Sickness from the Sea: A Panoply of Seafood Intoxications
August 1, 1998 6 minutes read
Sickness from the Sea: A Panoply of Seafood Intoxications
ABSTRACT & COMMENTARY
Synopsis: An outbreak of diarrhetic shellfish poisoning, one of a variety of intoxications resulting from ingestion of seafood, is described.
Source: Scoging A, Bahl M. Diarrhetic shellfish poisoning in the UK. Lancet 1998;352:117.
Forty-nine patients developed nausea, vomiting, diarrhea, abdominal pain, and a feverish feeling within 30 minutes of eating mussels (or, in one case, mussel soup) in one of two London restaurants. The symptoms lasted more than eight hours before spontaneous resolution.
Samples of mussels from the restaurants were positive in a mouse bioassay for diarrheic shellfish poisoning toxin, and high-pressure liquid chromatography was used to identify it as okadaic acid.
COMMENT BY STAN DERESINSKI, MD, FACP
Seafood, especially shellfish, are a common source of human illness throughout the world. Seafood were the third most common source of foodborne disease outbreaks between 1983 and 1992 in the United States.1 In addition to illnesses caused by the transmission via seafood of infectious agents, such as parasites, hepatitis A virus, and Vibrio parahaemolyticus, many illnesses are due to the ingestion of pre-formed toxins. (See Table.)
The most frightening of these intoxications is the often rapidly lethal paralytic syndrome associated with ingestion of improperly prepared pufferfish containing tetrodotoxin, a compound which appears to be a product of bacterial metabolism. While this disease predominantly occurs in Japan, cases have been observed on all continents as the result of ingestion of either locally caught or imported fish. Three cases occurred in California in 1996 after ingestion of fugu brought from Japan.2 Fatal tetrodotoxin poisoning has also occurred as the result of ingestion of newts.3
Scombroid fish poisoning is the result of ingestion of scombroid fish containing high concentrations of histamine as the result of histidine decarboxylation by contaminating bacteria, including Morganella morganii, Klebsiella oxytoca, Pleisomonas shigelloides, halophilic Vibrio spp., and others.1-4 The most commonly affected fish are skipjack, bonito and yellowfin tuna, mahi mahi, bluefish, mackerel, sardines, and amberjack. The symptoms resemble an acute allergic reaction and the severity is directly related to the amount of histamine ingested.5
Ciguatera seafood poisoning is the result of the consumption of subtropical and tropical marine fin fish containing ciguatoxin, which has accumulated as a result of ingestion of dinoflagellates clustered around deep coral reefs. The most commonly implicated fish are barracuda, grouper, snapper, mackerel, and triggerfish. A small outbreak occurred in U.S. soldiers in Haiti in 1995 after eating amberjack.6 The first symptom is usually perioral paresthesia, followed by gastrointestinal symptoms, paresthesias of the extremities, and muscular weakness. Severe cases may cause cardiovascular collapse and, occasionally, death. Perhaps the most intriguing symptom is a reversal of temperature sensation.
All the intoxications due to shellfish ingestion are the result of toxins that accumulate as the result of their filter feeding on affected dinoflagellates. Blooms of these toxic organisms may be increasing as the result of eutrophication of coastal waters. In 1987, neurotoxic shellfish poisoning was identified in 48 individuals and was attributed to ingestion of local oysters after the North Carolina coast was affected by a red tide due to P. brevis.7 The symptoms of this illness, caused by the polyether toxin, brevetoxin, are similar to those of ciguatera seafood poisoning but are usually mild and of relatively short duration. Paralytic shellfish poisoning, resulting from ingestion of saxitoxin, is associated with paresthesias, drowsiness, incoherent speech, and respiratory paralysis.
