Mushroom poisoning: overview …

Douglas J Lanska MD MS MSPH

Neurotoxicology

Updated 05.20.2024
Released 09.10.2021
Expires For CME 05.20.2027

Mushroom poisoning: overview

Author: Douglas J Lanska MD MS MSPH

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Mushroom poisoning: overview

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Introduction

Overview

Only a small fraction of known species of fungi is hazardous. Nevertheless, even if some species are considered edible, low concentrations of toxins can still be present, and either chronic ingestion or overconsumption can result in manifest toxicity. Thus, “mushrooms” and other higher fungi can be divided into edible, conditionally edible, and poisonous categories. For the conditionally edible group, edibility depends either on controlling both the frequency and amount of fungi ingested or on the elimination (where possible) of toxins by drying, soaking, cooking, and other pretreatments. At least eight distinct neurologic or myologic presentations of mushroom poisoning have been reported: (1) acute encephalopathy; (2) hallucinations; (3) CNS dysfunction, including cerebellar dysfunction; (4) seizures; (5) cholinergic (muscarinic) syndrome; (6) erythromelalgia; (7) a disulfiram-like reaction; and (8) rhabdomyolysis. Some mushroom toxins produce their associated toxidromes by affecting neurotransmission. Except for the myotoxic and false morel neurologic toxidromes, neurologic and myologic presentations of mushroom poisoning are rarely fatal. Fatalities have uncommonly occurred with other neurologic toxidromes (eg, cholinergic mushroom poisoning). Other serious and often permanent organ dysfunction or fatalities may result from accidentally ingesting a more toxic mushroom resembling one that is hallucinogenic, edible, or conditionally edible.

Key points

	• Only a small fraction of known species of mushrooms is hazardous.
	• Even if some species are considered edible, low concentrations of toxins can still be present, and either chronic ingestion or overconsumption can result in manifest toxicity.
	• Mushrooms and other higher fungi can be divided into edible, conditionally edible, and poisonous categories.
	• At least eight distinct neurologic or myologic presentations of mushroom poisoning have been reported: (1) acute encephalopathy; (2) hallucinations; (3) CNS dysfunction, including cerebellar dysfunction; (4) seizures; (5) cholinergic (muscarinic) syndrome; (6) erythromelalgia; (7) a disulfiram-like reaction; and (8) rhabdomyolysis.
	• Although for most neurologic and myologic presentations of mushroom poisoning, care is primarily supportive and symptomatic, some need specific management.
	• Some mushroom toxins produce their associated toxidromes by affecting neurotransmission.
	• Except for the myotoxic and false morel neurologic toxidromes, neurologic and myologic presentations of mushroom poisoning are rarely fatal.
	• Other serious and often permanent organ dysfunction or fatalities may result from accidentally ingesting a more toxic mushroom resembling one that is hallucinogenic, edible, or conditionally edible.

Historical note and terminology

Scope. This article considers neurotoxins and myotoxins originating in macroscopic higher fungi that are either intentionally or accidentally ingested. Some, but not all, of the responsible toxic fungi are stalked mushrooms (or “toadstools”); mushrooms are a subset of fungi from the phylum Basidiomycota (which also includes other fungi with nonmushroom structures like puffballs, bracket fungi, etc.), whereas the Ascomycota include a range of nonmushroom structures. Somewhat colloquially, we will consider the effects of ingesting these mushroom toxins collectively as “mushroom poisoning.”

So-called “mycotoxins” (eg, ergotamine) are not covered in this article. Like mushroom toxins (or “poisons”), mycotoxins are a chemically and pharmacologically heterogeneous assemblage of low-molecular-weight natural products produced as secondary metabolites by filamentous fungi. The definition of a “mycotoxin,” however, does not correctly apply to all fungal substances that are toxic to humans, other animals, or plants, even if some physicians (mis)use the terminology to refer to all fungal toxic substances as “mycotoxins,” including those produced by mushrooms (04; 05):

Other low-molecular-weight fungal metabolites such as ethanol that are toxic only in high concentrations are not considered mycotoxins. ... [In addition], although mushroom poisons are definitely fungal metabolites that can cause disease and death in humans and other animals, they are rather arbitrarily excluded from discussions of mycotoxicology. ... The distinction between a mycotoxin and a mushroom poison is based not only on the size of the producing fungus, but also on human intention. Mycotoxin exposure is almost always accidental. In contrast, with the exception of the victims of a few mycologically accomplished murderers [and accidental mushroom poisoning cases in young children], mushroom poisons are usually ingested by amateur mushroom hunters who have collected, cooked, and eaten what was misidentified as a delectable species (02). [emphasis added]

Classification of fungi. Within the kingdom Fungi is the subkingdom Dikarya (often referred to as the “higher fungi”). Dikarya includes two large divisions or phyla: Basidiomycota and Ascomycota.

