mushroom poisoning(redirected from GI/liver damage)
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Mushroom poisoning refers to the severe and often deadly effects of various toxins that are found in certain types of mushrooms. One type known as Amanita phalloides, appropriately called "death cap," accounts for the majority of cases. The toxins initially cause severe abdominal cramping, vomiting, and watery diarrhea, and then lead to liver and kidney failure.
The highest reported incidences of mushroom poisoning occur in western Europe, where a popular pastime is amateur mushroom hunting. Since the 1970s, the United States has seen a marked increase in mushroom poisoning due to an increase in the popularity of "natural" foods, the use of mushrooms as recreational hallucinogens, and the gourmet qualities of wild mushrooms. About 90% of the deaths due to mushroom poisoning in the United States and western Europe result from eating Amanita phalloides. This mushroom is recognized by its metallic green cap (the color may vary from light yellow to greenish brown), white gills (located under the cap), white stem, and bulb-shaped structure at the base of the stem. A pure white variety of this species also occurs. Poisoning results from ingestion of as few as one to three mushrooms. Higher death (mortality) rates of more than 50% occur in children less than 10 years of age.
Causes and symptoms
Poisonous mushrooms contain at least two different types of toxins, each of which can cause death if taken in large enough quantities. Some of the toxins found in poisonous mushrooms are among the most potent ever discovered. One group of poisons, known as amatoxins, blocks the production of DNA, the basis of cell reproduction. This leads to the death of many cells, especially those that reproduce frequently such as in the liver, intestines, and kidney. Other mushroom poisons affect the proteins needed for muscle contraction, and therefore reduce the ability of certain muscle groups to perform.
Symptoms of Amanita poisoning occur in different stages or phases. These include:
- First phase. Abdominal cramping, nausea, vomiting, and severe watery diarrhea occur anywhere from 6-24 hours after eating the mushroom and last for about 24 hours. These intestinal symptoms can lead to dehydration and low blood pressure (hypotension).
- Second phase. A period of remission of symptoms that lasts 1-2 days. During this time, the patient feels better, but blood tests begin to show evidence of liver and kidney damage.
- Third phase. Liver and kidney failure develop at this point and either lead to death within about a week or recovery within 2-3 weeks.
Other symptoms are due to either a decrease in blood clotting factors that leads to internal bleeding or reduced muscle function, with the development of weakness and paralysis.
In most cases, the fact that the patient has recently eaten wild mushrooms is the clue to the cause of symptoms. Moreover, the identification of any remaining mushrooms by a qualified mushroom specialist (mycologist) can be a key to diagnosis. When in doubt, the toxin known as alpha-amantin can be found in the blood, urine, or stomach contents of an individual who has ingested poisonous Amanita mushrooms.
It is important to remember that there is no specific antidote for mushroom poisoning. However, several advances in therapy have decreased the death rate over the last several years. Early replacement of lost body fluids has been a major factor in improving survival rates.
Therapy is aimed at decreasing the amount of toxin in the body. Initially, attempts are made to remove toxins from the upper gastrointestinal tract by inducing vomiting or by gastric lavage (stomach pumping). After that continuous aspiration of the upper portion of the small intestine through a nasogastric tube is done and oral charcoal (every four hours for 48 hours) is given to prevent absorption of toxin. These measures work best if started within six hours of ingestion.
In the United States, early removal of mushroom poison by way of an artificial kidney machine (dialysis) has become part of the treatment program. This is combined with the correction of any imbalances of salts (electrolytes) dissolved in the blood, such as sodium or potassium. An enzyme called thioctic acid and corticosteroids also appear to be beneficial, as well as high doses of penicillin. In Europe, a chemical taken from the milk thistle plant, Silybum marianum, is also part of treatment. When liver failure develops, liver transplantation may be the only treatment option.
The mortality rate has decreased with improved and rapid treatment. However, according to some medical reports death still occurs in 20-30% of cases, with a higher mortality rate of 50% in children less than 10 years old.
The most important factor in preventing mushroom poisoning is to avoid eating wild or noncultivated mushrooms. For anyone not expert in mushroom identification, there are generally no easily recognizable differences between nonpoisonous and poisonous mushrooms. It is also important to remember that most mushroom poisons are not destroyed or deactivated by cooking, canning, freezing, drying, or other means of food preparation.
"Alerts from the CDC." Experience Lab Page. 〈http://www.medsitenavigator.com〉.