Amnesic shellfish poisoning is caused by ingestion of domoic acid, which acts as an excitatory neurotransmitter, and is associated with vomiting, diarrhea, and abdominal pain, as well as confusion, short-term memory loss, seizures, and coma. An outbreak involving 156 cases resulted from ingestion of cultured blue mussels harvested off Prince Edward island; three patients, all elderly, died.8 PET scans reveal marked reduction of hippocampal glucose metabolism.9 Some patients are left with chronic residual memory deficits and motor neuronopathy or axonopathy.10
Diarrhetic shellfish poisoning is caused by ingestion of shellfish containing phycotoxins that they have accumulated as the result of their concentration of the marine dinoflagellates, Dinophysis and Prorocentrum. The most prominent of the implicated phycotoxins are a group of Dinophysis toxins and okadaic acid, the toxin implicated in the outbreak described above.11 Okadaic acid, which inhibits cellular protein phosphatases, increases the paracellular permeability of intestinal epithelia.12 Diarrhetic shellfish poisoning is predominantly found in Europe and Japan, but has also affected individuals in Australia, Indonesia, New Zealand, and both Americas. Okadaic acid, as well as domoic acid, has been detected in Gulf of Mexico shellfish and phytoplankton.13
Table
Common Types of Seafood Poisoning
Shellfish Poisoning |
Toxin |
Symptoms |
Common Shellfish Source |
Onset/Duration |
Neurotoxic |
Brevetoxins |
Paresthesias and numbness of lips, tongue, throat; myalgia, dizziness, temperature sensation reversal, vomiting |
Mussels, clams, cockles, scallops |
Minutes to hours/ Few hours to several days |
Paralytic |
Saxitoxin |
Dysphagea, paresthesias, drowsiness, paralysis |
Mussels, clams, cockles, scallops |
30-120 minutes/ Potentially fatal |
Diarrhetic |
Okadaic acid and dinophysis toxins, yessotoxin |
Nausea, vomiting, diarrhea, abdominal pain, fever |
Mussels, oysters, scallops |
30-180 minutes/2-3 days |
Amnesic |
Domoic acid |
Vomiting, diarrhea, abdominal pain, confusion, short-term memory loss, disorientation, seizure, coma |
Mussels |
GI within 24 hours; Neuro within 48 hours/Variable |
Red Whelk |
Tetramine (tetramethyl ammonium hydroxide) |
Vomiting, diarrhea or constipation, dizziness, mouth dryness, paralysis |
Red Whelk |
One to several hours |
Fish Poisoning |
Toxin/Metabolite |
Symptoms |
Common Fish Source |
Onset/Duration |
Scombroid |
Histamine |
Paresthesias of mouth, flushing, nausea, vomiting, urticaria, bronchospasm |
Tunas, mackerel, mahi mahi, bluefish, sardines, amberjack, abalone |
Immediate to30 minutes |
Ciguatera |
Ciguatoxin |
Perioral paresthesias spreading to extremities, nausea, vomiting, diarrhea, temperature sensory reversal, hypotension |
Groupers, barracuda, snapper, jack, mackerel, triggerfish, amberjack |
Within 6 hours/ Days to many months(may be fatal) |
Pufferfish (Fugu) |
Tetrodotoxin |
Lip and tongue numbness, paresthesias of face and extremities, vomiting, paralysis |
Pufferfish gonads, liver, intestines, skin |
20-180 minutes/ Death within4-6 hours in up to 50% |
Thus, the variety of intoxications associated with eating seafood are broad and the symptoms produced, which are determined by both the specific toxin and the amount ingested, often overlap. The situation can be even more confusing since outbreaks may be due to ingestion of combinations of toxins.14 In addition, there are additional types of intoxications reported, such as "red whelk poisoning."15 Some intoxications tend to be more prevalent within certain geographic areas. For example, paralytic shellfish poisoning and amnesic shellfish poisoning, as well as "red whelk poisoning," occur in Europe, while paralytic shellfish poisoning, neurotoxic shellfish poisoning, and amnesic shellfish poisoning occur in North America. However, climatic changes resulting in toxic algal blooms have the potential to alter these patterns. Furthermore, seafood is now transported throughout the world, erasing any remaining geographic confinement of these intoxications.
References
1. Lipp EK, Rose JB. Rev Sci Tech 1997;16:620-640.
2. MMWR Morb Mortal Wkly Rep 1996;45:389-390.
3. Bradley SG, Klika LJ. JAMA 1981;246:247.
4. Lopez-Sabater EI, et al. Int J Food Microbiol 1996; 28:411-418.
5. Morrow JD. N Engl J Med 1991;324:716-720.
6. Poli MA, et al. Toxicon 1997;35:733-741.
7. Morris PD, et al. Am J Public Health 1991;81:471-474.
8. Perl TM, et al. N Engl J Med 1990;322:1775-1780.
9. Gjedde A, et al. Can Dis Wkly Rep 1990;16(Suppl 1E):105-109.
10. Teitelbaum JS, et al. N Engl J Med 1990;322: 1781-1787.
11. PHLS. Comm Dis Rep Wkly 1997;7:1.
12. Tripuraneni J, et al. Gastroenterology 1997;112: 100-108.
13. Dickey RW, et al. Toxicon 1992;30:355-359.
14. Gago-Martinez A, et al. Nat Toxins 1996;4:72-79.
15. Fleming C. Brit Med J 1971;3:520-521.
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