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Hallucinogenic Mushroom Toxicity

  • Author: Louis Rolston-Cregler, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Apr 08, 2015
 

Background

Hallucinogenic mushroom toxicity is not a new phenomenon: Hallucinogenic fungi have been used in divinatory or religious contexts for at least 3000 years. However, it was not until the 1950s that the involved species of fungi were identified and the chemical nature of the active substances was determined.[1]

Consumption of hallucinogenic mushrooms continues to be popular today in some settings. Motives for their use include simple experimentation; a desire to enhance routine experiences, emotions, or social interactions; to disconnect from reality; to induce visions; as a psychotherapeutic tool; or for mystical or spiritual reasons.[2]

For the most part, mushrooms with significant psychoactive effects fall into the following 2 groups[3] :

  • Mushrooms containing ibotenic acid and muscimol (isoxazoles) – Amanita gemmata, Amanita muscaria (also called fly agaric or soma), and Amanita pantherina (also called panther or panther amanita); these are not to be confused with the deadly Amanita phalloides, Amanita verna, and Amanita virosa.
  • Mushrooms containing psilocybin – Psilocybe caerulipes, Psilocybe cubensis, Gymnopilus spectabilis, Panaeolus species (eg, Panaeolus foenisecii), and Psathyrella foenisecii

For centuries, A muscaria has been consumed in central Asia as a hallucinogen. Some Siberian tribes report that 3 fresh A muscaria mushrooms can be lethal, whereas others claim that eating as many as 21 of these mushrooms is safe. Various hallucinogenic mushrooms containing ibotenic acid and muscimol or psilocybin are found in the New World. Reports of toxicity associated with this group of mushrooms have increased as a consequence of their growing popularity as hallucinogens.[4]

The timing of symptom onset is important for distinguishing life-threatening or severe mushroom poisonings from less serious poisonings (eg, those involving hallucinogenic mushrooms), which typically have an onset of symptoms well within 5 hours of ingestion. If symptoms such as vomiting, diarrhea, and abdominal pain begin 5 hours or more after ingestion, mushrooms that can cause potentially life-threatening or severe toxicity (eg, A phalloides or Cortinarius spp) should be considered (see Presentation).

No particular diagnostic procedures are available or needed for most patients. Laboratory studies can be helpful in identifying complications of hallucinogenic mushroom abuse. Identification of the mushroom by a mycologist is desirable (see Workup).

Care is primarily supportive. Symptoms usually subside in 6-8 hours, though some may take as long as several days to resolve fully. Benzodiazepines may be used for sedation and treatment of panic attacks, hallucinations, and seizures. Psychiatric consultation and evaluation may be needed in some cases (see Treatment).

For patient education resources, see the Poisoning - First Aid and Emergency Center, as well as Poisoning and Activated Charcoal.

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Pathophysiology

A muscaria,A pantherina, and A gemmata contain ibotenic acid, muscimol, and muscazone. These isoxazole derivatives are present in various concentrations, depending on environmental conditions, the maturity of the fungus, and the season of the year. Ibotenic acid and muscimol are relatively stable: Toxic activity has been maintained in dried plants for as long as 7 years.

Other toxins are probably present in these mushrooms; pure extracts of ibotenic acid or muscimol do not reproduce all of the symptoms observed after their ingestion. Although muscarinic acid originally was isolated from A muscaria, as the name suggests, muscarine does not appear to be of particular clinical significance in A muscaria poisoning; in fact, anticholinergic findings may be observed in this setting. A muscaria also lacks the amatoxins seen in other Amanita species.

Ibotenic acid resembles glutamic acid and is an agonist at central glutamic acid receptors; its decarboxylated derivative, muscimol, is an agonist at gamma-aminobutyric acid (GABA) receptors. The central effects of these hallucinogenic mushrooms are thought to be attributable to these actions.[1] Both ibotenic acid and muscimol can cross the blood-brain barrier.[5]

Many of the central nervous system (CNS) effects of muscimol (eg, sedation) are ascribed to its ability to act as a GABA agonist. By comparison, ibotenic acid is more of a CNS stimulant, by virtue of its action on glutamic acid receptors. In humans, most of the ibotenic acid ingested is excreted unchanged in the urine, with only some of it being metabolized to muscimol. About one third of the muscimol ingested is excreted unchanged, another third is conjugated, and the remaining third is oxidized.[5]

The Psilocybe, Gymnopilus, Panaeolus, and Psathyrella species previously mentioned (see Background) contain the indoles psilocybin and psilocin. Psilocin and its phosphate ester, psilocybin, are similar in structure to lysergic acid diethylamide (LSD). They are structural analogues of serotonin (5-hydroxytryptamine [5-HT]); thus, hallucinogenic effects probably are mediated through effects on serotonergic receptors.[1]