Basidiomycota. Basidiomycota are filamentous fungi composed of hyphae and reproduce sexually. Basidiomycota includes inter alia some fungi that might be grown or foraged for food (eg, mushrooms, puffballs, bracket fungi, other polypores, and chanterelles) and fungi that infest plants and might be secondarily ingested (eg, smuts, bunts, rusts).

Ascomycota. Ascomycota, commonly known as the sac fungi, are defined by an “ascus” (meaning “sac” or “wineskin”), a microscopic sexual structure in which nonmotile spores, called ascospores, are formed. However, some species of the Ascomycota are asexual. Familiar edible or conditionally edible examples of sac fungi include morels and truffles, whereas others with much greater potential toxicity include false morels and Claviceps purpura (ergot).

Only a small fraction of known species of mushrooms is hazardous. Nevertheless, even if some species are considered edible, low concentrations of toxins can still be present, and either chronic ingestion or overconsumption can result in manifest toxicity. Thus, “mushrooms” and other higher fungi can be divided into edible, conditionally edible, and poisonous categories (13). For the conditionally edible group, edibility depends either on controlling both the frequency and amount of fungi ingested or on the elimination (where possible) of toxins by drying, soaking, cooking, and other pretreatments.

Classification of mushroom poisoning. Multiple classification systems or frameworks for mushroom poisoning have been proposed (Table 1) (01; 07; 32; 14; 03). Almost all of these consider fungal toxidromes for both mushroom and nonmushroom forms of higher fungi. However, most of these classifications do not address neurotoxic presentations thoroughly or effectively, nor have they kept up with subsequent descriptions of various novel toxidromes or the elaboration (in some cases) of the responsible toxins.

Table 1. Neurologic Components of Different Classifications of Mushroom Poisoning

Barbato, 1993 (01)
	Group B muscarine (cholinergic toxidrome)
	Group C Psilocybin (hallucinogenic toxidrome)
	Group D Muscimol (confusion, ataxia, and hallucinations)
	Group F Coprine (disulfiram-like reaction)
Blackman, 1994 (07)
	Group 2 Gyromitrin (monomethylhydrazine) poisoning
	Group 3 Coprine poisoning
	Group 4 Muscarine poisoning
	Group 5 Ibotenic acid -- Muscimol poisoning
	Group 6 Psilocybin poisoning (“magic mushrooms”)
White, 2019 (32)
	Group 2 - Neurotoxic mushroom poisoning Group 2A - Hallucinogenic mushrooms (psilocybin) Group 2B - Autonomic toxicity mushrooms (muscarine) Group 2C - Central nervous system toxicity mushrooms (ibotenic acid/muscimol) Group 2D - Morel neurologic syndrome (unknown toxin)
	Group 3 - Myotoxic mushroom poisoning Group 3A - Rapid onset myotoxicity (? carboxylic acid) Group 3B - Delayed onset myotoxicity (? saponaceolide B)
	Group 4 - Metabolic/endocrine toxicity mushroom poisoning Group 4A - GABA-blocking mushroom poisoning (gyromitrin) Group 4B - Disulfiram-like mushroom poisoning (coprine)
	Group 6 - Miscellaneous adverse reactions to mushrooms Group 6B - Erythromelalgia-like mushroom poisoning (acromelic acid) Group 6D - Encephalopathy syndrome (? hydrocyanic [prussic] acid)
Gummin and colleagues, 2020 (14)
	Group 2 Muscimol (Ibotenic acid) Group 3 Monomethylhydrazine (gyromitrin) Group 4 muscarine and histamine Group 5 Coprine Group 6 Hallucinogenics (psilocybin and psilocin)
*Note: Not included here are categories for (1) isolated gastrointestinal symptoms (probably multiple different toxins); (2) hepatic toxicity (eg, cyclopeptide amatoxins); or (3) nephrotoxicity (eg, orellanine or orellanin).

Table 2. Comparison of Classifications of Mushroom Poisoning

Phylum	Toxidrome	Type of Mushroom	Toxin	Classification System
				Barbato, 1993 (01)	Blackman, 1994 (07)	White and colleagues, 2019 (32)	Gummin and colleagues, 2020 (14)
Basidiomycota	Hallucinogenic	Psilocybe spp.	Psilocybin/psilocin	C	6	2A	6
		Gymnopilus spp.
		Inocybe spp.
		Panaeolus spp.
		Pholiotina spp.
		Pluteus spp.
		Amanita spp.	Muscimol/ibotenic acid	D	5	2C	2
	Encephalopathic	Pleurocybella porrigens	Pleurocybellaziridine			6D
	Autonomic (cholinergic)	Clitocybe and Inocybe spp.	Muscarine	B	4	2B	4
	Erythromelalgia	Clitocybe spp.	Acromelic acid			6B
	Disulfiram-like reaction	Coprinus atramentarius	Coprine	F	3	4B	5
		Echinoderma asperum
	Myotoxic (rhabdomyolysis)	Tricholoma equestre	Unknown			3B
		Russula subnigricans	Cycloprop-2-ene carboxylic acid			3A
Ascomycota	Encephalopathic	Morchella spp. (Morel)	Unknown			2D
	Encephalopathic (confusion and intractable seizures)	Gyromitra esculenta (False morel)	Gyromitrin/monomethylhydrazine		2	4A	3

White’s classification is the most detailed but makes some inadequately supported conclusions and several idiosyncratic organizational decisions (eg, the locations within the classification system of groups 4A, 6B, and 6D) (32). White incorrectly specified the toxin for Tricholoma equestre mushroom poisoning as saponaceolide B, when that toxin was identified in a related species, T. terreum, but not in T. equestre. Further, White considered T. equestre poisoning as “delayed,” when instead it appeared to require cumulative ingestions on several consequtive days, rather than a delayed response to a single ingestion.

