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Clinical manifestations and evaluation of mushroom poisoning

Clinical manifestations and evaluation of mushroom poisoning
Literature review current through: May 2024.
This topic last updated: Sep 28, 2023.

INTRODUCTION — The clinical manifestations of mushroom poisoning syndromes and the diagnostic evaluation of patients with mushroom poisoning are reviewed here.

The general management of mushroom poisoning and the diagnosis and treatment of poisoning caused by potentially lethal amatoxin-containing mushrooms (eg, Amanita phalloides) are discussed in detail separately:

(See "Management of mushroom poisoning (except amatoxin-containing mushrooms)".)

(See "Amatoxin-containing mushroom poisoning (eg, Amanita phalloides): Clinical manifestations, diagnosis, and treatment".)

EPIDEMIOLOGY — There are over 10,000 species of mushrooms worldwide, but of these, only 50 to 100 are potentially toxic [1-3]. In the United States, approximately 6000 to 8000 mushroom exposures occur annually [4-6]. The vast majority of exposures result in no toxic effects or only mild or moderate symptoms; deaths are rare. Over one-half of mushroom ingestions occur in children less than six years of age. In most cases, pediatric exposures are limited to a partial or single bite of nontoxic or minimally toxic mushrooms (picture 1 and picture 2). Even in the uncommon cases of amatoxin-containing mushroom exposures (picture 3 and picture 4), children typically do well because of the small amount of toxins ingested. In the United States, no pediatric fatalities due to ingestion of a single mushroom have been reported in over 25 years of National Poison Data System surveillance [3,7].

When serious toxicity or mortality after mushroom ingestion does occur, it typically results from consumption of misidentified mushrooms by foraging adults and others who shared the meal [3,4,8]. A common scenario involves amateur mushroom hunters or recent immigrants who mistake a toxic mushroom for an edible variety with similar morphologic features (eg, Gyromitra esculenta mistaken for Morchella esculenta (picture 5) or Amanita species (picture 3 and picture 4) mistaken for Agaricus species) [3,9]. Outbreaks of mushroom poisoning caused by self-harvesting of toxic species can occur when a variety of factors, including optimal weather conditions (rainfall and sunlight, along with soil and temperature conditions), lead to increased growth of mushroom species [10]. Public health surveillance by regional poison control centers and other agencies are critical in identifying these outbreaks and educating the public and health care providers of the toxic potential.

In up to 80 percent of cases, the species of mushroom ingested is not identified [4]. Thus, one must rely upon the presenting signs and symptoms to aid in the clinical diagnosis and to guide treatment recommendations. (See 'Mushroom poisoning syndromes' below and 'Evaluation' below and "Management of mushroom poisoning (except amatoxin-containing mushrooms)".)

MUSHROOM POISONING SYNDROMES

Concern for serious toxicity depends on timing of symptom onset — Classification of poisoning based upon clinical presentation (table 1) and timing of onset of symptoms is most helpful in achieving a working diagnosis, assessing the clinical concern for potentially serious toxicity, and guiding further treatment. There are 12 groups of identified mushroom toxins found in multiple different mushroom species with 14 described clinical syndromes (table 1). Mushrooms that only cause acute toxicity (<6 hours after ingestion) are rarely life threatening. Mushrooms that cause symptoms more than six hours after consumption are associated with serious and potentially lethal toxicity. However, early symptoms do not exclude the possibility of consumption of potentially lethal mushrooms, especially if more than one type of mushroom was eaten.

Acute symptom onset (<6 hours after ingestion)

Acute gastroenteritis — A variety of mushroom species cause acute gastroenteritis soon after ingestion without any further toxicity. Often these exposures occur when children take a bite of a "little brown mushroom" (picture 1) while playing outside in the backyard [2,3]. Chlorophyllum molybdites is one of the more common "backyard mushrooms" [11].