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Etiology

Hallucinogenic mushroom toxicity is caused by ingestion of fungi containing ibotenic acid, muscimol, psilocybin, or psilocin. Circumstances that could lead to such ingestion include the following:

  • Adults and adolescents seeking to achieve a state of intoxication – This is the most common reason for ingesting these mushrooms [3]
  • Incorrect mushroom identification by a naive forager (eg, a novice mushroom harvester or an immigrant who mistakes a local poisonous variety for an edible variety native to his or her homeland)
  • Intentional ingestion by a suicidal person
  • Unintentional ingestion by a child who found mushrooms growing in yards or outdoor play areas
  • Foul play, in which an individual is poisoned by someone else
  • Inadvertent poisoning from dried mushrooms purchased on the Internet or from other sources where the composition of the mushroom is unreliable or where the mushroom might be contaminated with unknown toxic compounds
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Epidemiology

United States statistics

Determination of the frequency of hallucinogenic mushroom toxicity is limited by the lack of a national reporting system or registry for mushroom poisoning and by the likelihood that many affected individuals may never seek medical attention. However, estimates based on small studies or surveillance systems using self-reporting are available.

In a study of 174 adolescents with a history of substance abuse, 45 (26%) reported having used hallucinogenic mushrooms at some point in their life, often in combination with alcohol or marijuana.[6]

On the basis of data collected from September 2008 to December 2009, the Youth Risk Behavior Surveillance System reported that 8% of students had used a hallucinogenic drug (eg, LSD, phencyclidine [PCP; angel dust], mescaline, or mushrooms) at least once in their life.[7] Hallucinogen use was more common among males and whites than among females and African Americans and Hispanics.

In 2009, 5902 mushroom ingestions were reported to the National Poison Data System of the American Association of Poison Control Centers (AAPCC).[8] Of these cases, 77% involved mushrooms of unknown type. Mushrooms containing ibotenic acid accounted for 61 cases, with 52 of the 61 involving single-substance exposures and 5 (10%) of these 52 involving children younger than 6 years. About 60% of all cases of ibotenic acid mushroom poisoning resulted from intentional ingestion, and 71% were treated at a healthcare facility.

One death was attributed to ibotenic acid mushrooms in 2004, whereas no deaths were reported in the preceding 12 years or the subsequent 5 years of data collection by the AAPCC. The manner in which A muscaria involvement in this fatality was confirmed was not described, and the fact that the mushroom was purchased on the Internet raised questions about the integrity of the contents.[9]

Age-related demographics

Few data exist on the age distribution of hallucinogenic mushroom users; however, some general observations may be made.

Adults are frequently involved as foragers for edible mushrooms; because of errors in identification, they may ingest toxin-containing lookalike mushrooms. Adults and adolescents may also be poisoned when they intentionally consume mushrooms, picked from the ground or purchased dried, to achieve intoxication. In particular, college students are known to abuse psilocybin mushrooms.[10, 11, 12]

Young children may experience mushroom poisoning when they unintentionally eat mushrooms found outside, typically in yards or outdoor play areas. Reports of seizurelike activity have been reported for children but are not typical in adults.[13, 14]

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Prognosis

Use of hallucinogenic mushrooms rarely results in life-threatening symptoms.[15] The prognosis is generally excellent. Many patients who ingest these mushrooms exhibit only minor symptoms or no symptoms at all. Symptoms typically are mild to moderate in severity and self-limited, though some effects of ibotenic acid poisoning, particularly headache, may take 2 days or more to resolve.[13, 14] Patients commonly recover without drug therapy. Fatalities from hallucinogenic mushroom poisoning are rare.

From 1999 to 2009, 35 deaths due to mushrooms were reported to US poison control centers through the AAPCC, and 1 death was attributed to mushrooms containing ibotenic acid.[9] The patient who died was a 44-year-old man who ate 6-10 freeze-dried mushrooms, purported to be A muscaria, which he obtained from the Internet. Paramedics found him in cardiac arrest, and he eventually died 10 days later with anoxic brain injury. The report did not mention whether and how the mushroom was confirmed to be A muscaria.

