Paralytic shellfish poisoning
Saxitoxin neutral.svg
The saxitoxin molecule shown in its unionized state

Paralytic shellfish poisoning (PSP) is one of the four recognized syndromes of shellfish poisoning, which share some common features and are primarily associated with bivalve mollusks (such as mussels, clams, oysters and scallops). These shellfish are filter feeders and accumulate neurotoxins, chiefly saxitoxin, produced by microscopic algae, such as dinoflagellates, diatoms, and cyanobacteria.[1] Dinoflagellates of the genus Alexandrium are the most numerous and widespread saxitoxin producers and are responsible for PSP blooms in subarctic, temperate, and tropical locations.[2] The majority of toxic blooms have been caused by the morphospecies Alexandrium catenella, Alexandrium tamarense, Gonyaulax catenella and Alexandrium fundyense,[3] which together comprise the A. tamarense species complex.[4] In Asia, PSP is mostly associated with the occurrence of the species Pyrodinium bahamense.[5]

Some pufferfish, including the chamaeleon puffer, also contain saxitoxin, making their consumption hazardous.[6]

PSP and cyanobacteria

Saxitoxin can be produced in both eukaryotic dinoflagellates as well as prokaryotic cyanobacteria (usually referred to as blue-green algae). The biosynthesis pathway of this toxin within cyanobacteria is well defined, while the pathway within dinoflagellates is mostly unknown.

Within cyanobacteria the saxitoxin pathway is complex with many steps, enzymes and chemical reactions. Using radioisotope tracing experiments scientists have determined how the initial reagent of the pathway, L-arginine (via acetyl-CoA), turns into this toxin. L-arginine goes through a rare reaction known as Claisen condensation forming four intermediates before turning into the final product of saxitoxin.[7]

Cyanobacteria is general responsible for the accumulation of PSP toxins, mainly being saxitoxin, within freshwater marine life. Studies have been completed showing that the Australian freshwater mussel Alathyria condola are highly susceptible to neurotoxin accumulation. This specific shellfish has shown upwards of 80 ug of neurotoxin accumulation for every 100g of the mussel after a 2-3 day of exposure to the cyanobacteria A. circinalis , which is significant enough to cause health risks for humans.[8]


The toxins responsible for most shellfish poisonings are water insoluble, heat and acid-stable, and ordinary cooking methods do not eliminate the toxins. The principal toxin responsible for PSP is saxitoxin. Some shellfish can store this toxin for several weeks after a harmful algal bloom passes, but others, such as butter clams, are known to store the toxin for up to two years.[9] Additional toxins are found, such as neosaxitoxin and gonyautoxins I to IV. All of them act primarily on the nervous system.

PSP and its associated toxin can cause paralysis in extreme cases by targeting the sodium ion channels. Saxitoxin is able to bind to the receptor site of a cellular membrane near the sodium ion channel, blocking the entrance and not allowing potassium or sodium to pass into the cell. This blockage restricts the transmission of signals between neurons potentially resulting in paralysis.[10]

PSP can be fatal in extreme cases, particularly in immunocompromised individuals. Children are more susceptible. PSP affects those who come into contact with the affected shellfish by ingestion.[1] Symptoms can appear ten to 30 minutes after ingestion, and include nausea, vomiting, diarrhea, abdominal pain, tingling or burning lips, gums, tongue, face, neck, arms, legs, and toes.[1] Shortness of breath, dry mouth, a choking feeling, confused or slurred speech, and loss of coordination are also possible.

PSP in wild marine mammals

PSP has been implicated as a possible cause of sea otter mortality and morbidity in Alaska, as one of its primary prey items, the butter clam (Saxidomus gigantea) bioaccumulates saxitoxin as a chemical defense mechanism.[11] In addition, ingestion of saxitoxin-containing mackerel has been implicated in the death of humpback whales.[12]

Additional cases where PSP was suspected as the cause of death in Mediterranean monk seals (Monachus monachus) in the Mediterranean Sea[13] have been questioned due to lack of additional testing to rule out other causes of mortality.[14]

Detection and treatment

In Vivo, in Vitro, analytical techniques and immunoassays can all be used in order to determine whether saxitoxin is present within shellfish or has been ingested by humans. The most common In Vivo method used is that of mouse bioassays, which provides quantitative and qualitative data regarding the relative toxicity of a suspected PSP infection. An in Vitro method of detection commonly used is that of receptor binding assays which provides similar data to that of mouse bioassays. Analytical techniques that can be used for PSP detection include High performance liquid chromatography (HPLC) and other forms of chromatography.[15]

These detection methods can be used on shellfish in order to determine the concentration of saxitoxin within the organism. Concentrations of saxitoxin greater than or equal to 80 ug per 100g of flesh within a shellfish are determined to be unsafe for human consumption.[16]

In terms of treatment there is no current antidote for the PSP disease that is able to combat the saxitoxin molecule. Most patients are able to recover without treatment, however biomedical devices such as mechanical respirators as well as oxygen supports can help treat any respiratory paralysis symptoms until the toxin passes through the patient's body

See also


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