With ingestion of these mushrooms, symptoms occur within 1 to 3 hours and include nausea, vomiting, and abdominal cramping as well as diarrhea [2]. Close attention to the history of ingestion and the timing associated with the onset of symptoms is important to differentiate acute gastroenteritis from the more concerning delayed gastroenteritis that may indicate consumption of a more lethal variety of mushroom toxins (eg, amatoxins, gyromitrin, or orellanine) [12]. (See 'Delayed gastroenteritis and liver toxicity' below and 'Delayed gastroenteritis, seizures, and liver toxicity' below and 'Delayed renal failure' below and 'Delayed rhabdomyolysis' below.)

An exception to this general rule applies to the Northwest United States, where patients who consume Amanita smithiana may develop acute gastroenteritis within two hours of ingestion, which is then followed by renal failure approximately 24 hours later. (See 'Acute gastroenteritis and delayed renal failure' below.)

Care of gastroenteritis is supportive and includes rehydration and assessment for electrolyte abnormalities. Rarely, hypovolemic shock may occur [13]. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Vomiting and diarrhea'.)

Hallucinations — The hallucinogenic effects produced by the ingestion of mushrooms containing psilocybin and psilocin (also known as "magic mushrooms") have been known for thousands of years by indigenous communities in North and South America [3]. Specific mushroom species that contain psilocybin and psilocin include Psilocybe, Conocybe, Gymnopilus, and Panaeolus [2]. These mushrooms grow throughout the United States and Europe, especially in warm, moist climates and are commonly abused for recreational purposes [14].

Psilocybin and psilocin are stable alkaloids from the chemical class tryptamines, which are chemically related to lysergic acid diethylamide (LSD) and serotonin. They are present in small amounts in both dried and fresh mushrooms [2]. Hallucinatory effects require the ingestion of several caps of fresh mushrooms (eg, 3 to 60 caps) and up to 2 g of dried mushrooms.

Feelings of euphoria and subsequent sensory distortion develop within 30 minutes to 2 hours after ingesting these mushrooms and are commonly associated with mild tachycardia and dilated pupils [2,3]. Frank hallucinations may also occur. The most common symptoms associated with emergency department presentation after "magic mushroom" consumption include anxiety, panic, suspiciousness, and paranoia [15]. The duration of symptoms is typically 4 to 12 hours after mushroom consumption. Treatment is supportive. Benzodiazepines may be necessary for anxiety or panic provoked by the psychoactive effects. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Agitation, delirium, and/or hallucinations'.)

CNS excitation and depression — This syndrome is caused by muscimol and ibotenic acid which are concentrated in the caps of Amanita muscaria, Amanita pantherina, and other related mushroom species (picture 6A-B) [16-18]. A. muscaria mushrooms are the prototypic large red or orange capped mushroom with white plaques or spots. These mushrooms are also known as fly agaric mushrooms because of their ability to attract and kill flies that land on them. A. muscaria and A. pantherina species have been used for thousands of years because of their psychoactive effects, and cases of poisoning still occur in individuals who ingest them for their hallucinatory effects. The toxins ibotenic acid and muscimol are water-soluble. Peeling the skin of the cap, parboiling the mushrooms, and discarding the water may detoxify the mushrooms prior to consumption [3].

Ibotenic acid and muscimol have very similar chemical structures, but opposite clinical effects [3]. Muscimol is a central nervous system (CNS) depressant with structural similarities to gamma aminobutyric acid (GABA). In contrast, ibotenic acid has excitatory effects at glutamic acid receptors in the CNS. Mushrooms in this class (including A. muscaria) do not contain sufficient muscarine to cause cholinergic effects. (See 'Cholinergic poisoning' below.)

Clinical findings typically occur within 30 minutes to 3 hours of ingestion and include [18-20]:

Somnolence, coma

Hallucinations

Dizziness

Dysphoria

Bizarre behavior

Seizures (primarily in children) [21]

Salivation

Nausea, vomiting, diarrhea, and abdominal cramping

Treatment of poisonings in this mushroom group is supportive and should include prompt management of delirium, agitation, or seizures and hydration in a monitored setting. Toxicity usually lasts between 4 and 24 hours. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Agitation, delirium, and/or hallucinations' and "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Seizures' and "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Vomiting and diarrhea'.)

Cholinergic poisoning — Cholinergic excess results from the ingestion of muscarine, a toxin present in many species of mushrooms throughout the world [2,3]. Among these, the species Inocybe and Clitocybe are frequently the source of poisoning. They commonly grow on lawns and in parks.

