An Outbreak of Toxic Encephalopathy Caused by Eating Mussels Contaminated with Domoic Acid

Abstract

In Canada in late 1987 there was an outbreak of an acute illness characterized by gastrointestinal symptoms and unusual neurologic abnormalities among persons who had eaten cultivated mussels. Health departments in Canada solicited reports of this newly recognized illness. A case was defined as the occurrence of gastrointestinal symptoms within 24 hours or of neurologic symptoms within 48 hours of the ingestion of mussels. From the more than 250 reports received, 107 patients met the case definition. The most common symptoms were vomiting (in 76 percent of the patients), abdominal cramps (50 percent), diarrhea (42 percent), headache, often described as incapacitating (43 percent), and loss of short-term memory (25 percent). Nineteen patients were hospitalized, of whom 12 required intensive care because of seizures, coma, profuse respiratory secretions, or unstable blood pressure. Male sex and increasing age were associated independently with the risks of hospitalization and memory loss. Three patients died. Mussels associated with this illness were traced to cultivation beds in three river estuaries on the eastern coast of Prince Edward Island. Domoic acid, which can act as an excitatory neurotransmitter, was identified in mussels left uneaten by the patients and in mussels sampled from these estuaries. The source of the domoic acid appears to have been a form of marine vegetation, Nitzschia pungens, also identified in these waters in late 1987. The contaminated mussels from Prince Edward Island were removed from the market, and no new cases have occurred since December 1987. We conclude that the cause of this outbreak of a novel and severe intoxication was the ingestion of mussels contaminated by domoic acid, a potent excitatory neurotransmitter.

Ischemic Cardiomyopathy Following Seizure Induction by Domoic Acid

“…1,5,6,8,21,22 Of direct relevance to development of our hypothesis were indications that systemic dosing with domoic and kainic acids provoke the formation of epileptiform activity originating primarily from the hippocampus. 49 Using intrahippocampal dosed animals, Sawant and colleagues 13 from our research group used electrocorticography to show that DOM-induced epileptiform discharges spread rapidly to surrounding extralimbic regions.…”

“…3,4 Clinical reports of neurological symptoms including seizures, amnesia, and coma coupled with postmortem evidence of hippocampal and amygdaloid nucleus necrosis and astrocytosis were particularly noted among severe cases of DOM ingestion. 1,5,6 Among these cases, the authors also reported cardiovascular disturbances, including cardiac arrhythmias and hypotension. 1 As a consequence of heightened interest in the mechanism of DOM toxicity, a number of experimental studies have investigated the consequences of DOM exposure on behavioral and neurological responses in laboratory animals.…”

“…1,5,6 Among these cases, the authors also reported cardiovascular disturbances, including cardiac arrhythmias and hypotension. 1 As a consequence of heightened interest in the mechanism of DOM toxicity, a number of experimental studies have investigated the consequences of DOM exposure on behavioral and neurological responses in laboratory animals. 4,[7][8][9][10][11][12][13] Within neuronal tissue, DOM has been shown to activate ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and kainic acid (KA) receptors and results in the release of glutamate.…”

Pathology of Domoic Acid Toxicity in California Sea Lions (Zalophus californianus)

“…DA gained notoriety as the causative agent of amnesic shellfish poisoning in 1987, when human consumption of contaminated mussels led to illness and deaths. 19 DA may also pose a risk to marine wildlife and has caused mass mortalities of seabirds 25,37 and marine mammals. 23 Initially described as the antihelmintic component of ''domoi,'' a Japanese folk medicine derived from the red algae Chondria armata, 28 DA is a potent agonist of the alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionate (AMPA) and kainate subclasses of the neuronal glutamate ionotropic receptors.…”

“…DA produced during a HAB may undergo trophic transfer by accumulating in algivorous or filter-feeding species such as anchovy, 13 Dungeness crab, razor clam, 36 or mussels. 19 Other algal toxins of concern in US waters include saxitoxin, brevetoxin, okadaic acid, ciguatoxin, and Pfeisteria-associated toxin. DA gained notoriety as the causative agent of amnesic shellfish poisoning in 1987, when human consumption of contaminated mussels led to illness and deaths.…”