Clinical manifestations

Presentation and course

	• Neurologic or myologic presentations of mushroom poisoning include acute encephalopathy, hallucinations, cerebellar dysfunction, intractable seizures, cholinergic (muscarinic) reactions, erythromelalgia, a disulfiram-like reaction, and rhabdomyolysis.
	• Within each of the major categories of mushroom poisoning, there is considerable clinical variation, depending on age, body weight, toxin concentration within the mushrooms ingested, the amount ingested, and various constitutional factors.

An exposure history should include the following: (1) quantity and description of mushrooms ingested; (2) preparation of the mushroom (eg, raw or cooked), although cooking may not alter toxicity for many mushroom neurotoxins; (3) source of the mushroom (eg, foraged, online purchase, other); (4) time of ingestion; (5) symptoms seen after ingestion and the time between ingestion and onset; (6) prehospital treatment, including any home remedies (eg, activated charcoal or ipecac); (6) medications regularly taken; and (7) a list of any co-ingestants (including alcohol and cannabis).

At least eight distinct neurologic or myologic presentations of mushroom poisoning have been reported: (1) acute encephalopathy; (2) hallucinations; (3) CNS dysfunction, including cerebellar dysfunction; (4) seizures; (5) cholinergic (muscarinic) syndrome; (6) erythromelalgia; (7) a disulfiram-like reaction; and (8) rhabdomyolysis. There is considerable clinical variation within each of these major categories, depending on age, body weight, toxin concentration within the mushrooms ingested, and the amount ingested. Other factors undoubtedly play a role, including co-ingested substances, medications, genetic susceptibility, and comorbidities (eg, renal or hepatic dysfunction). Clinical features are summarized in Table 3.

Table 3. Neurologic Presentations of Mushroom Poisoning

Toxidrome	Toxins	Presenting Neurologic Symptoms
Acute encephalopathy	Pleurocybellaziridine	Acute encephalopathy
Hallucinogenic	Psilocybin	Most commonly, perceptual distortions and alterations of thought or mood. CNS manifestations may include euphoria, irritability, fear, agitation, depressed level of consciousness (ranging from lethargy to coma), confusion or delirium, incoherent babbling, misperceptions, hallucinations, delusions, dizziness, ataxia, myoclonus, and seizures (mostly in young children).
Hallucinogenic	Muscimol or ibotenic acid	Variable CNS depression and excitation, variable obtundation, visual and auditory hallucinations and misperceptions, delusions, ataxia, ataxia and hyperkinetic behavior.
Cholinergic (muscarinic)	Muscarine	DUMBELS: D - Diaphoresis / Diarrhea / Defecation U - Urination M - Miosis B - Bronchorrhea / Bronchospasm / Bradycardia E - Emesis L - Lacrimation S - Salivation / Sweating SLUDGE: S - Salivation / Sweating L - Lacrimation U - Urination D - Diaphoresis / Diarrhea / Defecation G - Gastrointestinal distress or upset E - Emesis
Morel neurologic syndrome (encephalopathy)	Unknown	Most commonly, tremor, dizziness or ”inebriation,” visual disorders, and unsteadiness or ataxia. Other less common neurologic manifestations include headache, paresthesia, trismus or muscle spasms, drowsiness or confusion, dysarthria.
False morel neurologic syndrome (acute confusional state and intractable seizures)	Gyromitrin or monomethylhydrazine	Confusion and, in severe poisoning, seizures refractory to standard anticonvulsants; subacute motor neuron syndrome mimicking amyotrophic lateral sclerosis (21; 22)
Erythromelalgia	Acromelic acid	Erythromelalgia
Disulfiram-like reaction	Coprine	Disulfiram-like reaction after drinking alcohol: headache, nausea, vomiting, flushing, tachycardia, and, rarely, hypotension
Myotoxic [Tricholoma equestre mushroom poisoning]	Unknown	Rhabdomyolysis
Myotoxic [Russula subnigricans mushroom poisoning]	Cycloprop-2-ene carboxylic acid	Rhabdomyolysis

Prognosis and complications

In 2019, there were no fatalities in these categories of potentially neurotoxic mushroom exposures reported to poison control centers in the United States (14); however, 354 individuals were treated in a healthcare facility, and of these, 112 (32%) suffered a minor adverse outcome, 176 (50%) suffered a moderate adverse outcome, and 8 (2%) suffered a major adverse outcome.