Of the 52 cases of single-substance exposure to ibotenic acid−containing mushrooms reported by US poison control centers through the AAPCC in 2009, 27% had no or minor effects, 37% had moderate effects, 7% had major effects, 29% had unknown outcomes.[8]

In Slovenia, a 48-year-old man consumed several A muscaria mushrooms and began to experience vomiting and lethargy within 30 minutes.[16] He was found comatose, having a seizurelike episode; he then awoke and was oriented 10 hours after ingestion. By 18 hours after ingestion, the patient’s condition had deteriorated, and he became confused and uncooperative. Paranoid psychosis with visual and auditory hallucinations appeared, persisted for 5 days, and resolved with short-term drug therapy, without any subsequent recurrence.

In Poland, 5 young adults aged 18-21 years consumed dried A muscaria and a can of beer, and 4 of the 5 experienced heightened visual and auditory perceptions beginning about 20 minutes after ingestion.[17] Of these 4, 1 experienced severe hallucinations and lost consciousness, according to the others, who induced vomiting and gave her liquids. The next day, this person came to a hospital complaining of tiredness and gastric pain. She was evaluated, observed for several days, and sent home. No confirmation of the mushrooms was performed.

Also in Poland, 2 women ate 5 fried caps of A pantherina (later confirmed) and developed nausea, stomachache, diarrhea, and vomiting within 2 hours.[18] They subsequently developed ataxia, waxing and waning obtundation, altered perceptions, hyperkinetic movements, and altered speech. One patient’s symptoms lingered for several days, whereas the other had no symptoms at 6 hours after ingestion; the latter received activated charcoal and intravenous (IV) fluids.

In a series of 9 children aged 1-6 years who ingested A muscaria or A pantherina and were treated at a hospital in Seattle, Washington, symptoms developed within 30-180 minutes (median, 45 minutes) after ingestion and lasted for 4-14 hours (median, 9 hours).[13] Symptoms included lethargy (4 children), unresponsiveness (1), comalike sleep (1), ataxia (2), abnormal movements (3), tonic-clonic seizures (3), and agitation, babbling, or hysteria (5). All 9 children recovered uneventfully within 12 hours after admission.

Descriptions of cases reported to the toxicology section of the North American Mycological Association illustrate the typical course of many mushroom poisonings; however, these cases were not necessarily observed by health care professionals.[19]

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Contributor Information and Disclosures
Author

Louis Rolston-Cregler, MD Resident Physician, Department of Emergency Medicine, SUNY Downstate Medical Center, Kings County Hospital Center

Louis Rolston-Cregler, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Medical Student Association/Foundation, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association, Student National Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Acknowledgements

William Banner Jr, MD, PhD Medical Director, Oklahoma Poison Control Center; Clinical Professor of Pharmacy, Oklahoma University College of Pharmacy-Tulsa; Adjunct Clinical Professor of Pediatrics, Oklahoma State University College of Osteopathic Medicine

William Banner Jr, MD, PhD, is a member of the following medical societies: American College of Medical Toxicology

Disclosure: Nothing to disclose.

Peter A Chyka, PharmD, FAACT, DABAT Professor and Executive Associate Dean, College of Pharmacy, University of Tennessee Health Science Center

Peter A Chyka, PharmD, FAACT, DABAT is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Clinical Pharmacy, and American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Timothy E Corden, MD Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society

Disclosure: Nothing to disclose.

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT Associate Clinical Professor; Medical and Managing Director, South Texas Poison Center, Department of Surgery/Emergency Medicine and Toxicology, University of Texas Health Science Center at San Antonio

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Clinical Toxicologists, American College of Emergency Physicians, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, Society for Academic Emergency Medicine, and Texas Medical Association

Disclosure: Nothing to disclose.

Diane F Giorgi, MD, FACEP Attending Physician, Department of Emergency Medicine, Brooklyn Hospital Center

Diane F Giorgi, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American Association of Women Emergency Physicians, American College of Emergency Physicians, and American College of Physicians

Disclosure: Nothing to disclose.

Michael Hodgman, MD Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare

Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society

Disclosure: Nothing to disclose.

C Crawford Mechem, MD, MS, FACEP Professor, Department of Emergency Medicine, University of Pennsylvania School of Medicine; Emergency Medical Services Medical Director, Philadelphia Fire Department

C Crawford Mechem, MD, MS, FACEP is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Michael E Mullins, MD Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine

Michael E Mullins, MD is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Emergency Physicians

Disclosure: Johnson & Johnson stock ownership None; Savient Pharmaceuticals stock ownership None

Jeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center

Disclosure: Merck Salary Employment

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Fly agaric (Amanita muscaria).
Amanita pantherina.
Amanita muscaria.
Amanita muscaria var. guessowii with yellow cap surface, from Massachusetts.
Amanita muscaria var. formosa sensu Thiers, from Oregon.
 
 
 
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