Author: Matthew Turner, MD
Reviewed by: Sage Wiener, MD
Case
A 19-year-old man with no past medical history goes hiking in the woods near his college campus in search of “magic mushrooms”. He finds a patch of little brown mushrooms that look similar to the pictures of psilocybin mushrooms he saw on the internet. He eats a handful of the mushrooms back in his dorm room expecting to have a psychedelic experience. To his disappointment, his mental state is unchanged, but he does develop crampy abdominal pain, diarrhea, and vomiting six hours after the ingestion. He takes some Pepto-bismol, his symptoms improve, and he goes to sleep. The next day he develops right upper quadrant pain which worsens throughout the day prompting him to go to the ED. Testing in the ED is consistent with acute hepatitis. It turns out that the little brown mushrooms he ate were the amatoxin-containing, Galerina marginata.
This post will cover an approach to mushroom poisoning and some of the unique toxidromes
Approach to Mushroom Poisoning
Epidemiology
There are over 6,000 toxic mushroom exposures annually in the US [1]. Over ½ of exposures occurred in children less than 6 years of age. Pediatric exposures are often limited to a single bite and serious toxicity is less likely. Serious toxicity and mortality often occurs as the result of consumption of misidentified mushrooms by adults. An old adage goes, “There are old mushroom hunters and bold mushroom hunters, but there are no old, bold mushroom hunters”.
Identification
Don’t try to identify mushrooms yourself. Call poison control early for guidance. Poison control centers often have a mycologist (mushroom expert) they can call for help with identification. If a patient brings a mushroom into the ED, carefully place it in a wax paper bag and store it in a refrigerator in order to preserve it for identification by a mycologist.
History
Ask patients where the mushrooms were collected and what they looked like. This can help with identification. Ask when the mushrooms were ingested and when symptoms began in order to establish a timeline. Ask if multiple types of mushrooms were ingested or if there were other co-ingestions, including foraged plants. Ask about symptoms among others ingesting the same mushrooms. This can help differentiate mushroom poisoning from other kinds of food poisoning or other illnesses.
Pearls
The most common clinical manifestation of mushroom poisoning is acute gastroenteritis This can be caused by many different species of mushrooms [2]. This typically occurs within 6 hours of ingestion, is self limited, and requires only supportive care. Most life-threatening mushrooms have delayed presentations. Symptoms of gastroenteritis that occur greater than six hours after ingestion should alert clinicians that a life-threatening mushroom may have been consumed and should prompt further workup. An exception to this rule is Amanita smithiana, which causes acute gastroenteritis within 6 hours and delayed renal failure. Be aware that many mushroom toxins are not heat labile, so they will not be destroyed by cooking or freezing.
Poisonous Mushrooms and their Toxidromes
Cyclopeptide-containing mushrooms (Eg. Aminitia phalloides)
Toxin Amatoxin/Alpha-amanitin. There are 35 mushroom species known to contain amatoxin — Amanita phalloides is the mushroom most commonly involved in human exposures and fatalities [3].
Mechanism of Action Amatoxin is a cyclopeptide that inhibits RNA polymerase II, preventing mRNA formation and leading to apoptosis, with greatest effect on the rapidly dividing cells of the liver, GI mucosa, and renal tubular epithelium [4].
Clinical Presentation Symptom onset is 6 to 8 hours after ingestion with initial gastroenteritis followed by a quiescent period of apparent recovery. Hepatotoxicity begins 24 hours after ingestion and fulminant hepatic failure and multiorgan failure occurs within 2 to 4 days.
Management 1. GI decontamination: Activated charcoal (if ingested within 5 hours) 2. Antioxidant therapy –N-acetyl-cysteine (decreased mortality in systematic review [5]) –Cimetidine and vitamin C (Cytoprotective effects in animal models) 3. Amatoxin uptake inhibitors –Silymarin/silbinin (reduced mortality in retrospective studies [6]) –Penicillin G 4. Supportive care of liver toxicity 5. Transfer to liver transplant center
Psilocybe
Toxin Psilocybin/psilocin
Mechanism of Action Serotonin receptor agonist
Clinical Presentation Psilocybe mushrooms are often intentionally ingested for recreation or spiritual experience. Symptom onset is within 1 hour with duration of 6 to 12 hours. Patients will have sensory distortion and hallucination with euphoria or dysphoria. Look for tachycardia and mydriasis on exam.