The timing of symptom onset is important for distinguishing life-threatening or severe mushroom poisoning from less serious poisoning. Early symptom onset is generally good with mushroom toxicity because symptom onset in less serious mushroom poisoning generally occurs within 5 to 6 hours of ingestion (eg, with hallucinogenic mushrooms). If symptoms such as vomiting, diarrhea, and abdominal pain begin 5 to 6 hours or more after ingestion, mushrooms that can cause potentially life-threatening or severe toxicity (eg, A. phalloides, Gyromitra spp., or Cortinarius spp.) should be considered (07).

Hallucinogenic mushrooms (“magic mushrooms” or “shrooms”) continue to be fashionable among drug users, especially young drug users, in part because they are often believed to be relatively harmless compared to other hallucinogenic drugs (06). However, serious adverse outcomes have been reported, including myocardial infarction (08); psilocybin-induced takotsubo cardiomyopathy (20); severe rhabdomyolysis, acute renal failure, and posterior encephalopathy (06); psychosis and mania, complicated by violent behavior and rhabdomyolysis (31); and protracted paranoid psychosis (09). Ingestion of magic mushrooms may result in horror trips combined with self-destructive and suicidal behavior, especially among people with mental or psychiatric disorders (26; 15).

Despite the potential for serious adverse outcomes, magic mushroom ingestion is relatively safe (19). Out of 9233 magic mushroom users, 19 (0.2%) reported seeking emergency medical treatment in the past year, with a per-event risk estimate of 0.06%. Young age was the only predictor associated with a higher risk of emergency medical presentations. The most common symptoms were psychological: anxiety/panic and paranoia/suspiciousness. All but one returned to baseline within 24 hours.

Biological basis

	• Poisoning by ingested fungi, whether intentional or accidental, is associated with at least 10 different toxidromes.
	• Some mushroom toxins produce their associated toxidromes by affecting neurotransmission.
	• The hallucinogenic mushroom toxins psilocybin and psilocin are structurally similar to the neurotransmitter serotonin.
	• Muscimol is a potent, selective agonist for the GABAA receptors and has sedative-hypnotic, depressant, and hallucinogenic activity.
	• Muscimol binds to the same site on the GABAA receptor complex as GABA itself, in contrast to other GABAergic drugs, such as barbiturates and benzodiazepines, that bind to separate regulatory sites.
	• Ibotenic acid is a psychoactive toxin that occurs naturally in Amanita muscaria and related species of mushrooms found in the temperate and boreal regions of the northern hemisphere.
	• Ibotenic acid is a conformationally-restricted analogue of the neurotransmitter glutamate and acts as a particularly potent agonist of NMDA and multiple types of metabotropic glutamate receptors.
	• Ibotenic acid also serves as a prodrug to muscimol.
	• Muscarine is a cholinergic (muscarinic) agonist.
	• Gyromitrin is converted to a water-soluble toxin, monomethylhydrazine (MMH), which can bind to and inhibit pyridoxal phosphokinase.
	• Gyromitrin-induced pyridoxine kinase inhibition interferes with production of the active form of pyridoxine, pyridoxal 5-phosphate, which is an essential cofactor for glutamic acid decarboxylase (GAD), which catalyzes the decarboxylation of glutamate to gamma-aminobutyric acid (GABA) and CO2.
	• The resultant GABA deficiency from gyromitrin (through the action of its metabolite MMH), with loss of inhibitory neurotransmission, as well as the relative buildup of glutamate, with an increase in excitatory neurotransmission, may produce CNS excitation and seizures that are refractory to standard anticonvulsant therapy.
	• The mushroom-induced disulfiram-like reaction is caused by the fungal toxin coprine.

Etiology and pathogenesis

Poisoning by toxins of higher fungi of the phylum Basidiomycota is summarized in Table 4. There are at least nine toxidromes and toxin combinations affecting the nervous system or muscle as at least a prominent component.