Some species of Amanita, including Amanita muscaria (picture 6A-B), do contain very small amounts of muscarine, but not enough to cause cholinergic symptoms. (See 'CNS excitation and depression' above.)

Muscarine is structurally similar to acetylcholine and causes toxicity by binding to postganglionic cholinergic neurons in the autonomic nervous system. Muscarine does not readily cross the blood-brain barrier.

Clinical effects usually begin within 30 minutes after ingestion. Patients develop bradycardia, diaphoresis, salivation, lacrimation, bronchospasm, bronchorrhea, and incontinence. Unlike other cholinergic poisoning (eg, pesticide cholinesterase inhibitors), muscarine toxicity is not typically life-threatening and is usually short-lived unless large amounts of mushrooms were consumed [22]. However, death due to refractory bradycardia and shock occurring 10 hours after mushroom consumption in an adult has been described [23].

Treatment of muscarine poisoning consists of administration of anticholinergic agents (atropine or glycopyrrolate) and intravenous fluids to manage dehydration. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Cholinergic excess'.)

Disulfiram-like reaction — The toxin coprine, when ingested before consumption of ethanol, results in a disulfiram-like reaction [2,3,24]. Coprinus atramentarius, the "inky cap" mushroom, and related species (picture 7) are most commonly associated with this syndrome. Coprine is heat-stable, so boiling or cooking the mushrooms does not prevent toxicity.

The metabolites of coprine, including 1-aminocyclopropanol and cyclopropanone hydrate, irreversibly inhibit aldehyde dehydrogenase [2,3,24]. This effect causes a marked elevation of blood aldehyde when ethanol is ingested several hours to seven days after Coprinus mushroom consumption. However, if alcohol is ingested at the same time as coprine-containing mushrooms, toxicity often does not occur or is lessened because the metabolism of coprine is slower than the normal hepatic elimination of ethanol.

Clinical effects usually occur within two hours of ethanol ingestion and include:

Headache

Flushing of the face, neck, and trunk

Nausea and vomiting

Tachycardia

Palpitations

Chest pain

Dyspnea

Marked apprehensiveness

Rarely, hypotension, cardiac dysrhythmia, confusion, and/or coma

Treatment of toxicity is supportive. Clinical findings are self-limited and typically resolve after three to six hours, although, they can rarely persist as long as 24 hours [2]. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Vomiting and diarrhea'.)

Alcohol intolerance can also be precipitated by mushroom species other than Coprinus atramentarius (eg, Lepiota aspera). Although the pathophysiology of intolerance and toxicity is not well characterized, the treatment is the same [25].

Acute rhabdomyolysis — Certain mushroom species from the Russula family (eg, R. subnigrans) that are found throughout Europe and Asia can cause acute onset of rhabdomyolysis within hours after ingestion [26-28]; delayed rhabdomyolysis has been reported as well. Treatment is supportive. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Rhabdomyolysis'.)

Cycloprop-2-ene carboxylic acid is proposed as the potential myotoxin [26].

Delayed symptom onset (>6 hours after ingestion)

Acute gastroenteritis and delayed renal failure — Mushrooms that contain allenic norleucine, including Amanita smithiana (found in the Pacific Northwest), and other Amanita species found in France, Spain, Portugal, Germany, Italy, and Japan may cause acute renal failure [29-33]. Allenic norleucine is a heat-stable toxin (ie, cooking does not prevent toxicity) that causes renal tubular necrosis. Amanita smithiana may be mistaken for the edible mushroom Tricholoma magnivelare, also called the Matsutake mushroom, which is used extensively in Japanese cooking and has a similar habitat and appearance (picture 8). Unlike Cortinarius species, these mushrooms also cause gastroenteritis, typically within 2 to 6 (but up to 12) hours of ingestion. Evidence of renal toxicity is usually present at 12 to 24 hours after ingestion, suggesting that the renal injury occurs acutely after mushroom consumption. The initial manifestation of kidney failure is decreased urine output, which typically develops three to six days after ingestion. Most patients will recover full renal function with general supportive care over several weeks to months.