Management Provide supportive care and consider placing patients in a dark, quiet room to minimize sensory input. Benzodiazepines may be given for agitation or anxiety [2].
Amanita muscaria
Toxin Muscimol and ibotenic acid
Mechanism of Action Muscimol is a GABA type A receptor agonist Ibotenic acid is a glutamate receptor agonist
Clinical Presentation Onset occurs in 30 minutes to 2 hours with duration of 4 to 14 hours. Common symptoms include gastroenteritis and CNS excitation or depression. Pediatric patients tend to get more glutamatergic effects and are at increased risk for myoclonus or seizures.
Management Provide supportive care and give benzodiazepines for agitation or seizures.
Inocybe and Clitocybe
Toxin Muscarine
Mechanism of Action Acetylcholine muscarinic receptor agonist
Clinical Presentation Onset is within 30 minutes with a duration up to 12 hours. Patients will have muscarinic features of the cholinergic toxidrome which can be remembered by the mnemonic, DUMBBELS (Diarrhea, Urination, Miosis, Bradycardia, Bronchorrhea, Bronchoconstriction, Emesis, Lacrimation, Salivation).
Management Provide supportive care with oxygen, suctioning, and IV fluids to maintain euvolemia. Give atropine for bradycardia or bronchorrhea (2-5 mg IV q
5 minutes titrated to resolution of bronchorrhea) [2]. Consider intubation for airway protection if unable to tolerate secretions.
Gyromitra
Toxin Gyromitrin/Monomethylhydrazine
Mechanism of Action Decreases GABA production by inhibition of pyridoxal 5’-phosphokinase (same mechanism as isoniazid toxicity) [7]
Clinical Presentation Gyromitra resembles the edible morel mushroom and is sometimes eaten by mistake. Symptom onset occurs 6 hours after ingestion. Patients will have gastroenteritis, headache, weakness, and muscle cramping. Severe ingestions can cause seizures and delayed hepatotoxicity.
Management Provide supportive care. Give benzodiazepines and pyridoxine for seizures [7].
Take Home Points
Call poison control if you suspect a toxic mushroom ingestion
Most life-threatening mushroom ingestions have delayed presentations
Provide supportive care and consider early activated charcoal
References
[1] Brandenburg, W. E., & Ward, K. J. (2018). Mushroom poisoning epidemiology in the United States. Mycologia, 110(4), 637-641. [2] Auerbach, P. S., Cushing, T. A., & Harris, N. S. (2016). Auerbach’s Wilderness Medicine E-book. Elsevier Health Sciences. [3] Vetter, J. (1998). Toxins of Amanita phalloides. Toxicon, 36(1), 13-24. [4] Enjalbert, F., Rapior, S., Nouguier-Soulé, J., Guillon, S., Amouroux, N., & Cabot, C. (2002). Treatment of amatoxin poisoning: 20-year retrospective analysis. Journal of Toxicology: Clinical Toxicology, 40(6), 715-757. [5] Poucheret, P., Fons, F., Doré, J. C., Michelot, D., & Rapior, S. (2010). Amatoxin poisoning treatment decision-making: pharmaco-therapeutic clinical strategy assessment using multidimensional multivariate statistic analysis. Toxicon, 55(7), 1338-1345. [6] Ganzert, M., Felgenhauer, N., Schuster, T., Eyer, F., Gourdin, C., & Zilker, T. (2008). Amanita poisoning–comparison of silibinin with a combination of silibinin and penicillin. Deutsche medizinische Wochenschrift (1946), 133(44), 2261-2267. [7] Michelot, D., & Toth, B. (1991). Poisoning by Gyromitra esculenta–a review. Journal of applied toxicology, 11(4), 235-243.mturner1590
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