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Shellfish poisoning

Shellfish poisoning refers to a group of acute foodborne illnesses resulting from the ingestion of molluscan shellfish, such as clams, mussels, oysters, and scallops, contaminated with potent marine biotoxins produced by certain marine microalgae during harmful algal blooms (HABs). Cases are often underreported due to mild symptoms or misdiagnosis.^[1] The primary syndromes include paralytic shellfish poisoning (PSP), neurotoxic shellfish poisoning (NSP), amnesic shellfish poisoning (ASP), diarrhetic shellfish poisoning (DSP), and azaspiracid shellfish poisoning (AZP), each caused by distinct toxins that accumulate in filter-feeding bivalves without being degraded by cooking or freezing.^[2] These conditions are reported worldwide, particularly in coastal regions prone to algal proliferation influenced by factors like nutrient runoff and warmer waters, with the United States documenting cases along both Atlantic and Pacific coasts as well as the Gulf of Mexico.^[1] The toxins responsible originate from microscopic algae, including dinoflagellates and diatoms, which form dense blooms under favorable environmental conditions and release heat-stable biotoxins that shellfish ingest while filtering seawater.^[2] For instance, PSP is induced by saxitoxins from dinoflagellates like Alexandrium species, NSP by brevetoxins from Karenia brevis, ASP by domoic acid from Pseudo-nitzschia diatoms, DSP by okadaic acid from dinoflagellates such as Dinophysis, and AZP by azaspiracids from Azadinium species.^[1] These toxins target the nervous system, gastrointestinal tract, or both, with no specific antidotes available; treatment relies on supportive measures like hydration, respiratory assistance, and symptom management.^[2] Symptoms typically onset rapidly—within minutes to hours after consumption—and vary by toxin type, ranging from mild gastrointestinal upset to severe neurological effects.^[1] PSP often presents with tingling around the mouth, nausea, paralysis, and potential respiratory failure, which can be fatal without prompt intervention; NSP causes similar tingling, dizziness, and ataxia alongside vomiting and diarrhea; ASP leads to vomiting, confusion, memory loss, and seizures; DSP primarily involves diarrhea, abdominal cramps, and nausea; while AZP manifests as prolonged vomiting and bloody diarrhea.^[2] Although most cases resolve within days, severe ASP or PSP can result in permanent neurological damage or death, with global incidence tied to seasonal blooms and affecting thousands annually.^[1] Prevention centers on regulatory monitoring of shellfish harvesting areas, where authorities test for toxins and issue closures during blooms, alongside consumer advisories to check harvest tags and avoid wild shellfish from unverified sources.^[2] International standards, such as those from the Codex Alimentarius, guide safe toxin levels (e.g., 800 micrograms of saxitoxin per 100 grams of shellfish meat for PSP), and programs like the U.S. National Shellfish Sanitation Program ensure compliance through sanitation and traceability.^[1] Climate change may exacerbate HAB frequency, underscoring the need for ongoing surveillance to mitigate risks.^[2]

Overview

Definition and Scope

Shellfish poisoning encompasses a range of acute intoxications resulting from the consumption of bivalve mollusks, such as clams, oysters, and mussels, and certain crustaceans contaminated with biotoxins produced by harmful algal blooms in marine environments. These filter-feeding shellfish accumulate neurotoxins and other algal-derived biotoxins, like saxitoxins, without being harmed themselves, leading to potentially severe human illness upon ingestion.^[1]^[2]^[3] The condition's scope includes five main syndromes—paralytic shellfish poisoning (PSP), neurotoxic shellfish poisoning (NSP), amnesic shellfish poisoning (ASP), diarrhetic shellfish poisoning (DSP), and azaspiracid shellfish poisoning (AZP)—each linked to distinct toxin groups from dinoflagellates, diatoms, or other phytoplankton.^[1] It primarily impacts humans via oral exposure to contaminated seafood from coastal and brackish waters, with global occurrences concentrated in temperate and tropical regions prone to algal proliferation, such as the U.S. coasts, Gulf of Mexico, Europe, and parts of Asia. Not all shellfish are equally affected; filter-feeders like bivalves concentrate toxins more readily than non-filtering species, heightening risks during seasonal blooms.^[1]^[2]^[4] Those most vulnerable are locals and tourists in endemic coastal areas who harvest or consume recreationally gathered shellfish, as commercial monitoring may not cover all sources. No immunity develops from prior exposures, since the diverse toxin profiles vary by bloom event, allowing subsequent incidents to occur without diminished severity.^[3]^[5]^[6]

