Shellfish Poisoning

Shellfish Poisoning

Source

■■  Shellfish (especially oysters, clams, mussels, and scallops) contaminated by dinoflagellates. Other sources include univalve mollusks, starfish, limpets, sand crabs, whelks, turban shells, top shells, xanthid crabs and various fish.

Types

Paralytic Shellfish Poisoning

There are actually several paralytic shellfish toxins (PSP toxins). PSP toxins are a group of 21 structurally related neurotoxins, and are among the most common and deadly phycotoxins. The main toxin is saxitoxin which is produced by the following dinoflagellates (unicellular algae): Pyrodinium, Gymnodinium and Alexandrium.

Because dinoflagellates can occur in tropical and moderate climate zones, shellfish can accumulate these toxins worldwide. While the primary areas of poisoning have been the east and west coasts of the United States and Canada, the area around Japan, and the area from Southern Norway to Spain, of late, reports of paralytic shellfish poisoning (PSP) have been coming in from regions of the world where it had not been previously reported. In tropical regions, Pyrodinium bahamense var.compressa has been a source of PSP. These toxins affect thecentral nervous system and can produce muscular nerve block and paralysis. Paralytic shellfish poisoning is often associated with “red tide” blooms, but may occur with or without the red tide (Fig 33.18). These are natural phenomena triggered by a series of events, which can include human pollution. Over 300 phytoplankton species can produce red tides*, but only 60 to 70 species are actually harmful. Swimming in the “red tide” may produce pruritus and skin irritation

The incubation period is usually 30 minutes (occasionally can extend to 3 hours). There are 3 grades of severity:

·            Mild: Tingling and numbness of the tongue and lips, that soon spreads to the face, neck, arms, fingers and toes; headache and nausea. Diarrhoea may also occur. Moderate: Limb weakness, ataxia, incoherent speech, difficulty breathing, hypersalivation, and sweating.

·              Giddiness, rash, fever, tachycardia, hypertension, and dyspnoea can occur. Temporary blindness has been reported.

·              Severe: Muscle paralysis, “choking” sensation, severe respiratory difficulty, and respiratory failure.

Other effects:

o     Nystagmus, temporary blindness, iridoplegia, jaw and facial muscle incoordination, loss of gag reflex, immobilisation of the tongue, and difficulty speaking may occur after exposure.

o     Tachycardia, T wave changes, and occasionally hypertension or hypotension may occur following exposure.

o     Most patients remain conscious and alert, and reflexes are frequently normal throughout progres-sion of the illness. Muscle weakness may last for weeks. Patients who survive the first 12–24 hours generally have a good prognosis and recover without sequelae. Exposure to PSP toxins offer no immunity; in fact subsequent attacks can be more severe.

Diagnosis is by mouse bioassay or enzyme immunoassay. HPLC, liquid chromatography-mass spectrometry (LC-MS), immunoaffinity chromatography (IAC), and capillary elec- trophoresis have also been developed to evaluate seafood and environmental samples. Saxitoxin, the main toxin found in PSP, is heat and acid-stable, and does not alter the odour or taste of food. Cooking or freezing are not effective in destroying the toxin.

Treatment

·              In symptomatic patients, the following should be moni- tored closely: haemodynamic status, acid-base, serum electrolytes, BUN, creatinine, calcium, magnesium, phos- phorous, urine output, CPK, ECG, pulse oximetry, and cardiac rhythm.

·              Decontamination: Activated charcoal.

·              Since saxitoxin is excreted mainly via urine, diuresis can enhance renal excretion

·              Supportive measures: Most patients recover with supportive care alone. Monitor for respiratory depression. Patients with significant neurotoxicity may need endotracheal intubation and mechanical ventilation.

·              Because saxitoxin acts by blocking sodium channels, sodium bicarbonate may be effective in reversing ventric- ular conduction delays and arrhythmias, though this has not been proved: administer 1 to 2 mEq/kg sodium bicarbonate as a bolus, and repeat as necessary.

Neurotoxic Shellfish Poisoning

Neurotoxic shellfish poisoning results from eating shellfish (cockles, oysters, whelks, and clams) that have consumed the dinoflagellates containing brevetoxins. The main dinoflagellate involved is Ptychodiscus brevis (formerly called Gymnodiniumbreve). “Red tides” are caused by several non-protein, lipid-soluble, neurotoxins and haemolysins such as brevetoxins found in these dinoflagellates. Besides causing major fish kills, these toxins produce various ill effects in man and other shore animals.

Brevetoxins are heat stable, and are not destroyed by boiling or cooking. Unlike saxitoxin, they produce a stimulatory rather than a depressant nervous effect, and open the sodium channels in nerves, while saxitoxin closes them.

The incubation period is usually about 3 hours (range: 15 minutes to 18 hours). Main features include nausea, vomiting, diarrhoea, abdominal pain, rectal burning, paraesthesias of the face, throat, fingers, and toes, burning sensation of the mucous membranes, reversal of hot and cold temperature sensation, myalgia, vertigo, ataxia, headache, dysphagia, bradycardia, decreased reflexes, and mydriasis. Paralysis does not occur. Seizures are seen occasionally. Coughing, sneezing, and diffi-culty in breathing has occurred. Severe poisoning can cause respiratory arrest.

Diagnosis is by mouse bioassay, ELISA, or RIA. Treatment involves decontamination, administration of beta₂ adrenergic agonists and corticosteroids. In animal studies, 0.5 mg/kg of atropine reversed the bronchoconstrictive and bradycardic effects of brevetoxins.

Amnestic Shellfish Poisoning

The main toxin involved is domoic acid, produced by the diatom Nitzschia pungens. Incubation period is usually about 5 hours (range: 15 minutes to 38 hours). The main features include nausea, vomiting, diarrhoea, abdominal pain, amnesia, hemiparesis, grimacing, purposeless chewing, ophthalmo-plegia, convulsions, and coma. There may be unstable blood pressure with cardiac arrhythmias. In some patients, memory loss may persist for a long time. Diagnosis is by mouse bioassay or HPLC. Treatment involves supportive and symptomatic measures.