Table 4. Basidiomycota with Clinically Important Neurotoxins and Myotoxins

Order	Family	Scientific names (common names)	Toxidrome (toxin)
Agaricales (gilled mushrooms)	Hymenogastraceae	Psilocybe spp., including: P. semilanceata (“liberty cap”) P. cubensis (“golden teacher”)	Hallucinogenic (psilocybin)
	Bolbitiaceae	Pholiotina spp.
	Strophariaceae	Gymnopilus spp.
	Inocybaceae*	Inocybe spp.
	Incertae sedis	Panaeolus spp.
	Pluteaceae	Pluteus spp.
	Amanitaceae	Amanita muscaria (“fly agaric”) A. pantherina (“panther cap,” or “false blusher”); A. aprica (“sunshine amanita”)	Hallucinogenic (muscimol/ibotenic acid)
	Tricholomataceae**	Clitocybe spp., especially: Clitocybe dealbata (Sowerby) Gillet (“ivory funnel”) Clitocybe rivulosa (Pers.) P. Kumm. (“false champignon,” or “fool's funnel”)	Cholinergic (muscarine)
	Inocybaceae*	Inocybe spp.
	Tricholomataceae**	Paralepistopsis acromelalga Paralepistopsis amoenolens (“paralysis funnel”)	Mushroom-induced erythromelalgia (acromelic acid)
	Agaricaceae	Coprinus atramentarius (“ink cap”) Echinoderma asperum or Lepiota aspera (“freckled dapperling”)	Mushroom-induced disulfiram-like reaction (coprine)
	Marasmiaceae	Pleurocybella porrigen (sugihiratake [Japan]; “angel wings” [North America])	Mushroom-induced acute encephalopathy (pleurocybellaziridine)
	Tricholomataceae**	Tricholoma equestre (“man on horseback,” or “yellow knight”)	Myotoxic (unknown toxin)
	Omphalotaceae	Gymnopus dryophiloides***
Boletales	Boletaceae	Anthracoporus nigropurpureus***	Dizziness, blurred vision, and variable headache, weakness, muscle cramps, tremors
Russulales	Russulaceae	Russula subnigricans Hongo	Myotoxic, causing rhabdomyolsis (cycloprop-2-ene carboxylic acid)
* Inocybaceae are associated with hallucinogenic (psilocybin) and cholinergic (muscarine) toxidromes.
** Tricholomataceae are associated with cholinergic (muscarine), mushroom-induced erythromelalgia (acromelic acid), and myotoxic toxidromes.
*** Only single reports are available for Gymnopus dryophiloides (23) and Anthracoporus nigropurpureus (24).
# Hemolysis occurred in a patient with glucose-6-phosphate dehydrogenase deficiency (27).

Poisoning by toxins of higher fungi of the phylum Ascomycota is summarized in Table 5. There are two known toxidromes affecting the nervous system as at least a prominent component.

Table 5. Ascomycota with Clinically Important Neurotoxins and Myotoxins

Order	Family	Scientific name(s)	Toxidrome (toxin)
Pezizales	Morchellaceae	Morchella spp. (“morel”)	Morel neurologic syndrome (unknown toxin)
	Discinaceae	Gyromitra species, especially: Gyromitra esculenta (“false morel,” “turban fungus”) G. gigas (Kromb.) Cooke (non Phill.) (“giant's false morel,” “snow false morel,” “calf brain,” or “bull nose”)	False morel neurologic syndrome (gyromitrin/monomethylhydrazine)
	Helvellaceae	Helvella crispa (“white saddle,” “elfin saddle,” or “common helvel”) H. lacunosa (“slate grey saddle,” or “fluted black elfin saddle”) H. elastica (“flexible Helvella,” or “elastic saddle”) H. macropus (“felt saddle”)
Helotiales	Cudoniaceae	Cudonia circinans
Leotiales	Leotiaceae	Leotia lubrica (“jelly baby”)

Given the structural diversity of chemicals responsible for the multiple forms of mushroom poisoning, it is not surprising that the mechanisms of action vary considerably as well.

Some mushroom toxins produce their associated toxidromes by affecting neurotransmission:

	(1) Psilocybin and psilocin are both indolealkylamines that can be considered derivatives of tryptamine and are structurally similar to the neurotransmitter serotonin (5-hydroxytryptamine) (33).
	(2) Muscimol is a potent, selective agonist for the GABAA receptors, activating the receptor for the brain's principal inhibitory neurotransmitter and displaying sedative-hypnotic, depressant, and hallucinogenic activity (17). Muscimol binds to the same site on the GABAA receptor complex as GABA itself, in contrast to other GABAergic drugs, such as barbiturates and benzodiazepines, that bind to separate regulatory sites.
	(3) Ibotenic acid or (S)-2-amino-2-(3-hydroxyisoxazol-5-yl)-acetic acid, is a psychoactive toxin that occurs naturally in Amanita muscaria and related species of mushrooms that are found in the temperate and boreal regions of the northern hemisphere. It is a conformationally-restricted analogue of the neurotransmitter glutamate and acts as a particularly potent agonist of the NMDA and multiple types of metabotropic glutamate receptors. Ibotenic acid also serves as a prodrug to muscimol.
	(4) Muscarine is a cholinergic (muscarinic) agonist.
	(5) Gyromitrin rapidly decomposes to form acetaldehyde and N-methyl-N-formylhydrazine, which is converted to a water-soluble toxin, monomethylhydrazine (MMH). MMH can bind to and inhibit pyridoxal phosphokinase (16). Pyridoxine kinase inhibition interferes with production of the active form of pyridoxine, pyridoxal 5-phosphate. Pyridoxal 5-phosphate is an essential cofactor for various enzymes, including glutamic acid decarboxylase (GAD), which catalyzes the decarboxylation of glutamate to gamma-aminobutyric acid (GABA) and CO2. MMH also may inhibit GAD directly. The resultant GABA deficiency, with loss of inhibitory neurotransmission as well as the relative build-up of glutamate, with an increase in excitatory neurotransmission, may produce CNS excitation and seizures that are refractory to standard anticonvulsant therapy.