Historical Context

Early accounts of phenomena potentially linked to shellfish poisoning date back to ancient times, with biblical references in the Book of Exodus describing the Nile River turning to blood around 2000 BCE, which some scholars interpret as a possible red tide event causing fish kills and toxic conditions.^[7] Ancient Greeks similarly named the Red Sea for its reddish hue during seasonal algal blooms, documented as early as the classical period and associated with toxic marine events over millennia.^[8] By the 18th century, European explorers encountered suggestive cases; in 1793, members of Captain George Vancouver's crew in British Columbia suffered severe illness and one death after consuming mussels, marking one of the earliest recorded instances of paralytic shellfish poisoning (PSP) symptoms in a European-linked context.^[9] The 20th century brought more systematic recognition through major outbreaks on the U.S. Pacific Coast. In 1927, a significant PSP incident near San Francisco affected multiple individuals, leading to six deaths and prompting the first formal identification of the syndrome as a public health threat. This event spurred research that culminated in the 1930s with the isolation of saxitoxin, the primary neurotoxin responsible for PSP, by Hermann Sommer and colleagues from toxic Alaskan butter clams, enabling the development of the first mouse bioassay for toxin detection.^[10] Regulatory and scientific progress accelerated in subsequent decades. The U.S. Food and Drug Administration (FDA) expanded its National Shellfish Sanitation Program in the 1970s to include enhanced biotoxin monitoring, building on earlier frameworks to routinely test shellfish for toxins like saxitoxin amid rising awareness of harmful algal blooms (HABs).^[11] A pivotal outbreak in 1987 on Prince Edward Island, Canada, involving contaminated mussels, resulted in three deaths and over 100 cases of amnesic shellfish poisoning (ASP), the first recognized instance of this syndrome caused by domoic acid.^[8] The 2000s saw global advancements in HAB research, including the launch of the GEOHAB program by UNESCO-IOC in 2001, which integrated multidisciplinary studies to better predict and mitigate toxin-producing algal proliferations affecting shellfish worldwide.^[12]

Causes and Mechanisms

Marine Toxins Involved

Shellfish poisoning arises from the ingestion of marine biotoxins produced by certain phytoplankton during harmful algal blooms (HABs), which accumulate in filter-feeding bivalves such as clams, mussels, oysters, and scallops. These biotoxins are not metabolized or degraded by the shellfish, leading to their bioaccumulation and persistence in tissues for extended periods, sometimes months to years, thereby posing risks to human consumers. The primary toxins responsible include saxitoxins, brevetoxins, domoic acid, okadaic acid, and azaspiracids, each originating from specific marine microorganisms and exerting distinct physiological effects through disruption of cellular processes.^[2]^[13] Saxitoxins, a group of over 20 carbamate alkaloids, are potent neurotoxins produced primarily by dinoflagellates of the genus Alexandrium species during HABs. These water-soluble toxins bind to voltage-gated sodium channels in nerve cells, blocking sodium ion influx and thereby preventing nerve impulse transmission, which can lead to rapid onset of paralysis in affected organisms. Variants such as saxitoxin (STX), neosaxitoxin, and gonyautoxins differ in carbamoyl groups and toxicity levels, with STX being the most potent.^[2]^[14]^[15] Brevetoxins, lipid-soluble polyether compounds, are generated by the dinoflagellate Karenia brevis, commonly associated with red tides in regions like the Gulf of Mexico. Unlike saxitoxins, brevetoxins bind to site 5 on voltage-gated sodium channels, causing persistent channel opening and uncontrolled sodium influx, which results in membrane depolarization, repetitive nerve firing, and neuromuscular dysfunction. This mechanism underlies neurotoxic effects, with toxins such as PbTx-1 and PbTx-2 varying in ladder-like polycyclic structures that enhance their lipophilicity and cellular penetration.^[2]^[16]^[13] Domoic acid, a water-soluble amino acid analog of the neurotransmitter glutamate, is synthesized by diatoms of the genus Pseudo-nitzschia during nutrient-rich HABs, particularly along coastal upwelling zones. It acts as an excitotoxin by mimicking glutamate and overstimulating kainate and AMPA receptors, leading to excessive calcium influx, neuronal depolarization, and selective damage to hippocampal and amygdala regions, potentially causing long-term neurological impairment. Shellfish like razor clams and Dungeness crabs can retain high levels of domoic acid in viscera.^[2]^[17]^[13] Okadaic acid, along with related dinophysistoxins, comprises lipophilic polyether fatty acids produced by dinoflagellates such as Dinophysis and Prorocentrum species in temperate and subtropical waters. These toxins inhibit serine/threonine protein phosphatases (PP1 and PP2A), disrupting cellular signaling pathways, promoting hyperphosphorylation of proteins, and altering intestinal epithelial integrity, which contributes to fluid secretion and gastrointestinal effects. Unlike the neurotoxins, okadaic acid's action is primarily enteric, with no significant neural targeting.^[2]^[18]^[13] Azaspiracids, lipophilic polyether toxins, are produced by dinoflagellates of the genus Azadinium during HABs. They accumulate in bivalve shellfish and cause severe gastrointestinal illness, with mechanisms not fully elucidated but involving disruption of cytoskeletal structures, tight junction alterations in intestinal epithelium, and potential modulation of ion channels such as chloride channels, leading to fluid accumulation and mucosal damage.^[2]^[19] These toxins are released into the marine environment during HABs triggered by factors like eutrophication, temperature shifts, and ocean currents, allowing dinoflagellates and diatoms to proliferate and contaminate shellfish vectors. Bivalves filter large volumes of water, concentrating the indigestible toxins in their digestive glands without detoxification, facilitating transfer to humans via consumption. Monitoring programs by agencies like the FDA enforce regulatory limits to mitigate risks.^[2]^[20]^[21]

