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Toxicity, Shellfish

Updated: Oct 29, 2009

Introduction

Background

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.

Pathophysiology

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 2008 Annual Report of the American Association of Poison Control Centers' National Poison Data System documented 752 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.

Clinical

History

All 4 shellfish syndromes can produce symptoms lasting from a few minutes to several hours after ingestion of contaminated shellfish.

Paralytic shellfish poisoning
- The onset generally is noted with paresthesias of the lips, tongue, and gums. Symptom onset usually occurs within 30 minutes of ingestion.
- Symptoms at onset rapidly progress to involve the distal extremities.
- Other symptoms include a sensation of floating, headache, ataxia, muscle weakness, paralysis, and cranial nerve dysfunction.
- Gastrointestinal symptoms are less common and may include nausea, vomiting, diarrhea, and abdominal pain. Fatalities are usually within the first 12 hours of symptom onset and are caused by unsupported respiratory failure.
- PSP usually lasts 3 days, but muscle weakness may persist for weeks.
Neurologic shellfish poisoning
- The illness encountered with NSP is milder than that with PSP. Symptom onset ranges from 15 minutes to 18 hours postingestion, and the duration of toxicity ranges from 1-72 hours (usually <24 h) postingestion.
- Presenting symptoms include gastroenteritis; rectal burning; paresthesias of the face, trunk, and limbs; myalgias; ataxia; vertigo; and reversal of hot/cold sensation.
- Other less common features include tremor, dysphagia, bradycardia, decreased reflexes, and mydriasis.
- This syndrome presents much like ciguatera poisoning but without a paralytic component, and it may last from several hours to a few days.
- The brevetoxins, unlike the other shellfish toxins, can become aerosolized by the surf and produce an allergic response characterized by rhinorrhea, conjunctivitis, bronchospasm, and cough in sensitive individuals along the shore.
Diarrheal shellfish poisoning
- DSP is most common in Japan and Europe.
- Gastroenteritis develops shortly after ingestion and generally lasts 1-2 days.
Amnestic shellfish poisoning
- The only reported outbreak occurred in 1987 and affected more than 100 people after eating mussels harvested off Prince Edward Island, Canada.
- Gastroenteritis followed by headache and short-term memory loss occurred.
- In a few cases, severe cognitive dysfunction to the point of interfering with the patient's ability to perform normal daily activities was noted.
- Seizures, coma, hemiparesis, and ophthalmoplegia were noted in the most severe cases. The mortality rate is 3%.

Physical

Findings vary according to the syndrome involved.
- Gastrointestinal symptoms occur less often in PSP than in the other syndromes.
- Paresthesias of the face and extremities are noted only in PSP and NSP.
- ASP is the only shellfish syndrome with cognitive dysfunction as an early finding.
Volume depletion from gastrointestinal symptoms is common to all syndromes.

Causes

Ingestion of raw or cooked mollusks that contain the toxin in sufficient quantities ensures the development of symptoms.

Differential Diagnoses

CBRNE - Botulism	Toxicity, Scombroid
Gastroenteritis	Toxicity, Tetrodotoxin
Toxicity, Ciguatera
Toxicity, Organophosphate and Carbamate
Toxicity, Phenytoin

Workup

Laboratory Studies

Direct human serum assays for shellfish toxins are not yet available to clinicians. Research in this area is ongoing, and a reliable assay for several of these specific toxins should be available soon.
Saxitoxin can be assayed by using a mouse bioassay, ELISA, and high-performance liquid chromatography (HPLC). Brevetoxin can be assayed by using a mouse bioassay, ELISA, and antibody radioimmunoassay (RIA). Liquid chromatography, mass spectrometry, and ELISA techniques have been developed for domoic acid.
A new assay was used to quantify saxitoxin and neosaxitoxin in human urine samples, with results suggesting that few false-positive outcomes would occur when attempting to identify people exposed to these toxins.⁵

Treatment

Prehospital Care

Support and maintenance of the airway are of crucial importance in PSP.