Treatment should consist of general supportive care for acute kidney injury with close monitoring of the serum creatinine. Hemodialysis is occasionally required as a temporary measure for two to five weeks, and in one case, it was required for six months [29,32,33]. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Renal failure'.)

Delayed gastroenteritis and liver toxicity — Delayed onset of vomiting and diarrhea approximately 6 to 12 hours after mushroom ingestion followed by progressive liver toxicity is characteristic of amatoxin-containing mushrooms. These highly toxic mushrooms include species from three different genera: Amanita (picture 3 and picture 4), Galerina, and Lepiota, all of which grow primarily in Europe and North America. The vast majority of fatalities after mushroom ingestion are associated with exposures to Amanita species. (See "Amatoxin-containing mushroom poisoning (eg, Amanita phalloides): Clinical manifestations, diagnosis, and treatment", section on 'Amatoxin-containing mushrooms'.)

Toxicity typically consists of three distinct clinical phases (see "Amatoxin-containing mushroom poisoning (eg, Amanita phalloides): Clinical manifestations, diagnosis, and treatment", section on 'Clinical manifestations'):

The first phase typically starts more than six hours after mushroom consumption and includes gastrointestinal effects which include a cholera-like diarrhea, vomiting, abdominal pain and subsequent dehydration.

The second phase begins 24 to 36 hours after ingestion and is a quiescent interval where the patient typically improves with regard to symptoms although there may be laboratory evidence of evolving hepatotoxicity.

During the third phase of poisoning, more than two days after mushroom consumption, progressive hepatic insufficiency occurs, characterized in severe cases by coagulopathy, acidosis, encephalopathy proceeding to hepatic coma (seizures may occur), hemorrhage, renal failure, and, within four to seven days, death.

Aggressive gastrointestinal decontamination, including interruption of enterohepatic circulation of the toxin, and supportive care are the mainstays of therapy. The treatment for amatoxin-containing mushroom exposures is discussed in greater detail separately. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Vomiting and diarrhea' and "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Liver failure' and "Amatoxin-containing mushroom poisoning (eg, Amanita phalloides): Clinical manifestations, diagnosis, and treatment", section on 'Management'.)

Delayed gastroenteritis, seizures, and liver toxicity — In most patients exposed to Gyromitra species, gastrointestinal symptoms predominate and develop approximately six hours after ingestion (although onset of symptoms sometimes occurs earlier). With severe poisoning, neurologic symptoms, including vertigo, ataxia, tremors, weakness and seizures can develop in conjunction with hepatotoxicity [2,3,34-36]. Gyromitrin is present in many mushrooms of the Gyromitra genus, with Gyromitra esculenta (picture 5) being one of the most commonly ingested species. These mushrooms grow in North America, Europe, and Asia. Paxina species, Sarcosphaera coronaria, and Cyathipodia micropus also contain gyromitrin, but are less commonly encountered.

Toxicity of the gyromitrin-containing mushrooms varies by geographic location. Toxicity from gyromitrin-containing mushrooms can be differentiated from toxicity due to hepatotoxic Amanita species based on seasonal considerations: Gyromitra mushrooms grow in the spring and early summer, whereas Amanita species grow in the fall. The appearance of the mushrooms can also be used to differentiate the two species. Gyromitra are described as having a "brain-like" appearance whereas Amanita are typically "umbrella-shaped" and have gills [36].

Most commonly, Gyromitra esculenta (false morel) is mistaken for the similar appearing Morchella esculenta (morel). Although certain methods of preparation may limit the toxicity of gyromitrin-containing mushrooms (eg, parboiling), it is still recommended that all members of this family be avoided.

Gyromitrin is hydrolyzed by liver alcohol dehydrogenase into acetaldehyde and monomethyl hydrazine, a substance similar to the hydrazines in rocket fuel [35]. The mechanism of toxicity is inhibition of pyridoxal phosphate-related enzymatic reactions, which causes functional pyridoxine deficiency and ultimately leads to a depletion of the inhibitory neurotransmitter, gamma-aminobutyric acid (GABA). Thus, delayed seizures intractable to anticonvulsant therapy may result.