Sources in Shellfish

Shellfish poisoning primarily arises from the accumulation of marine toxins produced by harmful algal blooms (HABs), which are driven by environmental factors such as nutrient runoff from agricultural and urban sources, warming ocean temperatures, and coastal upwelling that brings nutrient-rich deep waters to the surface.^[22]^[23]^[24] These conditions promote rapid proliferation of toxin-producing phytoplankton, like dinoflagellates that release saxitoxins during bloom peaks, often in late summer or fall when water temperatures exceed 15–20°C.^[25] Toxin release intensifies as blooms decay or under stress from light and salinity changes, leading to elevated concentrations in surrounding waters that shellfish can ingest.^[26] The biology of shellfish, particularly filter-feeding bivalves such as mussels, clams, and oysters, facilitates toxin uptake as they strain large volumes of seawater—up to 50 liters per day for a single mussel—to capture planktonic food.^[27] These toxins, including saxitoxins, accumulate primarily in the digestive glands and viscera, where they bind to tissues and resist metabolism, with retention periods lasting weeks to months post-bloom; for instance, butter clams can hold paralytic toxins for up to a year.^[28] In contrast, non-bivalve shellfish like crabs and lobsters accumulate toxins mainly in their viscera rather than muscle meat, making the latter generally safer if properly eviscerated, though overall risk is lower due to their predatory or scavenging habits rather than direct filter-feeding.^[29]^[30] Depuration occurs slowly through excretion and growth dilution, varying by species, temperature, and toxin type, but bivalves often remain contaminated long after blooms dissipate.^[31]^[32] Geographic hotspots for toxin accumulation in shellfish cluster in temperate coastal regions, including the U.S. Northeast (e.g., Gulf of Maine), where paralytic toxins frequently contaminate bivalves due to recurrent Alexandrium blooms; northwestern Europe, with high diarrhetic toxin incidents in areas like Scandinavia and the UK; and Japan, particularly along the Pacific coast, known for seasonal saxitoxin outbreaks.^[16] Climate change exacerbates these risks by extending warm seasons, intensifying nutrient delivery via heavier rainfall, and shifting bloom distributions poleward, leading to more frequent and widespread HAB events in these areas.^[33]^[34]

Types of Poisoning

Paralytic Shellfish Poisoning

Paralytic shellfish poisoning (PSP) is caused by the ingestion of saxitoxins, a group of potent neurotoxins produced by certain marine dinoflagellates such as Alexandrium species, which accumulate in filter-feeding bivalve shellfish like mussels, clams, and oysters.^[13] These toxins include saxitoxin itself and over 50 derivatives, all of which are water-soluble and heat-stable, rendering standard cooking, freezing, or steaming ineffective at destroying them.^[35] In brief, saxitoxins exert their paralytic effects by blocking voltage-gated sodium channels in nerve cells, preventing nerve impulse transmission.^[3] PSP exposure is most prevalent in temperate and cold waters, particularly along the Pacific coast of North America including Alaska, and in Scandinavian regions like Norway and Sweden where algal blooms periodically contaminate local shellfish harvests.^[13]^[36] Symptoms typically onset within 30 minutes to 3 hours after consuming contaminated shellfish, progressing from perioral tingling and numbness to more severe neurological effects such as muscle weakness, ataxia, and dysphagia.^[32] A lethal dose can be as low as 0.5 mg of saxitoxin for an average adult, highlighting the toxin's extreme potency.^[37] Severe PSP cases pose unique risks, including respiratory failure due to diaphragmatic paralysis, which can lead to death within 2 to 12 hours if untreated, necessitating mechanical ventilation in critical scenarios.^[3] Recreational harvesters face higher incidence rates, as evidenced by outbreaks in Alaska where non-commercial gathering from unmonitored areas has accounted for the majority of reported illnesses.^[38]

Neurotoxic Shellfish Poisoning

Neurotoxic shellfish poisoning (NSP) is a syndrome caused by the consumption of shellfish contaminated with brevetoxins, a group of potent lipid-soluble polyether neurotoxins produced by the dinoflagellate Karenia brevis.^[16] These toxins primarily include two structural classes: type A brevetoxins (e.g., PbTx-1) and type B brevetoxins (e.g., PbTx-2), which accumulate in filter-feeding bivalve mollusks such as oysters, clams, and mussels during harmful algal blooms known as red tides.^[16] Brevetoxins bind to and activate voltage-gated sodium channels in nerve and muscle cells, leading to persistent sodium influx, membrane depolarization, and disruption of normal neurological function.^[39] NSP is endemic to subtropical and tropical regions, particularly the Gulf of Mexico coastal areas of the United States (including Florida and Texas) and New Zealand, where K. brevis blooms occur seasonally.^[16] Outbreaks are relatively rare due to rigorous monitoring and harvest closures by regulatory agencies, but notable incidents include a 1987 event in North Carolina affecting 48 individuals and a 1992–1993 outbreak in New Zealand impacting over 180 people.^[16] In the U.S., cases are most commonly associated with recreational shellfish harvesting during red tides, while commercial shellfish are subject to strict controls under the National Shellfish Sanitation Program.^[2] A distinctive feature of NSP is the potential for pre-ingestional exposure through aerosolized brevetoxins generated by wave action on beachfronts during blooms, which can cause respiratory irritation including coughing, sneezing, and eye/throat discomfort even without consuming shellfish.^[40] Symptoms from ingestion typically onset within 30 minutes to 3 hours and include gastrointestinal effects such as nausea, vomiting, and diarrhea, alongside neurological manifestations like paresthesias of the lips, tongue, and extremities, reversal of hot and cold sensations, dizziness, ataxia, and muscle aches.^[41] The syndrome is self-limiting, with symptoms generally resolving within 48 hours to 3 days without long-term sequelae, and no fatalities have been reported.^[16] However, aerosol exposure or ingestion can severely exacerbate symptoms in individuals with asthma, leading to bronchoconstriction, reduced pulmonary function, and increased emergency room visits during blooms.^[41]

