Other important mushroom toxins are methylhydrazine (contained in the Gyromitra species) and muscarine (Inocybe and Clitocybe species). The former gives rise to a clinical picture much like that caused by the cyclopeptides. The symptoms of muscarine poisoning, which appear within 30 to 60 min of ingestion, are essentially those of parasympathetic stimulation—miosis, lacrimation, salivation, nausea, vomiting, diarrhea, perspiration, bradycardia, and hypotension. Tremor, seizures, and delirium occur in cases of severe poisoning.
The mushroom toxins have no effective antidotes. If vomiting has not occurred, it should be induced with ipecac, following which activated charcoal should be administered orally in order to bind what toxin remains in the gastrointestinal tract. A local poison control center may help identify the poisonous mushroom and its toxin. Even more important, the gathering and ingestion of field varieties of mushrooms should be left to those absolutely certain of their identity.
A rapidly progressive and sometimes fatal paralysis follows the ingestion of the small fruit of the buckthorn shrub that is indigenous to northern Mexico and the neighboring southwestern parts of the United States. The responsible toxin causes a predominantly motor polyneuropathy, probably of axonal type. Except for a normal CSF protein concentration, the disorder closely resembles Guillain-Barré syndrome and tick paralysis (see later), and its recognition depends on awareness of ingestion of the fruit in endemic areas.
Ingestion of marine toxins that block neural sodium channels is a common form of poisoning throughout coastal areas and islands of the world. It results from eating fish that have fed on toxin-containing microscopic dinoflagellates. Reef fish and shellfish ingest high concentrations of these organisms during periodic upswings in the population of the dinoflagellates. They may be so profuse as to color the surrounding water (red tide).
Although the toxins differ (tetrodotoxin—fugu, puffer fish; ciguatoxin—snails; saxitoxin and brevetoxin—shellfish), the neurologic and gastrointestinal symptoms that follow the ingestion of poisoned fish are similar. The initial symptoms are diarrhea, vomiting, or abdominal cramps coming on minutes to hours after the ingestion. These are followed by paresthesias that begin periorally and then involve the limbs distally. Hot and cold sensory stimuli (e.g., ice cream) are characteristically associated with electrical-like or burning paresthesias in the mouth. Muscle aches and shooting pains are also mentioned by most patients. In puffer fish poisoning, and in advanced stages of poisoning from other fish, weakness occurs, and there have been a few reports of coma and of respiratory failure.
The recognition of this type of fish poisoning is straightforward in endemic areas, in some of which there is a seasonal clustering of cases. In tourists returning home from endemic areas, and in persons consuming imported fish, the illness may be mistaken for Guillain-Barré syndrome. Prominent perioral paresthesias should suggest the correct diagnosis. Supportive treatment is all that is required but treatment with intravenous mannitol is said to hasten recovery.
Pearn has reviewed the biochemistry and physiologic and clinical effects of the various marine toxins and points out a form of chronic intoxication that is apparently endemic in certain island communities. The main chronic effects are severe fatigue and asthenic weakness. The problem of distinguishing this syndrome from depression is acknowledged by the author and the cases on which we have consulted locally almost always fall into the psychiatric category. One of our patients developed chronic paresthesias.
Venoms, Bites, and Stings