Abstract

Domoic acid is an excitatory neurotoxin that is produced by a number of marine algae, including the diatom Pseudo-nitzschia australis. Acute domoic acid toxicity can result in a number of neurologic signs in affected California sea lions (Zalophus californianus) such as ataxia, disorientation, seizure, and possibly death. However, the long-term, sublethal effects of domoic acid toxicity have not been fully investigated. This study describes the neurologic lesions associated with the long-term effects of acute exposure to domoic acid in stranded sea lions, and it investigates the survival of animals with these lesions using satellite-linked telemetry. Animals in the study were suspected of having long-term effects of domoic acid toxicity if they exhibited neurologic signs typical of domoic acid toxicity yet stranded during a time of no known domoic acid-producing algal blooms, re-stranded after initial treatment for domoic acid toxicity, or continued to exhibit neurologic signs after multiple courses of anti-convulsant therapy. The animals were then screened for other causes of neurologic disease by performing complete blood counts, serum biochemistry analysis, serology for Toxoplasma sp. and Sarcocystis sp., radiographs, cerebrospinal fluid evaluation, and magnetic resonance imaging (MRI). If the animals showed no clinical signs of neurologic disease for at least 10 days after the end of anti-convulsant therapy, they were fitted with a satellite-linked transmitter and released.

Ten animals (two male, eight female) were suspected of having long-term effects of domoic acid toxicity and entered into the study. Eosinophilia was noted in eight animals. Radiographs and cerebrospinal fluid evaluation did not reveal any significant abnormalities. Markedly elevated and rising Toxoplasma sp. titers were detected using an immunofluorescent antibody test in one animal, while weak positive titers were found in two additional animals. Evaluation of MRI studies in the animals revealed a variety of lesions. The most common MRI findings were varying degrees of unilateral and bilateral hippocampal atrophy found in all 10 animals.

Additional lesions suggestive of cerebritis in two animals and cerebral hemorrhage in one animal that were seen with MRI and confirmed with histopathology were not considered to be typical of domoic acid toxicity. Histopathology from the other three animals that either died or were euthanatized revealed neuronal necrosis and gliosis in the limbic system considered typical of California sea lions naturally exposed to high doses of domoic acid. One animal was released without a satellite-linked transmitter. Five animals were released with satellite-linked transmitters and monitored for up to 106 days post-release. Of these five, two animals restranded and were euthanatized, one animal had questionable success after release due to premature failure of the telemetry system, one animal displayed normal behavior after release, and it is still too early to evaluate the success of the last animal. This study highlights the difficulties encountered with the diagnosis of long-term effects due to acute domoic acid toxicity in stranded California sea lions. The variable post-release success of animals diagnosed with long-term effects of domoic acid toxicity suggests that diagnosis of the severity of lesions must be improved in order to better evaluate the prognosis for affected California sea lions.