Shellfish Toxicity 

Infectious agents cause most shellfish-associated illness. Hepatitis A, Norwalk virus, Vibrio parahaemolyticus, and Vibrio vulnificus all have been transmitted through shellfish ingestion. Toxic illness caused by shellfish has been recognized for several hundred years.

Native Americans are known to have warned early settlers to avoid shellfish during the summer months. Since that time, at least 4 distinct shellfish-poisoning syndromes have been identified, as follows:

• Paralytic shellfish poisoning (PSP)
• Neurologic shellfish poisoning (NSP)
• Diarrheal shellfish poisoning (DSP)
• Amnestic shellfish poisoning (ASP)

All 4 syndromes share some common features and primarily are associated with bivalve mollusks (eg, mussels, clams, oysters, scallops). These shellfish are filter feeders and, therefore, accumulate toxins produced by microscopic algae in the form of dinoflagellates and diatoms.

The toxins responsible for most shellfish poisonings are water-soluble, are heat and acid-stable, and are not inactivated by ordinary cooking methods. The main toxins responsible for each of the shellfish syndromes are as follows:

• PSP - Saxitoxin
• NPS - Brevetoxin
• DSP - Okadaic acid
• ASP - Domoic acid

The saxitoxins act by blocking sodium ion movement through voltage-dependent sodium channels in nerve and muscle cell membranes. Conduction block occurs principally in motor neurons and muscle. The toxin is made by dinoflagellates of the Gonyaulax species (red tide). Brevetoxins are polycyclic ethers that, like ciguatoxin, bind to and stimulate sodium flux through voltage-gated sodium channels in nerve and muscle. Brevetoxins are made by the dinoflagellate Ptychodiscus brevis. Okadaic acid binds to intestinal epithelial cells and increases their permeability. This toxin is made by dinoflagellates of the species Dinophysis and Prorocentrum. A group of these toxins associated with diarrheal shellfish poisoning has collectively been called pectenotoxins.^[1]

Domoic acid is structurally similar to the excitatory neurotransmitter glutamate. Domoic acid binds to and stimulates the kainic acid glutamate receptor,^[2] which allows sodium influx and a small amount of potassium efflux—neuronal depolarization results. Domoic acid has been associated with necrosis of the glutamate-rich hippocampus and amygdala in autopsied cases. Domoic acid is produced by the diatom Nitzschia pungens.

Frequency

United States

Toxic outbreaks often are associated with algal blooms of single-celled dinoflagellates, which can cause a red-brown discoloration of the water. This proliferation of toxic dinoflagellates, known as red tide, is favored by warmer weather. This phenomenon has led to the general teaching in North America that shellfish are safe to eat only if harvested in a month containing the letter "r."

Education, surveillance, and strict regulation by public health officials appear to be decreasing the incidence of shellfish poisoning in the United States. Additionally, enzyme-linked immunosorbent assay (ELISA) screening techniques are making detection of these toxins simple and rapid. Most recent cases of PSP have occurred along the northeast Atlantic coast, northwest Pacific coast, or Alaska. Most cases have involved recreational shellfish collectors, not commercial vendors. Since 1927, a total of 500 cases of PSP and 30 deaths have been reported in California. Sporadic and continuous outbreaks of NSP occur along the Gulf coast from Florida to Texas. In May 2002, 13 cases of saxitoxin poisoning were reported in Florida residents who ate pufferfish caught in waters near Titusville, Florida.^[3]

The 2009 Annual Report of the American Association of Poison Control Centers' National Poison Data System documented 136 single exposures to paralytic shellfish; no deaths occurred.^[4]

International

Sporadic outbreaks have been reported in Europe, Asia, Africa, and the Pacific Islands. Red tide and its resultant massive kills of various birds and marine animals have become an enormous concern in Europe, prompting numerous international congresses to address the problem.

Mortality/Morbidity

Fatality rates from PSP, the most severe of the 4 syndromes, ranges from 1-12% in isolated outbreaks. Its high mortality rate in some areas is caused by poor access to advanced life support capabilities. The mortality rate in the only known outbreak of ASP was 3%. To date, no deaths have been reported for NSP or DSP.

Age

Based on mortality figures from recent outbreaks, children appear to be more sensitive to the saxitoxins of PSP than adults. To date, all the reported deaths from ASP have been in elderly persons who had more severe neurologic symptoms.