Emergency Department Care

Therapy for all shellfish poisonings is supportive and symptom-driven.
Gastrointestinal decontamination with activated charcoal is recommended for patients who present within 4 hours of ingestion. Nasogastric or orogastric lavage may be performed if the patient presents within 1 hour of ingestion, but this is often unnecessary.
If gastric lavage is performed, the use of isotonic sodium bicarbonate solution as a lavage irrigant has been suggested because many of the shellfish toxins have reduced potency in an alkaline environment.
Okadaic acid undergoes enterohepatic recycling that could be interrupted by delayed or repeat charcoal administration.
The greatest danger is respiratory paralysis. Close monitoring for at least 24 hours and aggressive airway management at any sign of respiratory compromise should prevent severe morbidity and mortality.
Neostigmine and edrophonium have been used to improve muscle weakness following tetrodotoxin intoxication, which is similar to saxitoxin intoxication. Nonetheless, no clinical trials have evaluated the use of these drugs for saxitoxin exposures.

Medication

Care is primarily symptomatic and supportive.

GI decontaminant

GI decontaminants are empirically used to minimize systemic absorption of the toxin. They may only be beneficial if administered within 1-2 h of ingestion.

Activated charcoal (Liqui-Char)

Emergency treatment in poisoning. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water. For maximum effect, administer within 30 min of ingesting poison.
Cathartic not to be used in children <2 y.

Dosing

Adult

1 g/kg (50-100 g) PO, with or without cathartic (eg, sorbitol)

Pediatric

1 g/kg (15-30 g) PO
<2 years: Cathartic not recommended

Interactions

May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decreases with coadministration; do not mix with sherbet, milk, or ice cream (decreases adsorptive properties)

Contraindications

Documented hypersensitivity; poisoning or overdose of mineral acids and alkalies; unprotected airway with absent gag reflex

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before administration; after emesis with ipecac syrup, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black; protect airway; monitor for bowel sounds before readministration to minimize risk of charcoal ileus

Follow-up

Deterrence/Prevention

Routine surveillance of shellfish beds for known toxins should prevent most forms of shellfish poisoning.
Consumption of shellfish harvested outside of regulated areas or during times known to be associated with red tide is dangerous and should be avoided.
The feasibility and effectiveness of degrading saxitoxins through chlorination is currently being investigated.⁶

Patient Education

For excellent patient education resources, visit eMedicine's Poisoning Center, Poisoning - First Aid and Emergency Center, and Wilderness Emergencies Center. Also, see eMedicine's patient education articles Wilderness: Shellfish Poisoning, Gastrointestinal, Wilderness: Shellfish Poisoning, Paralysis, Food Poisoning, and Activated Charcoal.

Miscellaneous

Medicolegal Pitfalls

Failure to adequately treat dehydration associated with gastroenteritis from shellfish poisoning
Failure to recognize subtle respiratory paralysis and provide airway support early in PSP syndromes
Failure to recognize shellfish poisoning as a potential etiology of a disease outbreak

Special Concerns

Shellfish gastroenteritis caused by viral agents is at epidemic proportions and, for many, has become an unacceptable risk associated with consumption of raw shellfish.
Callistin shellfish poisoning has been associated with the Japanese callista clam during spawning months of May to September. It causes a syndrome of cholinergic crisis with muscarinic and nicotinic symptoms.
Venerupin shellfish poisoning has been associated with 2 specific Japanese lake-harvested oysters and clams. From December through April, these mollusks occasionally feed on a toxic dinoflagellate that produces a potent hepatotoxin. This toxin has resulted in death from fulminant hepatic failure in 33% of cases to date.