The mushroom-induced disulfiram-like reaction is caused by the fungal toxin coprine (25; 18). Metabolites of coprine inhibit aldehyde dehydrogenase. If alcohol is ingested hours to days after eating coprine-containing mushrooms, the affected individual experiences a constellation of symptoms identical to that from drinking alcohol after taking disulfiram: headache, nausea, vomiting, flushing, tachycardia, and, rarely, hypotension.

For most of the remaining toxidromes, either the responsible toxin is unknown or the mechanism of action of an identified toxin is not understood at a molecular level.

Epidemiology

	• Collectively, the most common symptoms of mushroom poisoning are nausea and vomiting, followed by diarrhea, syncope, abdominal pain, and hallucinations.
	• In three quarters of mushroom-poisoning events reported to poison control centers, the mushroom is unknown or unidentified.
	• The largest category of identified mushroom exposures reported to poison control centers in the United States was represented by psilocybin- or psilocin-containing hallucinogenic mushrooms.

In a retrospective 11-year review of mushroom poisoning in a Swiss emergency department, the authors identified 87 cases (30). The most common symptoms were nausea and vomiting (82%), followed by diarrhea (68%), syncope (10%), abdominal pain (8%), and hallucinations (7%). Three quarters (74%) exhibited early symptoms (appearance less than 6 hours after ingestion), and one quarter (26%) exhibited late symptoms (appearance more than 6 hours after ingestion). Eleven patients (13%) required hospitalization over 24 hours. Patients with late symptoms tended to have longer in-hospital lengths of stay. Nearly half (44%) were part of cluster presentations (in which more than one person was simultaneously affected).

In the 2019 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (14), there were 5799 reports of single-substance exposures to mushrooms, of which the type of mushroom was unknown or unidentified in 76%. Categories of potentially neurotoxic exposures with substantial numbers of individuals affected were (using their classification system): Group 2 (muscimol or ibotenic acid) 33 cases; Group 3 (monomethylhydrazine) 49 cases; Group 4 (muscarine/histamine) 18 cases; Group 5 (coprine) 10 cases; and Group 6 (psilocybin/psilocin) 590 cases. Thus, most with potentially neurotoxic exposures were for hallucinogenic mushrooms (Groups 2 and 6).

The largest category of identified mushroom exposures reported to poison control centers in the United States was represented by psilocybin or psilocin-containing hallucinogenic mushrooms (14). Of 590 case mentions, there were 387 single exposures, meaning that many of these exposures involved multiple individuals simultaneously. Of the 387 exposures, 144 involved individuals ages 13 to 19 years, 188 involved individuals aged 20 years and older, and 14 involved adults of unknown age. Of these 346 exposures in adolescents and adults, 331 (96%) were acknowledged to have been intentional.

In 2019, no fatalities in these categories of potentially neurotoxic mushroom exposures were reported to poison control centers in the United States (14). However, 354 individuals were treated in a healthcare facility, and of these, 112 (32%) suffered a minor adverse outcome, 176 (50%) suffered a moderate adverse outcome, and 8 (2%) suffered a major adverse outcome.

Exposure to toxic mushrooms is generally accidental in cases of nonhallucinogenic mushroom poisoning (29).

Diagnostic workup

	• The diagnosis of mushroom poisoning should be based on the presenting syndrome and supported, if possible, by the description and toxicologic analysis of the mushroom.
	• Unfortunately, the exact mushroom species and toxins in cases of mushroom poisoning go unidentified in at least three quarters of the cases.
	• Ideally, a sample of the mushrooms ingested should be obtained so a mycologist can confirm identification.
	• No particular diagnostic procedures are available or needed for most patients with hallucinogenic mushroom toxicity.
	• The regional poison control center may be contacted for consultation, referral, and assistance in mushroom identification.
	• In the United States, a nationwide telephone number automatically directs calls to the nearest poison control center (1-800-222-1222).

The diagnosis of mushroom poisoning should be based on the presenting syndrome and supported, if possible, by the description and toxicologic analysis of the mushroom (10; 11). Unfortunately, according to data from the American Association of Poison Control Centers, the exact mushroom species and toxins in cases of mushroom poisoning go unidentified in at least three quarters of the cases (10; 11; 14). Ideally, a sample of the mushrooms ingested should be obtained so a mycologist can confirm identification. Unfortunately, in most cases, the mushroom in question has already been digested, but collecting the patient’s gastric contents using gastric lavage or after emesis might yield identifiable spores.

No particular diagnostic procedures are available or needed for most patients with hallucinogenic mushroom toxicity, although identification of the mushroom by a mycologist is still desirable. The regional poison control center may be contacted for consultation, referral, and assistance in mushroom identification. In the United States, a nationwide telephone number automatically directs calls to the nearest poison control center (1-800-222-1222). A mycologist can also be contacted through the North American Mycological Association, a local university, or sometimes a botanical garden.