Amnesic Shellfish Poisoning

Amnesic shellfish poisoning (ASP) is a neurotoxic syndrome resulting from the consumption of contaminated bivalve shellfish that have accumulated domoic acid, a water-soluble amino acid produced by certain diatoms of the genus Pseudo-nitzschia.^[1] Domoic acid structurally resembles the neurotransmitter glutamate and acts as a potent agonist at kainate and AMPA subtypes of ionotropic glutamate receptors, leading to excessive neuronal excitation and subsequent hippocampal damage through excitotoxicity.^[17] This selective vulnerability of the hippocampus underlies the syndrome's hallmark amnestic features.^[42] ASP was first identified during a major outbreak in late 1987 on Prince Edward Island, Canada, where more than 100 individuals fell ill after consuming cultured blue mussels (Mytilus edulis) contaminated with high levels of domoic acid, resulting in three deaths and numerous cases of acute gastrointestinal and neurological symptoms followed by chronic sequelae.^[43] In this event, affected patients exhibited permanent anterograde amnesia, with memory deficits persisting for years or even indefinitely in some survivors, particularly those who consumed larger quantities of toxin.^[42] The toxin's identification as the causative agent marked the discovery of ASP as a distinct clinical entity, distinct from other shellfish poisonings due to its enduring neurotoxic effects.^[44] Unlike acute syndromes, ASP disproportionately affects elderly and vulnerable populations, with advanced age correlating to more severe neurotoxicity even at moderate exposure doses, as older individuals exhibit heightened sensitivity to domoic acid's disruptive effects on cognitive function.^[45] Repeated low-dose exposures, such as through chronic consumption of subtly contaminated shellfish like razor clams, can accumulate to produce subtle but measurable cognitive impairments, including difficulties with everyday memory tasks, without overt acute illness.^[46] Beyond human health, domoic acid intoxication has been linked to mass mortality events in wildlife, including seizures, disorientation, and death in marine mammals such as California sea lions (Zalophus californianus) and seabirds like brown pelicans (Pelecanus occidentalis), where bioaccumulation in prey leads to widespread ecological impacts during harmful algal blooms.^[47] These incidents underscore the toxin's broad neurotoxic potential across species, with hippocampal and related brain region damage observed in affected animals.^[48]

Diarrhetic Shellfish Poisoning

Diarrhetic shellfish poisoning (DSP) is a gastrointestinal illness resulting from the ingestion of contaminated bivalve mollusks, such as mussels and scallops, that have accumulated lipophilic toxins produced by marine dinoflagellates of the genera Dinophysis and Prorocentrum. The primary toxins responsible are okadaic acid (OA) and its derivatives, including dinophysistoxins-1 (DTX-1) and dinophysistoxins-2 (DTX-2), which belong to the okadaic acid group and are potent inhibitors of protein phosphatases 1 and 2A.^[13]^[49] These toxins disrupt cellular signaling in the intestinal epithelium, leading to increased permeability and fluid secretion, which manifests as profuse diarrhea.^[18] Symptoms of DSP typically include abdominal pain, nausea, vomiting, and non-bloody diarrhea, with chills and headache occasionally reported; the onset occurs 30 minutes to 6 hours after consumption, and the condition is self-limiting, resolving within 1 to 3 days without specific treatment.^[50]^[13] DSP is the most prevalent form of shellfish poisoning worldwide, with frequent outbreaks in temperate regions such as Europe and Japan, where monitoring has identified it as a leading marine biotoxin syndrome.^[50]^[51] No fatalities have been documented, reflecting the toxin's low lethality and primarily acute gastrointestinal effects.^[13] A distinctive feature of DSP is its frequent co-occurrence with other shellfish toxins in contaminated bivalves, as dinoflagellate blooms often produce multiple biotoxin groups simultaneously, complicating attribution in outbreaks.^[49] Additionally, DSP is often underreported and underdiagnosed due to its flu-like symptoms mimicking common viral gastroenteritis, leading to potential underestimation of its public health impact.^[52]

Azaspiracid Shellfish Poisoning

Azaspiracid shellfish poisoning (AZP) is a gastrointestinal syndrome caused by ingestion of shellfish contaminated with azaspiracids, a group of lipophilic polyether toxins produced by small dinoflagellates of the genus Azadinium, which accumulate in filter-feeding bivalves such as mussels.^[53]^[19] These toxins are heat-stable and target the gastrointestinal tract, though their precise mechanism remains under investigation, potentially involving disruption of cellular fluid balance similar to other diarrheic toxins.^[54] AZP was first recognized in 1995 during an outbreak in Ireland, where consumption of contaminated mussels led to symptoms in several individuals, initially misattributed to diarrhetic shellfish poisoning due to overlapping features.^[54] Since then, cases have been reported primarily in Europe (e.g., Ireland, Norway, Scotland), with emerging detections in other regions including Morocco, Chile, and Australia as of 2020.^[55] Symptoms typically onset within 30 minutes to a few hours and include nausea, vomiting, severe watery diarrhea, and abdominal cramps, often lasting 2-3 days but occasionally persisting for weeks; neurological symptoms are rare, and no fatalities have been recorded.^[53]^[56] The syndrome is generally mild and self-limiting, with treatment focused on hydration, but its increasing global detection highlights the need for expanded monitoring, as azaspiracids can co-occur with other toxins in blooms.^[13]