"Cyclopeptide-Containing Mushroom Toxicity." The Toxikon Multimedia Project Page. http://www.uic.edu/com/er/toxikon/mushroo.htm.
"Mushroom Poisoning in Children." American Association of Family Physicians. 〈http://www.aafp.org/patient-info/mushroom.html〉.
Mushroom Toxins from the FDA. 〈http://vm.cfsan.fda.-gov/∼mow/chap40.html〉.
the fruiting body of any of a variety of fleshy fungi of the order Agaricales, especially one that is edible. Poisonous species are popularly called toadstools.
mushroom poisoning poisoning resulting from ingestion of mushrooms; potentially deadly mushrooms include Amanita phalloides, A. verna, A. virosa, and certain other species that contain neurotoxins. Rapid identification of mushroom poisoning and treatment is critical. According to the Center for Food Safety and Applied Nutrition of the Food and Drug Administration, persons who have ingested poisonous mushrooms and are treated immediately have a mortality rate of 10 per cent, whereas those who are treated 60 or more hours later have a 60 to 90 per cent mortality rate.
my·ce·tism, mycetismus (mī'sē-tizm, -tiz'mŭs),
Poisoning by certain species of mushrooms.
[G. mykēs, fungus]
a toxic condition caused by the ingestion of certain mushrooms, particularly species of the genus Amanita. Muscarine in A. muscaria produces intoxication in a few minutes to 2 hours. Symptoms include lacrimation, salivation, sweating, vomiting, labored breathing, abdominal cramps, diarrhea and in severe cases convulsions, coma, and circulatory failure. More deadly but slower-acting phalloidin in A. phalloides and A. verna causes similar symptoms, as well as liver damage, renal failure, and death. Rapid identification of mushroom poisoning and treatment is critical. According to the Center for Food Safety and Applied Nutrition of the Food and Drug Administration, persons who have ingested poisonous mushrooms and are treated immediately have a mortality rate of 10%, whereas those who are treated 60 or more hours later have a 60% to 90% mortality rate. Also called phalloidine poisoning.
mushroom poisoningToxicology Intoxication with substances derived from mushrooms, which are divided into those of rapid and delayed onset
GI symptoms, due to unknown toxins; onset within 1-3 hrs of ingestion, most commonly due to Chlorophyllum molybdites–aka Lepiota morgani, characterized by severe vomiting and diarrhea
Alcohol sensitization, due to coprine, which results in an Antabuse-like reaction, which affects the ingestant for up to 5 days after mushroom intake, most commonly due to Coprinus atramentarium, the symptoms include face flushing, tingling of fingers, and a metallic taste in mouth
PSL syndrome A symptom complex occurring 15 mins to 1 hr after ingesting the mushroom and characterized by perspiration, salivation, and lacrimation, caused by muscarine, a cholinergic toxin, which is accompanied by vomiting, diarrhea, and ↑ urination; most commonly due to Inocybe spp, Clitocybe spp, and others; antidote atropine
Hallucinogenic effect Toxins psilocybin and psilocin; symptoms begin 15 mins to 3 hrs after ingesting Psilocybe spp and others, and include delusions, euphoria, anxiety, distortion of the time-space continuum, and seizures, most commonly in children
Intoxication/delirium Toxins ibotenic acid/muscimol; symptoms begin 30 mins to 2 hrs after ingesting Amanita muscaria and others, and include apparent intoxication, incoordination, hyperactivity, muscle spasms, collapse, anxiety, altered vision, vomiting, and a coma-like state
GI/headache/liver damage Toxin monomethylhydrazine–MMH; symptoms begin within 6-12 hrs of ingestion, and include bloating, nausea, vomiting, diarrhea, abdominal pain, muscle cramps, and vertigo; MMH is present in Gyromitra esculenta
GI/liver damage Toxin amatoxin; symptoms occur in three stages: 12-24 hrs with nausea and severe abdominal pain, followed by a short period in which the symptoms appear to remit, followed by a resumption of symptoms, and fatal–in up to 50% of cases liver failure in 4-7 days; amatoxins are present in Amanita phylloides, and other Amanita spp
Kidney/liver damage Toxin orellanine; symptoms are delayed, beginning between 36 hrs and 14 days, and include extreme thirst, ↑ urinary frequency, lumbar pain, chills or fever, diarrhea or constipation
my·ce·tism, mycetismus (mī'sĕ-tizm,-tiz'mŭs)
Poisoning by certain species of mushrooms.
[G. mykēs, fungus]