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  • Updated 06.19.2022
  • Released 08.23.2021
  • Expires For CME 06.19.2025

Shellfish poisoning

Introduction

Key points

• Shellfish poisoning includes three neurotoxic syndromes that share some common features and are primarily associated with bivalve mollusks (eg, mussels, clams, oysters, and scallops).

• The neurologic shellfish poisoning syndromes are (1) amnesic shellfish poisoning, (2) neurotoxic shellfish poisoning, and (3) paralytic shellfish poisoning.

• About 40% of affected individuals require hospitalization, but fatalities are rare.

• Treatment is generally supportive and symptomatic.

• There are no available antitoxins for any of the neurologic forms of shellfish poisoning.

• Some survivors may have permanent neurologic disabilities after neurologic forms of shellfish poisoning, including potentially permanent short-term memory loss after amnesic shellfish poisoning.

Historical note and terminology

Toxic algal blooms and “red tides” have been documented for millennia (19). Ancient Greeks named the Red Sea for its appearance during red tides. The Bible (Exodus 7:20-21) refers to toxic algal blooms: “the waters that were in the rivers were turned to blood, and the fish in the rivers died, and the river stank...”

Shellfish poisoning includes four syndromes that share some common features and are primarily associated with bivalve mollusks (eg, mussels, clams, oysters, and scallops). As filter feeders, these shellfish can accumulate toxins produced by microscopic algae, such as cyanobacteria, diatoms, and dinoflagellates.

The neurologic shellfish poisoning syndromes are:

(1) Amnesic shellfish poisoning

(2) Neurotoxic shellfish poisoning

(3) Paralytic shellfish poisoning

The fourth type of shellfish poisoning is diarrheal shellfish poisoning, which is outside of the scope of this article except as it concerns the differential diagnosis. Diarrheal shellfish poisoning toxins typically include okadaic acid and dinophysistoxins and can be considered to include the more recently identified toxin azaspiracid, although human disease due to the latter toxin is often separated as azaspiracid shellfish poisoning. These are considered briefly in tabular form under differential diagnosis.

Amnesic shellfish poisoning was first discovered in the autumn of 1987 when a serious outbreak of food poisoning occurred in eastern Canada (07; 62; 19). Three deaths and 105 confirmed cases of acute intoxication followed consumption of mussels from this area. Some surviving victims suffered long-term neurologic problems, including memory loss. The outbreak was traced to cultured blue mussels (Mytilus edulis) from the Cardigan Bay region of eastern Prince Edward Island. The toxin, identified as domoic acid, had not previously been found in any shellfish, and this outbreak was the first known occurrence of human poisoning by this neurotoxin. A plankton bloom at the time of the outbreak consisted almost entirely of the diatom Nitzschia pungens f. multiseries. Symptoms of intoxication in humans included abdominal cramps, vomiting within the first few hours, and neurologic abnormalities involving disorientation and memory loss that could persist indefinitely (22). In mid-December 1987, the toxin in mussels was identified as domoic acid (09; 22; 68).

The first paralytic shellfish poisoning event was reported in 1927 near San Francisco (41; 59), although clinical descriptions suggestive of paralytic shellfish poisoning have been documented for centuries (19). The outbreak was traced to shellfish contaminated with a toxin from the dinoflagellate Alexandrium catenella. There were six deaths among 102 individuals affected. This event eventually led to the institution of extensive shellfish monitoring programs in the United States and establishment of regulatory limits on the associated neurotoxins in shellfish (50; 66).

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