Clinical Presentation

General Symptoms

Shellfish poisoning presents with overlapping gastrointestinal and neurological symptoms shared across toxin-induced syndromes. Gastrointestinal manifestations commonly include nausea, vomiting, diarrhea, and abdominal pain, which can lead to significant fluid loss.^[3] Neurological features often begin with paresthesias, such as tingling or numbness in the lips, tongue, and mouth, potentially extending to the face, neck, and extremities, accompanied by dizziness and headache.^[13] These symptoms reflect the neurotoxic and irritant effects of marine biotoxins accumulated in shellfish.^[52] The timeline for symptom onset varies from as little as 15–30 minutes to up to 18 hours post-ingestion, depending on the specific toxin and individual factors.^[3] Duration typically ranges from several hours in acute presentations, such as those seen in paralytic shellfish poisoning (PSP), to days or even chronic neurological sequelae in cases like amnesic shellfish poisoning (ASP).^[13] For instance, gastrointestinal symptoms may resolve within 24–72 hours, while neurological effects can persist longer without intervention.^[52] Severity is dose-dependent and often classified as mild (e.g., localized paresthesias with gastrointestinal upset), moderate (e.g., widespread numbness and ataxia), or severe (e.g., muscle weakness approaching paralysis), guiding clinical management needs.^[52] Complications such as dehydration from protracted vomiting and diarrhea, or respiratory arrest in high-dose exposures, underscore the potential for life-threatening outcomes in untreated severe cases.^[3] Exposure to these toxins does not confer long-term immunity, as they are non-immunogenic and do not stimulate an adaptive immune response.^[57]

Syndrome-Specific Manifestations

Paralytic shellfish poisoning (PSP) is characterized by rapid-onset neurological symptoms due to saxitoxin and related neurotoxins blocking sodium channels in nerve cells. Initial manifestations often include tingling, numbness, or burning sensations (paresthesia) in the lips, mouth, tongue, and fingertips, progressing within minutes to hours to generalized numbness of the extremities, face, and neck.^[13] More severe cases involve ataxia, dysphagia, muscle weakness, and paralysis, potentially leading to respiratory failure if diaphragmatic muscles are affected; these effects can occur as early as 30 minutes post-ingestion and may require mechanical ventilation in up to 10% of cases.^[38] Cardiovascular irregularities, such as bradycardia or hypotension, may accompany the paralysis, distinguishing PSP from other syndromes by its potent neuromuscular blockade.^[2] Neurotoxic shellfish poisoning (NSP), caused by brevetoxins from Karenia brevis, primarily affects the gastrointestinal and neurological systems but is notable for sensory reversals and respiratory involvement. Symptoms typically emerge within 3-6 hours and include nausea, vomiting, diarrhea, and abdominal cramps, alongside neurological signs like dizziness, vertigo, ataxia, and slurred speech.^[41] A hallmark is the reversal of temperature sensation (hot feels cold and vice versa), often with myalgia, paresthesia, and tremors; bronchial constriction leading to cough, wheezing, and shortness of breath is common, particularly in asthmatics.^[13] Unlike PSP, NSP symptoms are generally milder, self-resolve within 48 hours with rest, and rarely progress to paralysis, though cardiovascular effects like tachycardia or hypertension can occur.^[2] Amnesic shellfish poisoning (ASP) stands out for its prominent neurological and amnestic effects from domoic acid, an excitotoxin mimicking glutamate. Gastrointestinal symptoms such as vomiting, diarrhea, and abdominal pain usually appear first within 24 hours, but the syndrome's uniqueness lies in delayed-onset neurological manifestations like headache, dizziness, confusion, and disorientation developing up to 48 hours later.^[13] In severe instances, seizures, motor weakness, coma, and permanent short-term memory loss (amnesia) can result, with histopathological evidence of hippocampal damage; this differentiates ASP by its potential for lasting cognitive impairment, affecting up to 20% of hospitalized cases in major outbreaks.^[1] Diarrhetic shellfish poisoning (DSP), induced by okadaic acid and dinophysistoxins inhibiting protein phosphatases, is dominated by intense gastrointestinal distress with limited neurological involvement. Onset is swift, within 30 minutes to 6 hours, featuring profuse watery diarrhea, nausea, vomiting, and abdominal pain, often accompanied by chills and low-grade fever.^[13] Unlike neurotoxic syndromes, DSP rarely causes significant paresthesia, paralysis, or amnesia, though mild headache or myalgia may occur; symptoms typically resolve in 2-3 days without sequelae, emphasizing its primarily enteric pathology.^[2] Azaspiracid shellfish poisoning (AZP), caused by azaspiracid toxins from Azadinium species, primarily involves severe gastrointestinal effects similar to DSP but potentially more prolonged. Symptoms onset within hours of ingestion and include nausea, vomiting, abdominal pain, and watery or bloody diarrhea lasting up to several days, with occasional reports of mild neurological symptoms like headache.^[2] Unlike other syndromes, AZP is generally self-limiting and non-fatal, resolving without long-term sequelae, though dehydration from fluid loss requires supportive care.^[56]