References

Burgess V, Shaw G. Pectenotoxins--an issue for public health: a review of their comparative toxicology and metabolism. Environ Int. Oct 2001;27(4):275-83. [Medline].
Lefebvre KA, Robertson A. Domoic acid and human exposure risks: A review. Toxicon. Jun 6 2009;[Medline].
Centers for Disease Control and Prevention. Update: Neurologic illness associated with eating Florida pufferfish, 2002. MMWR Morb Mortal Wkly Rep. May 17 2002;51(19):414-6. [Medline].
Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057. [Medline]. [Full Text].
Johnson RC, Zhou Y, Statler K, Thomas J, Cox F, Hall S, et al. Quantification of saxitoxin and neosaxitoxin in human urine utilizing isotope dilution tandem mass spectrometry. J Anal Toxicol. Jan-Feb 2009;33(1):8-14. [Medline].
Nicholson BC, Shaw GR, Morrall J, Senogles PJ, Woods TA, Papageorgiou J, et al. Chlorination for degrading saxitoxins (paralytic shellfish poisons) in water. Environ Technol. Nov 2003;24(11):1341-8. [Medline].
Ahmed FE. Seafood safety. Committee on Evaluation of the Safety of Fishery Products. Food & Nutrition Board, Institute of Medicine. National Academy Press; 1991.
Chandrasekaran A, Ponnambalam G, Kaur C. Domoic acid-induced neurotoxicity in the hippocampus of adult rats. Neurotox Res. 2004;6(2):105-17. [Medline].
Economou V, Papadopoulou C, Brett M, Kansouzidou A, Charalabopoulos K, Filioussis G, et al. Diarrheic shellfish poisoning due to toxic mussel consumption: the first recorded outbreak in Greece. Food Addit Contam. Mar 2007;24(3):297-305. [Medline].
Gessner BD, Middaugh JP, Doucette GJ. Paralytic shellfish poisoning in Kodiak, Alaska. West J Med. Nov 1997;167(5):351-3. [Medline].
Jeffery B, Barlow T, Moizer K, Paul S, Boyle C. Amnesic shellfish poison. Food Chem Toxicol. Apr 2004;42(4):545-57. [Medline].
Kawatsu K, Hamano Y, Noguchi T. Production and characterization of a monoclonal antibody against domoic acid and its application to enzyme immunoassay. Toxicon. Nov 1999;37(11):1579-89. [Medline].
Poli MA, Musser SM, Dickey RW, Eilers PP, Hall S. Neurotoxic shellfish poisoning and brevetoxin metabolites: a case study from Florida. Toxicon. Jul 2000;38(7):981-93. [Medline].
Stommel EW, Watters MR. Marine Neurotoxins: Ingestible Toxins. Curr Treat Options Neurol. Mar 2004;6(2):105-114. [Medline].
Usleber E, Dietrich R, Burk C, Schneider E, Martlbauer E. Immunoassay methods for paralytic shellfish poisoning toxins. J AOAC Int. Sep-Oct 2001;84(5):1649-56. [Medline].
Vale P, Sampayo MA. Comparison between HPLC and a commercial immunoassay kit for detection of okadaic acid and esters in Portuguese bivalves. Toxicon. Nov 1999;37(11):1565-77. [Medline].
Van Dolah FM. Marine algal toxins: origins, health effects, and their increased occurrence. Environ Health Perspect. Mar 2000;108 Suppl 1:133-41. [Medline].

Keywords

paralytic shellfish poisoning, PSP, neurologic shellfish poisoning, NSP, diarrheal shellfish poisoning, DSP, amnestic shellfish poisoning, ASP, brevetoxin, brevotoxin, shellfish toxicity, shellfish poisoning, shellfish exposure, shellfish ingestion, hepatitis A, Norwalk virus, Vibrio parahaemolyticus, Vibrio vulnificus, toxic shellfish, saxitoxin, okadaic acid, domoic acid

Contributor Information and Disclosures

Author

Thomas Arnold, MD, Medical Director, Louisiana Poison Control Center, Associate Professor and Chairman, Department of Emergency Medicine, Section of Clinical Toxicology, Louisiana State University Health Sciences Center
Thomas Arnold, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Louisiana State Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert L Norris, MD, Associate Professor, Department of Surgery; Chief, Division of Emergency Medicine, Stanford University Medical Center
Robert L Norris, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, California Medical Association, International Society of Toxinology, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Michael J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center
Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

Further Reading