The following blood studies are recommended for most patients evaluated on an emergency basis with possible mushroom toxicity: complete blood count, basic serum metabolic profile, baseline liver and renal function studies, and creatine kinase. Urine drug testing should also be considered, especially if the patient exhibits alterations of behavior or mental status or if substance abuse, suicidal intent, or foul play is suspected.

Management

	• For most neurologic and myologic presentations of mushroom poisoning, care is primarily supportive and symptomatic.
	• Most patients with hallucinogenic mushroom toxicity can be treated without medications.
	• Cholinergic (muscarinic) mushroom poisoning should be treated with atropine.
	• Intensive care may be needed for patients with myotoxic mushroom poisoning and severe rhabdomyolysis.
	• Pyridoxine should be given after substantial ingestion of gyromitrin-containing (false morel) mushrooms or if central nervous system toxicity is present; repeat doses may be needed.
	• Diazepam should be administered intravenously if seizures persist despite pyridoxine in patients exposed to gyromitrin-containing (false morel) mushrooms.

The management recommendations presented here do not apply to poisoning with nonneurologic toxins, such as those that cause solely gastrointestinal symptoms or those more dangerous hepatotoxic and nephrotoxic varieties that are associated with high case-fatality rates.

Gastrointestinal decontamination. There is a limited and somewhat controversial role for gastrointestinal decontamination in cases of mushroom poisoning, with some advocating use of activated charcoal in the first hour and others discounting this as insufficient evidence of efficacy. Furthermore, the CNS manifestations of hallucinogenic mushroom toxicity, for example, develop rapidly after ingestion, with absorption before activated charcoal is usually considered. A reasonable approach is to consider activated charcoal administration in alert patients who present for care within 1 hour of potentially toxic mushroom ingestion. Patients admitted to the hospital are typically given activated charcoal to stop the toxic compound’s absorption and to prevent further intoxication, even though adsorption to activated charcoal has not been demonstrated for these fungal toxins. Supportive evidence for the efficacy of activated charcoal administration in this setting is largely indirect, from animal studies and from analogy with other toxic ingestions. Because of the potential for further volume depletion, combining a cathartic (eg, sorbitol) and activated charcoal is not generally recommended. Syrup of ipecac administration in remote locations soon after pediatric ingestion of toxic mushrooms may prevent or minimize toxicity, but unsupervised children typically only try exploratory nibbles of mushrooms in their local environments and, thus, rarely have serious consequences. Because most serious mushroom poisonings are only detected hours after ingestion, gastric emptying by gastric lavage or syrup of ipecac in the emergency department is not likely to be beneficial. If treatment occurs within the first hour of ingestion, gastric lavage may be considered, although this recommendation also lacks strong empiric evidence. Nasogastric aspiration in alert patients to obtain a sample for spore analysis can be considered if no other mushroom sample of what was ingested is available and gastric contents might still contain partially digested mushrooms.

Hallucinogenic mushroom toxicity. Care is primarily supportive in hallucinogenic mushroom toxicity, the most frequent form of neurotoxic mushroom poisoning. Most patients can be treated without medications. Toxicity usually lasts between 6 and 8 hours, but some symptoms may take several days to subside. Occasionally, benzodiazepines may be needed for sedation and to help control associated agitation and panic attacks. Intravenous fluids may sometimes be necessary to correct volume loss from vomiting.

Seizures are uncommon with hallucinogenic mushroom poisoning, except in young children. Various anticonvulsants have been used to treat seizures in such patients, but respiratory depression may occur when some of these agents (eg, benzodiazepines) are administered intravenously. Preparations must, therefore, be made to support the airway if necessary.

In rare cases, anticholinergic drugs, such as atropine, may be needed. With A muscaria poisoning, anticholinergic drugs (eg, atropine) are rarely, if ever, needed; the species name was applied because muscarine was first identified from preparations of this mushroom, even though few muscarinic effects are observed following ingestion of these mushrooms.

In the absence of a clinically evident infection, treating a low-grade fever with antipyretics is unnecessary in an agitated or hyperactive patient with hallucinogenic mushroom ingestion.

If symptoms such as vomiting, diarrhea, and abdominal pain begin 5 to 6 hours or more after ingestion, mushrooms that can cause potentially life-threatening or severe toxicity (eg, A. phalloides or Cortinarius spp.) should be considered.

Other neurologic and myotoxic forms of mushroom poisoning. Care is also primarily supportive and symptomatic for most other neurologic and myologic presentations of mushroom poisoning.

Cholinergic (muscarinic) mushroom poisoning should be treated with atropine.

Intensive care may be needed for patients with myotoxic mushroom poisoning and severe rhabdomyolysis.

Pyridoxine should be given after substantial ingestion of gyromitrin-containing (false morel) mushrooms or if central nervous system toxicity is present; repeat doses may be needed. Diazepam should be administered intravenously if seizures persist despite pyridoxine in patients exposed to gyromitrin-containing (false morel) mushrooms.