Diagnosis and Management

Diagnostic Methods

Diagnosis of shellfish poisoning begins with a thorough clinical evaluation, focusing on the patient's history of recent shellfish consumption from potentially contaminated sources, combined with the onset of syndrome-specific symptoms such as gastrointestinal upset, neurological disturbances, or memory impairment.^[58] A detailed neurological examination is essential, particularly to assess for paresthesia—manifesting as tingling or numbness starting around the mouth and spreading to the extremities—which is a hallmark of paralytic shellfish poisoning (PSP) and neurotoxic shellfish poisoning (NSP).^[16] This exam helps identify sensory deficits and motor weaknesses, aiding in the initial suspicion of toxin involvement.^[8] Laboratory confirmation is critical for definitive diagnosis, as clinical presentation alone cannot distinguish between shellfish poisoning syndromes or rule out mimics. The mouse bioassay remains the historical gold standard for detecting paralytic shellfish toxins (PSTs) in PSP, involving the intraperitoneal injection of shellfish extracts into mice to measure toxicity based on time to paralysis or death, as standardized by the Association of Official Analytical Chemists (AOAC).^[59] However, due to ethical concerns over animal use, this method is increasingly supplemented or replaced by non-animal alternatives.^[60] For diarrhetic shellfish poisoning (DSP), neurotoxic shellfish poisoning (NSP), and azaspiracid shellfish poisoning (AZP), similar bioassays have been adapted, though their specificity varies.^[61] Advanced instrumental methods, particularly liquid chromatography-mass spectrometry (LC-MS/MS), provide precise identification and quantification of multiple marine biotoxins, including saxitoxins (PSP), brevetoxins (NSP), domoic acid (amnesic shellfish poisoning, ASP), okadaic acid derivatives (DSP), and azaspiracids (AZP), in shellfish tissue, serum, or urine samples.^[62] These techniques offer high sensitivity and specificity, enabling detection at regulatory limits without relying on animal testing, and are endorsed by international bodies like the European Food Safety Authority for routine monitoring and clinical confirmation.^[63] In ASP cases, where neurological sequelae predominate, electroencephalography (EEG) may reveal epileptiform activity in severe presentations, while magnetic resonance imaging (MRI) can demonstrate hippocampal atrophy or lesions in chronic or high-dose exposures, supporting toxin-related brain damage.^[17] Diagnostic challenges include the absence of rapid, point-of-care field tests for toxin detection in patients, often necessitating shipment to specialized labs, which delays confirmation.^[64] Additionally, differentiation from conditions like botulism—characterized by descending flaccid paralysis without sensory symptoms—or ciguatera fish poisoning, which features temperature dysesthesia and longer duration, relies on exposure history, symptom patterns, and targeted toxin assays to avoid misdiagnosis.^[3]

Treatment Approaches

Treatment for shellfish poisoning primarily involves supportive and symptomatic care, as no specific antidotes exist for the toxins involved.^[65] Initial management may include gastrointestinal decontamination if ingestion was recent, such as administration of activated charcoal to limit toxin absorption, along with intravenous fluids to address dehydration and electrolyte imbalances.^[13] Antiemetics can be used to control nausea and vomiting, and close monitoring of respiratory function is essential, particularly in cases with potential neurotoxic effects.^[65] Most patients recover fully with these measures, as the illnesses are often self-limiting without long-term sequelae.^[13] Syndrome-specific therapies tailor supportive care to the predominant symptoms. For paralytic shellfish poisoning (PSP), caused by saxitoxins, mechanical ventilation is critical in severe cases to manage respiratory paralysis, with prompt airway support preventing fatalities.^[13] Neurotoxic shellfish poisoning (NSP), due to brevetoxins, is typically milder and self-resolving, but respiratory support, antihistamines, and bronchodilators may be provided for bronchospasm or wheezing if present.^[65] In amnesic shellfish poisoning (ASP) from domoic acid, treatment focuses on seizure control with anticonvulsants and possible intravenous mannitol to reduce intracranial pressure, alongside general supportive measures for confusion and ataxia.^[66] Diarrhetic shellfish poisoning (DSP) and azaspiracid shellfish poisoning (AZP), resulting from okadaic acid and related compounds or azaspiracids, respectively, require fluid and electrolyte replacement to counter severe diarrhea, with antiemetics for gastrointestinal distress.^[65] Emerging research explores targeted interventions beyond supportive care. Experimental approaches include saxitoxin-binding proteins derived from frog skin, which show promise in neutralizing the toxin in preclinical models for PSP.^[67] Additionally, biocatalytic methods using enzymes to detoxify paralytic shellfish toxins have been investigated in laboratory settings, though none are clinically approved.^[68] These advances aim to address the lack of antidotes, but current practice relies on supportive therapies for resolution in the majority of cases.^[65]

