Overview of shellfish and pufferfish poisoning
- Erin N Marcus, MD, MPH, FACP
Erin N Marcus, MD, MPH, FACP
- Associate Professor of Clinical Medicine
- University of Miami Miller School of Medicine
- Section Editors
- Daniel F Danzl, MD
Daniel F Danzl, MD
- Section Editor — Environmental Emergencies
- Professor of Emergency Medicine
- University of Louisville School of Medicine
- Michele M Burns, MD, MPH
Michele M Burns, MD, MPH
- Section Editor — Pediatric Toxicology
- Assistant Professor of Pediatrics
- Harvard Medical School
- Stephen J Traub, MD
Stephen J Traub, MD
- Section Editor — Toxicology
- Associate Professor of Emergency Medicine
- Mayo Medical School
As world travel and trade grow, physicians are increasingly likely to encounter patients poisoned by marine toxins. The world's oceans harbor hundreds of different types of marine toxins, and the epidemiology and clinical manifestations of these toxins vary widely. Several of these toxins are produced by dinoflagellates or phytoplankton during algae or marine diatom blooms. Shellfish and pufferfish poisoning arise from consumption of seafood that is contaminated by various toxins (table 1) [1-3]. In most instances the ingested seafood smells, appears, and tastes normal. Clinical features of the most common forms of shellfish or pufferfish poisoning typically develop within minutes to hours of ingestion. A food history that identifies ingestion of seafood commonly associated with the specific toxin, clinical features consistent with the specific poisoning, and detection of elevated levels of the toxin in the ingested seafood provides the diagnosis. Treatment is supportive.
An overview of paralytic shellfish poisoning, neurotoxic shellfish poisoning, diarrheic shellfish poisoning, and pufferfish poisoning is provided here. Scombroid (histamine) poisoning, ciguatera fish poisoning and marine envenomations, such as coral abrasions and sea urchin injuries, are discussed separately. (See "Scombroid (histamine) poisoning" and "Ciguatera fish poisoning" and "Marine envenomations from corals, sea urchins, fish, or stingrays".)
PARALYTIC SHELLFISH POISONING
●Epidemiology – Paralytic shellfish poisoning (PSP) occurs after ingestion of shellfish contaminated with neurotoxins formed by algae, primarily saxitoxins . It has been linked to algal blooms called "red tides," even though it can occur in the absence of red tides. PSP primarily occurs in temperate climates, although it has been described in shellfish from tropical waters . Potential vectors for PSP include bivalve mollusks (eg, cockles, salt- and fresh-water mussels, or butter/little neck clams), gastropod mollusks (eg, whelk, moon snails, or abalone), crustaceans (eg, Dungeness crabs, shrimp, or lobsters), pufferfish (saxitoxin pufferfish poisoning), and zooplanktivorous fish (eg, Atlantic salmon, herring, and mackerel) [4,6]. Of these, outbreaks of human disease are most commonly associated with salt-water bivalve mollusks, especially mussels or clams.
PSP has been described worldwide . In the United States, PSP primarily occurs in seafood harvested from the Northeast, Pacific Northwest, and Alaskan waters . As an example, from 2010 to 2011, there was a marked increase in the number of PSP cases in southeast Alaska, all of which stemmed from the ingestion of non-commercially harvested shellfish (specifically, cockles, blue mussels, butter/little neck clams, and Dungeness crabs) . A subsequent CDC report noted that non-commercially-harvested Alaskan shellfish can have high levels of PSP toxin at any time of year . Clinicians were urged to report suspected cases to health officials and to collect and freeze patient urine and shellfish samples (if available) for testing. In contrast, commercial shellfish are routinely monitored for PSP toxin in Alaska and are safe to consume .
●Pathophysiology – The toxins that cause PSP are formed by dinoflagellates of the genus Alexandrium and are collectively known as saxitoxins [4,9,10]. These toxins are taken up by seafood vectors, most commonly, bivalve mollusks such as mussels, clams, scallops, and oysters, as well as by crabs and snails, with no apparent ill effect. The PSP toxins are not destroyed by heat, marinating, or freezing. Contaminated seafood smells, tastes, and appears normal.
●Clinical manifestations and diagnosis – In humans, the PSP toxins block sodium ion channels and rapidly cause neurologic symptoms ranging from perioral tingling, ataxia, difficulty swallowing, dizziness, paresthesias, weakness to paralysis, brainstem dysfunction, and respiratory failure [4,7,9]. Onset of symptoms ranges from a few minutes to approximately four hours. In untreated patients, the case fatality rate is as high as 12 percent , and death may occur within 2 to 12 hours of seafood ingestion of contaminated seafood. With proper supportive care, most patients survive. Neurotoxic symptoms tend to improve gradually after 12 hours and are resolve completely within a few days [4,9].
A working diagnosis of paralytic shellfish poisoning is made when there is a history of consumption of a known seafood vector of PSP followed by the onset of neurologic symptoms, including paralysis . Frequently ingestion of a noncommercial harvest of shellfish or crabs is noted and a cluster of cases is identified. The diagnosis is confirmed by the detection of saxitoxin in the urine of affected patients or samples of the seafood. The local health department should be contacted to assist with laboratory confirmation.
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