exposure. Peracutely, there was microvesicular hydropic degeneration within the neuropil of the hippocampus, amygdala, pyriform lobe, and other limbic structures. Acutely, there was ischemic neuronal necrosis, particularly apparent in the granular cells of the dentate gyrus and the pyramidal cells within the hippocampus cornu ammonis (CA) sectors CA4, CA3, and CA1. Dentate granular cell necrosis has not been reported in human or experimental animal DA toxicity and may be unique to sea lions. Chronically, there was gliosis, mild nonsuppurative inflammation, and loss of laminar organization in affected areas.

Prey, parasites and pathology associated with the mortality of a juvenile gray whale (Eschrichtius robustus) stranded along the northern California coast.

An eastern Pacific gray whale (Eschrichtius robustus) stranded off Pelican Point, Tomales Bay, California, USA, was examined for physiological parameters, prey, parasites and associated pathology. The whale was emaciated, and hematological examination revealed an elevation in hematocrit, serum sodium, potassium, electrolyte values and hypoglycemia. Parasites recovered included 5 species, 1 ectoparasite (Cyamus scammoni), and 4 helminths (Anisakis simplex, Ogmogaster antarcticus, Ogmogaster pentalineatus, Bolbosoma balanae) with the latter causing multifocal transmural abscesses. Histological examination indicated severe acute lung congestion, minimal, multifocal, lymphocytic, interstitial myocarditis, and mild hepatocellular and Kupffer cell hemosiderosis. The prey taxa present in the stomach indicated the whale was feeding on hard bottom communities prior to death.

Mortality of sea lions along the central California coast linked to a toxic diatom bloom.

Over 400 California sea lions (Zalophus californianus) died and many others displayed signs of neurological dysfunction along the central California coast during May and June 1998. A bloom of Pseudo-nitzschia australis (diatom) was observed in the Monterey Bay region during the same period. This bloom was associated with production of domoic acid (DA), a neurotoxin that was also detected in planktivorous fish, including the northern anchovy (Engraulis mordax), and in sea lion body fluids. These and other concurrent observations demonstrate the trophic transfer of DA resulting in marine mammal mortality. In contrast to fish, blue mussels (Mytilus edulus) collected during the DA outbreak contained no DA or only trace amounts. Such findings reveal that monitoring of mussel toxicity alone does not necessarily provide adequate warning of DA entering the food web at levels sufficient to harm marine wildlife and perhaps humans.