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A variety of illnesses can be seen after ingestion of, and less commonly from dermal or inhalational contact with, fish or shellfish toxins. The most common types of seafood-related toxins include ciguatera, scombroid, neurotoxic shellfish poisoning, paralytic shellfish poisoning, and tetrodotoxin. Less commonly encountered toxins will be discussed briefly. Shellfish-induced bacterial diarrhea is described on (Table II–26).

  1. Mechanism of toxicity. The mechanism varies with each toxin. Marine toxins are generally tasteless, odorless, and heat-stable. Therefore, cooking the seafood does not prevent illness.

    1. Ciguatera. The toxins, ciguatoxin and related compounds such as maitotoxin, are produced by dinoflagellates, which are then consumed by reef fish. Ciguatoxin binds to voltage-sensitive sodium channels, causing increased sodium permeability and depolarization of excitable membranes. Stimulation of central or ganglionic cholinergic receptors may also be involved.

    2. Diarrheic shellfish poisoning is caused by several identified toxins, all of which appear to be produced by marine dinoflagellates. Suspected toxins include okadaic acid, dinophysistoxins, pectenotoxins, and azaspiracids. Yessotoxin is often classified as a diarrheic toxin, although animal testing suggests that its target organ is the heart.

    3. Domoic acid, the causative agent for amnesic shellfish poisoning, is produced by phytoplankton, which are concentrated by filter-feeding fish and shellfish. The toxin is thought to bind to glutamate receptors, causing neuroexcitatory responses.

    4. Neurotoxic shellfish poisoning is caused by ingestion of brevetoxins, which are produced by “red tide” dinoflagellates. The mechanism appears to involve stimulation of sodium channels, resulting in depolarization of nerve fibers.

    5. Palytoxin is produced by dinoflagellates. It alters Na+ and K+ flux across cell membranes by activation of the sodium-potassium-ATPase pump, causing depolarization and contraction of smooth, skeletal, and cardiac muscles. It is also a potent vasoconstrictor.

    6. Paralytic shellfish. Dinoflagellates (“red tide”), and less commonly cyanobacteria from fresh water, produce saxitoxin and 21 other related toxins, which are concentrated by filter-feeding clams and mussels and rarely by nontraditional vectors such as puffer fish, crabs, and lobsters. Saxitoxin blocks sodium conductance and neuronal transmission in skeletal muscles.

    7. Scombroid. Scombrotoxin is a mixture of histamine and histamine-like compounds produced when histidine in fish tissue decomposes.

    8. Tetrodotoxin, produced primarily by marine bacteria, is found in puffer fish (fugu), California newts, some gastropod mollusks, horseshoe crab eggs, and some South American frogs. It blocks the voltage-dependent sodium channel in nerve cell membranes, interrupting neuromuscular transmission.

  2. Toxic dose. The concentration of toxin varies widely, depending on geographic and seasonal factors. The amount of toxin necessary to produce symptoms is unknown in most cases. An oral dose of 0.1 mcg of ciguatoxin can produce symptoms in a human adult. Saxitoxin is extremely potent; the estimated lethal dose in humans is 0.3–1 mg, and contaminated mussels may contain 15–20 mg. For many marine toxins (eg, ciguatoxin, tetrodotoxin), ingestion of the organs or viscera is associated with greater symptom severity than eating only the fillet.

  3. Clinical presentation. The onset of symptoms and clinical manifestations vary with each toxin (Table II–27). In the majority of cases, the seafood ...

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