Outcomes

Except for the myotoxic and false morel neurologic toxidromes, neurologic and myologic presentations of mushroom poisoning are rarely fatal. Fatalities have uncommonly occurred with other neurologic toxidromes (eg, cholinergic mushroom poisoning).

Other serious and often permanent organ dysfunction or fatalities may result from accidentally ingesting a more toxic mushroom resembling one that is hallucinogenic, edible, or conditionally edible. For example, some individuals who intend to harvest or procure “magic mushrooms” (ie, hallucinogenic mushrooms) obtain instead more toxic species, like some species of mushrooms of the genus Cortinarius, which are nephrotoxic (28). A common feature among all species in the genus Cortinarius is that young specimens have a “cortina” (veil) between the cap and the stem, hence the name, meaning curtained. The renal toxicity of these mushrooms can vary, presumably based on toxin dose and physical constitution, from mild, transient renal failure to irreversible total acute renal failure that necessitates continual dialysis (28). The nephrotoxicity of Cortinarius orellanus was first recognized in the 1950s when this mushroom was identified as the cause of a mass poisoning of 135 people in Bydgoszcz, Poland, which resulted in 19 deaths (12). Affected individuals develop an acute tubulointerstitial nephritis (with severe interstitial nephritis, acute focal tubular damage, and interstitial fibrosis). The responsible toxin was identified to be orellanine, a bipyridine N-oxide compound. Renal symptom onset is typically delayed 1 to 2 weeks after ingestion, although patients may have gastrointestinal discomfort in the latency period (12).

Factors that increase the risk of a fatal outcome include age (eg, young children or the elderly) and amount ingested.

References

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34: References especially recommended by the author or editor for general reading.

Patient Profile

Age range of presentation: Typical: all ages
Sex preponderance: No sex preponderance
Heredity: No hereditary factors
Population groups selectively affected: No population group selective affected.
Occupation groups selectively affected: No occupation group selectively affected.

ICD & OMIM codes

ICD-10: Toxic effect of ingested mushrooms, accidental (unintentional): T62.0X1A
ICD-11: Unintentional exposure to or harmful effects of other or unspecified substances chiefly nonmedicinal as to source: PB36

Intentional self-harm by exposure to or harmful effects of other or unspecified substances chiefly nonmedicinal as to source: PD05

Exposure to or harmful effects of undetermined intent of other or unspecified substances chiefly nonmedicinal as to source: PH56

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Mushroom poisoning: overview

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Clinical Categories

Neurotoxicology

	• Prevention is optimally achieved by eating only nonhallucinogenic mushrooms that are commercially cultivated for human consumption.
	• Wild mushrooms should be regularly removed from areas where young children are routinely present.
	• Illicit recreational hallucinogenic mushrooms, if used, should be kept out of reach of children.
	• Mushroom foragers should eat only one type of wild mushroom and save a sample in a dry paper bag for later identification, if this proves necessary.

Mushroom poisoning: overview …

Mushroom poisoning: overview

Introduction

Overview

Key points

Historical note and terminology

Table 1. Neurologic Components of Different Classifications of Mushroom Poisoning

Table 2. Comparison of Classifications of Mushroom Poisoning

Clinical manifestations

Presentation and course

Table 3. Neurologic Presentations of Mushroom Poisoning

Prognosis and complications

Biological basis

Etiology and pathogenesis

Table 4. Basidiomycota with Clinically Important Neurotoxins and Myotoxins

Table 5. Ascomycota with Clinically Important Neurotoxins and Myotoxins

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Outcomes

References

Contributors

Author

Patient Profile

ICD & OMIM codes

This is an article preview.
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to access the full version.

Questions or Comment?

Also in This Category

Metal neurotoxicity

Medications and substances causing headache

Mercury neuropathy

Thallium neuropathy

Occupational neurotoxicology: metals

Occupational neurotoxicology: overview

Mass poisoning events with neurotoxic agents

Para-occupational poisoning

Mushroom poisoning: overview

Introduction

Overview

Key points

Historical note and terminology

Table 1. Neurologic Components of Different Classifications of Mushroom Poisoning

Table 2. Comparison of Classifications of Mushroom Poisoning

Clinical manifestations

Presentation and course

Table 3. Neurologic Presentations of Mushroom Poisoning

Prognosis and complications

Biological basis

Etiology and pathogenesis

Table 4. Basidiomycota with Clinically Important Neurotoxins and Myotoxins

Table 5. Ascomycota with Clinically Important Neurotoxins and Myotoxins

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Outcomes

References

Contributors

Author

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Metal neurotoxicity

Medications and substances causing headache

Mercury neuropathy

Thallium neuropathy

Occupational neurotoxicology: metals

Occupational neurotoxicology: overview

Mass poisoning events with neurotoxic agents

Para-occupational poisoning

This is an article preview.
Start a Free Account
to access the full version.