Prognosis

The prognosis for shellfish poisoning varies by syndrome, with low overall mortality rates due to the rarity of severe cases and effective supportive care.^[3] Paralytic shellfish poisoning (PSP) carries the highest risk, with case fatality rates up to 12% in some regions, primarily from respiratory failure if untreated.^[69]^[70] In contrast, neurotoxic shellfish poisoning (NSP), diarrhetic shellfish poisoning (DSP), and azaspiracid shellfish poisoning (AZP) have no reported fatalities, as their effects are typically self-limiting without respiratory compromise.^[16]^[71] Most patients achieve full recovery across syndromes, though timelines and potential sequelae differ. NSP, DSP, and AZP generally resolve within days—often 1-3 days—with complete restoration of function following supportive treatment.^[72]^[71] PSP survivors typically recover fully within hours to days if ventilation is provided promptly, without long-term deficits.^[73] Amnesic shellfish poisoning (ASP), however, may lead to permanent cognitive impairments, including short-term memory loss, in severe cases due to domoic acid's neurotoxic effects on the hippocampus.^[74] Prognostic outcomes are influenced by several key factors, including the ingested toxin dose, patient age, and timeliness of medical intervention. Higher doses correlate with greater severity and risk of complications across syndromes.^[75] Vulnerable groups such as children and the elderly face worse outcomes due to reduced physiological reserve.^[76] Prompt access to supportive care, particularly mechanical ventilation for PSP, significantly improves survival and recovery rates.^[59] Survivors of any syndrome rarely experience recurrence without re-exposure to contaminated shellfish.^[3]

Prevention and Regulation

Monitoring Programs

Monitoring programs for harmful algal blooms (HABs) and shellfish contamination are essential for detecting and mitigating risks associated with shellfish poisoning worldwide. These systems involve coordinated efforts by governmental agencies to sample water and shellfish tissues regularly, analyze for phytoplankton and biotoxins, and implement harvest closures when safety thresholds are exceeded. Such programs target key toxin groups, including paralytic, diarrhetic, and amnesic shellfish toxins, to prevent human exposure through contaminated seafood.^[77] In the United States, the National Oceanic and Atmospheric Administration (NOAA) operates the Harmful Algal Bloom Monitoring System (HABMM), which provides near real-time data on bloom locations, intensities, and forecasts using satellite imagery, in-situ sensors, and modeling. This system supports state-level shellfish sanitation programs under the National Shellfish Sanitation Program (NSSP), where routine monitoring by health departments ensures compliance with federal safety standards. NOAA's efforts, including the Monitoring and Event Response for Harmful Algal Blooms (MERHAB) program, enhance detection methods and training for local agencies, enabling rapid response to emerging threats.^[77]^[78] The European Union maintains a harmonized framework for biotoxin monitoring under Regulation (EC) No 854/2004, requiring member states to conduct year-round surveillance of classified shellfish production areas. The European Food Safety Authority (EFSA) provides scientific advice on toxin limits and risk assessments, while the European Reference Laboratory for Marine Biotoxins (EURLMB) coordinates method validation and proficiency testing across countries. National programs, such as those managed by the UK's Centre for Environment, Fisheries and Aquaculture Science (Cefas), involve classified area inspections and toxin analysis to enforce uniform standards.^[79]^[80]^[81] Japan has enforced stringent monitoring since the 1950s, mandating the mouse bioassay for paralytic shellfish toxins (PSTs) and diarrhetic shellfish toxins (DSTs) in all commercial shellfish under the Food Sanitation Act. The Ministry of Health, Labour and Welfare oversees nationwide testing, with samples collected from major production areas like Hokkaido and the Pacific coast, where PST outbreaks have historically been prevalent. This long-standing protocol uses intraperitoneal injection of extracts into mice to detect toxicity levels, supplemented by chemical methods for confirmation.^[82]^[61] Common methods across these programs include weekly phytoplankton netting and microscopy to identify HAB species, followed by chemical or bioassay testing of shellfish tissues for toxin accumulation. For instance, high-performance liquid chromatography (HPLC) or liquid chromatography-mass spectrometry (LC-MS/MS) quantifies toxins, while closures are triggered when concentrations exceed regulatory thresholds, such as 80 μg saxitoxin equivalents per 100 g of shellfish tissue for PSTs. These protocols allow for dynamic area classifications, reopening sites once toxins dissipate below safe levels.^[77]^[14]^[83] The implementation of these monitoring systems has significantly reduced the incidence of shellfish poisoning outbreaks by enabling proactive harvest bans and keeping contaminated products off the market. In monitored regions, rigorous surveillance since the 1990s has prevented numerous potential illnesses, with U.S. programs alone averting widespread exposure during HAB events through timely alerts and closures. Similar successes in the EU and Japan underscore the value of sustained investment in detection technologies for public health protection.^[20]^[84]

