Saxitoxin lethality

Saxitoxin paralyzes the peripheral nervous system and alters cardiac chronotrophy. Symptoms include gastrointestinal complaints and paresthesias of the face, followed by (in severe cases) muscle paralysis. The estimated lethal dose in humans is 0.3-1 mg. A single contaminated shellfish may contain 50 lethal doses. Mortality for reported cases is 5.9%, but has a... 

Marine toxins may be developed from marine organisms. Examples include saxitoxin, tetrodotoxin, palytoxin, brevetoxins, and microcystin. Saxitoxin is a sodium-channel blocker and is most toxic by inhalation compared to the other routes of exposure. Saxitoxin and tetrodotoxin are similar in mechanical action, toxicity, and physical attributes. They can be lethal within a few minutes when inhaled. It has not yet been chemically synthesized efficiently, or easily created in large quantities from natural sources. Palytoxin is produced from soft coral and is highly toxic. It is, however, difficult to produce or harvest from nature. 

Microcystis, Nostoc, and Oscillatoria (Planktothrix). Cyanobacteria toxins (cyanotoxins) include cytotoxins and biotoxins (neurotoxins anatoxin-a, anatoxin-a(s) and saxitoxins, and the hepatotoxins microcystins MCs, and nodularins), with biotoxins being responsible for acute lethal, acute chronic, and subchronic poisonings of wild/domestic animals and humans. In most of the reported cases, afflicted animals consumed water from water bodies where there was an obvious presence of cyano-bacterial scum on the water surface. More recent measurements of cyanobacterial toxins using sensitive modem analytical methods have often revealed high frequencies of toxic blooms even when animal poisonings have not been reported. 

Saxitoxin, the best known example of this group, is a potent neurotoxin found in shellfish such as mussels, clams, and scallops. Saxitoxin is a sodium channel-blocking agent and is more toxic by inhalation than by other routes of exposure. Unlike oral intoxication with saxitoxin (paralytic shellfish poisoning), which has a relatively slow onset, inhala-tional intoxication with saxitoxin can be lethal in a few minutes. Saxitoxin could be used against our troops as an antipersonnel weapon, but because it cannot currently be chemically synthesized efficiently, or produced easily in large quantities from natural sources, it is unlikely to be seen as an area aerosol weapon on the battlefield. 

Saxitoxin. Some neurotoxins, such as saxitoxin and tetrodotoxin, can kill an individual very quickly after inhalation of a lethal dose (within minutes). These toxins act by blocking nerve conduction directly and cause death by paralyzing muscles of respiration. Yet, at just less than a lethal dose, the exposed individual may not even feel ill, or may only feel dizzy. 

Because of the rapid onset of signs after inhalation, prophylaxis (either immunization or pretreatment) would be required to protect soldiers from these two rapidly acting neurotoxins. Unprotected soldiers who inhale a lethal dose would probably die before they could be helped, unless they could be intubated and artificially ventilated immediately. Although the mechanism of death after inhalation of saxitoxin is believed to be the same as when the toxin is administered intravenously, it is more toxic if inhaled. 

II. Toxic dose. The concentration of toxin varies widely depending on geographic and seasonal factors. The amount of toxin necessary to produce symptoms is unknown. Saxitoxin is extremely potent the estimated lethal dose in humans is 0.3-1 mg, and contaminated mussels may contain 15-20 mg. 

Saxitoxin Gonyaulax catanella, dinoflagellate marine algae (proposed for lethal steel darts one-fifth the thickness of a human hair shot by an air pistol)... 

Benton BJ, Keller SA, Spriggs DL, Capacio BR, Chang FC (1998) Recovery from the lethal effects of saxitoxin a therapeutic window for 4-aminopyridine (4-AP). Toxicon 36 571-588... 

Saxitoxin acts quickly, and can kill an individual within a few minutes of inhalation of a lethal dose. It acts by directly blocking nerve conduction, and causes death by paralyzing muscles of respiration. At slightly less than the lethal dose, the victim may not experience any effects at aU. Botulinum toxin needs to invade nerve terminals in order to block the release of neurotransmitters, which under normal conditions control muscle contraction. The symptoms from botulinum toxin are slow to develop (from hours to days), but are just as lethal, causing respiratory failure. This toxin blocks biochemical action in the nerves, which activate the muscles necessary for respiration, which leads to snffocation. Unlike saxitoxin, toxicity for botulinum is greater through ingestion than inhalation. 

---