Mushroom Poisoning

There are bold mushroom hunters and there are old mushroom hunters, but there are no old bold mushroom hunters. — A wise person

As spring approaches, one thing we can count on: mushrooms in the yard, woods, roadsides, etc. We can also count on children’s curiosity getting the best of them as they pick and eat the mushrooms. Mushroom “hunters” may mistakenly pick false morels (Gyromitra) and eat them at the dinner table. These ingestions may lead to emergency room visits. Why? Unfortunately, it is often difficult to differentiate poisonous mushrooms from edible types, even for trained mycologists. In addition, toxic and non-toxic mushrooms can grow side by side. For these reasons, the best prevention against mushroom poisonings is to assume that all wild mushrooms are poisonous.

A basic awareness of the types of mushroom poisonings and important features that distinguish mild from severe exposures may prove valuable when assessing the patient with potential mushroom toxicity. Symptoms range from nausea and vomiting, drowsiness and confusion, to heart, liver and kidney damage. One mushroom, the “inky cap” (coprine), only makes a patient ill when alcoholic beverages are consumed with the mushroom. The timing of symptoms also varies. Symptoms can occur soon after eating a mushroom or can be delayed 6 to 24 hours.

Fortunately, the most commonly ingested poisonous mushrooms are gastrointestinal irritants. These mushrooms cause self-limited nausea, vomiting, diarrhea and stomach pain. The onset of symptoms is rather rapid (0.5 to 3 hours). In contrast, there is a characteristic delayed onset of symptoms (> 6 hours) for more severe types of poisoning, such as toxicity associated with cyclopeptide toxicity (amatoxin, phallotoxin, virotoxin). Therefore, laboratory analysis including hepatic and renal function and prolonged observation may be warranted for any patient who presents with delayed onset of nausea and vomiting.

The table below has been developed to outline onset of symptoms, specific symptoms and the toxic class of mushroom to aide in identification and diagnosis.

Treatment is primarily symptomatic and supportive. Activated charcoal may be beneficial to limit absorption if administered within one hour of the ingestion. With amatoxin ingestions, delayed administration of activated charcoal may be appropriate due to enterohepatic recirculation of the toxin. Multiple dose activated charcoal have also been advocated for amatoxins because of enterohepatic recirculation. Benzodiazepines can be used for agitation and hallucinations. If GI symptoms predominate, antiemetics and fluid resuscitation should be considered. In cases of renal failure, hemodialysis may be needed.

Because cyclopeptide mushroom poisoning can be fatal, there has been research in search for treatment. Silymarin (Legalon^® SIL), an antidote for cyclopeptide mushroom poisoning, is isolated from the seed of the milk thistle (Silibin marianum) and inhibits the uptake of the amatoxin by the hepatocytes allowing more rapid clearing from the body. The drug is used to treat patients with suspected amatoxin poisoning caused by the ingestion of Amanita phalloides or other amatoxin containing mushrooms which are found predominantly in the Pacific Northwest. Treatment success using Legalon^®SIL is highly correlated to its prompt initiation following known or suspected amatoxin mushroom poisoning. Upon request, the Missouri Poison Center has more information about this antidote and how to obtain Legalon^®SIL in the case of suspected amatoxin mushroom poisoning.

The Missouri Poison Center stands ready to consult on mushroom exposures. Specially-trained and experienced health care professionals are just a phone call away at 1-800-222-1222.