Public Health Measures

Public health measures for shellfish poisoning primarily involve regulatory frameworks to restrict contaminated products, educational initiatives to inform consumers and food handlers, and technological innovations to enhance detection and prevention. Regulations include harvest bans imposed during harmful algal blooms, when toxin levels exceed safe thresholds, such as the 80 μg STX equivalents per 100 g of shellfish tissue for paralytic shellfish toxins.^[85] These bans are triggered by monitoring data from programs like the U.S. National Shellfish Sanitation Program (NSSP), which enforces sanitary controls across harvesting, processing, and distribution.^[86] For farmed shellfish, labeling requirements mandate indications of production method (e.g., "farm-raised") and country of origin to ensure traceability and compliance with safety standards, helping consumers identify potentially lower-risk sources.^[87] Internationally, the Codex Alimentarius Commission sets maximum levels for biotoxins in bivalve molluscs, such as 800 μg/kg for saxitoxins and 20 mg/kg for domoic acid, providing harmonized guidelines adopted by many countries to protect global trade and public health.^[88] Education efforts focus on disseminating warnings through media and digital tools to alert the public about closures and risks. Health authorities issue advisories via press releases, websites, and interactive maps, such as those from the California Department of Public Health, urging avoidance of sport-harvested shellfish during contamination events.^[89] Mobile apps and online platforms, like the BC Centre for Disease Control's shellfish harvesting status map, enable real-time access to safety information for recreational harvesters.^[90] For food service professionals, training programs emphasize recognizing biotoxin risks in raw or undercooked shellfish; initiatives like FDA's food safety education highlight proper sourcing and handling to prevent outbreaks in restaurants.^[91] Innovations in prevention include biosensors for rapid on-site toxin detection, offering quicker results than traditional lab methods and enabling timely regulatory responses. Aptamer-based electrochemical biosensors, for instance, detect paralytic shellfish toxins at low concentrations within minutes, supporting proactive closures.^[92] In aquaculture, controls such as Hazard Analysis and Critical Control Points (HACCP) plans identify and mitigate contamination risks through site selection, water quality monitoring, and detoxification protocols, like controlled purging to reduce toxin levels in mussels and clams before market release.^[93]^[94]

Epidemiology

Global Incidence

Shellfish poisoning, encompassing syndromes such as paralytic (PSP), neurotoxic (NSP), amnesic (ASP), diarrhetic (DSP), and azaspiracid (AZP) types, affects individuals globally, primarily through consumption of toxin-contaminated bivalve mollusks like mussels, clams, and oysters. For PSP, an estimated 2,000 cases occur annually worldwide, with cases reported across every inhabited continent as of 2025.^[95]^[69] Comprehensive global figures for all syndromes are limited due to underdiagnosis and underreporting. In the United States, reported biotoxin shellfish poisoning cases number in the low dozens annually, with higher numbers during peak harmful algal bloom (HAB) seasons along coastal regions such as the Pacific Northwest and Gulf of Mexico.^[13] These figures, drawn from surveillance by organizations like the Centers for Disease Control and Prevention (CDC) and World Health Organization (WHO), likely underestimate the true burden due to underdiagnosis and mild cases going unreported.^[13] Incidence of HAB-related events has increased over recent decades, attributed in part to climate change effects on ocean temperatures and nutrient cycles that promote HAB proliferation.^[96] HAB frequency and geographic range have expanded globally since the 1980s, correlating with warmer sea surface temperatures. In warming regions like the Mediterranean Sea, contamination events involving DSP toxins have become more frequent since 2000, linked to recurrent blooms of toxin-producing dinoflagellates such as Dinophysis species.^[97] Underreporting remains a significant challenge in developing nations, where limited monitoring infrastructure and reliance on subsistence fishing obscure the full scale of occurrences.^[69]

Risk Factors and Outbreaks

Risk factors for shellfish poisoning primarily involve the consumption of bivalve mollusks, such as mussels, clams, oysters, and scallops, that have accumulated biotoxins produced by harmful algal blooms (HABs) in marine environments.^[3] These blooms, often triggered by nutrient pollution, warmer water temperatures, and coastal upwelling, lead to rapid proliferation of toxin-producing dinoflagellates like Alexandrium species for paralytic shellfish poisoning (PSP), Karenia brevis for neurotoxic shellfish poisoning (NSP), Pseudo-nitzschia for amnesic shellfish poisoning (ASP), and Dinophysis species for diarrhetic shellfish poisoning (DSP). Recreational or subsistence harvesting from unmonitored areas heightens exposure, as does consuming the entire shellfish, including toxin-concentrated viscera, rather than just the adductor muscle.^[98] Vulnerable populations include older adults and young children, who may experience more severe neurological symptoms due to reduced physiological resilience, though all age groups are susceptible.^[3] Climate change exacerbates risks by potentially increasing HAB frequency and intensity in temperate and coastal regions.^[99] Outbreaks of shellfish poisoning are episodic and geographically variable, often coinciding with seasonal algal blooms in coastal waters. The 1987 ASP outbreak in Prince Edward Island, Canada, affected over 100 individuals who consumed contaminated mussels containing domoic acid, resulting in three deaths and persistent memory loss in some survivors, marking the first recognition of this syndrome.^[3] In 1992–1993, New Zealand experienced the largest recorded NSP outbreak, with more than 180 cases linked to brevetoxin-laden shellfish from K. brevis blooms, primarily causing gastrointestinal and neurological symptoms without fatalities.^[16] A major PSP event in Hong Kong in March 2005 involved 36 clusters of cases from fresh scallops (Atrina vexillum), where viscera consumption was identified as the key risk factor amplifying toxin intake, leading to paresthesia and respiratory distress in affected individuals.^[98] More recently, the 2024 PSP outbreak in Oregon, United States, was the state's largest on record, with 42 cases (39 presumptive, three confirmed) reported from May to July after consuming mussels and clams harvested north of 45.12535°N latitude, where saxitoxin levels exceeded regulatory limits by 44–68 times.^[99] Of those affected, 54% sought medical care, 17% required hospitalization, and one needed mechanical ventilation; cases were more severe among older individuals in rural coastal areas who delayed seeking treatment.^[99] Globally, PSP remains the most fatal syndrome, with outbreaks reported in regions like the Philippines (2013) and Nicaragua, underscoring the need for ongoing monitoring to mitigate public health impacts.^[3]

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