Clinical manifestations of gyromitrin toxicity include:

Delayed gastroenteritis (nausea, vomiting, abdominal pain, diarrhea) typically beginning 6 to 10 hours after ingestion

Headaches, weakness, and muscle cramping

Delayed seizures

Delayed hepatoxicity, including liver failure

Hemolysis (uncommon)

Methemoglobinemia (uncommon)

Most patients return to baseline health within a couple of days. However, mortality up to 10 percent has been reported in Eastern Europe [2]. Prompt treatment of seizures, hemolysis, and methemoglobinemia along with supportive care of gastroenteritis and hepatotoxicity are key aspects of treatment. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Seizures' and "Methemoglobinemia", section on 'Methylene blue (MB)'.)

Delayed renal failure — The toxins orellanine, orellinine, cortinarin A, and cortinarin B, have been associated with acute renal failure occurring 3 to 20 days after ingestion of mushrooms, such as Cortinarius orellanus, Mycena pura, and Omphalatus orarius [2,3,37]. This syndrome has been described in the Pacific Northwest United States, Europe, and Japan.

The toxin orellanine has chemical similarities with the herbicides paraquat and diquat, and is concentrated in the kidney where it produces interstitial nephritis and tubulointerstitial fibrosis [38]. The cortinarins appear to have similar toxic effects but may require conversion by cytochrome oxidases in the liver to toxic metabolites [3]. Although orellanine is typically not detectable in blood or urine by the time patients come to medical attention, it can be detected in renal tissue obtained by biopsy up to six months after exposure [39].

Initial symptoms due to Cortinarius ingestion are nonspecific and commonly consist of a headache, general malaise, nausea, vomiting, diarrhea, abdominal pain, myalgias, and dizziness that occur within four days of mushroom consumption [40]. Subsequently, renal toxicity is heralded by lumbar and back pain, oliguria, or polyuria with active urinary findings of pyuria, hematuria, and/or proteinuria.

Treatment should consist of general supportive care for acute kidney injury with close monitoring of the serum creatinine [2,3]. The impairment in renal function is frequently severe. In a systematic review of Cortinarius species mushroom poisoning in 90 patients, 62 patients developed evidence of renal toxicity [40]. Forty-six patients required hemodialysis, 10 developed end stage renal failure, and 12 received kidney transplantation. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Renal failure'.)

Delayed rhabdomyolysis — The mushroom Tricholoma equestre, also known as "man on horseback," has been reported to cause rhabdomyolysis when ingested in large amounts or in repeat meals [41-43]. T. equestre can be found throughout Europe or in North America in the late summer or early fall. The onset of symptoms from T. equestre poisoning typically occurs within 24 to 72 hours after mushroom consumption and include general fatigue with nausea, myalgias, and progressive weakness. Laboratory abnormalities include an elevated serum potassium and creatine kinase. Although the myotoxin contained in T. equestre remains unknown, extracts from this mushroom have produced muscle toxicity in an animal model. Treatment is supportive. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Rhabdomyolysis'.)

Delayed severe rhabdomyolysis with acute kidney injury and cardiomyopathy has also been described after ingestion of certain mushroom species from the Russula family (eg, R. subnigrans) found in Europe and Asia [26,44].

Rare manifestations — In addition to the above relatively common syndromes, several other disorders have been rarely described.

Erythromelalgia — Mushrooms that contain acromelic acid (eg, Clitocybe acromelalga and C. amoenolens) have been associated with the following clinical findings [3,45,46]:

Sensory abnormalities, including distal paresthesias, allodynia (severe tactile pain), and burning pain in the extremities

Erythema of the affected limbs

Limb edema

Symptoms are often delayed after ingestion of the mushrooms by more than 24 hours and may persist for several months in affected individuals. Persistent numbness and paresthesias have been reported in some individuals. Poisonings associated with Clitocybe species typically lack gastrointestinal symptoms. Because of the long latency between symptom development and consumption of the toxin it is often difficult to identify the specific source of exposure [46]. Treatment is primarily supportive although use of nicotinic acid has been proposed. (See "Management of mushroom poisoning (except amatoxin-containing mushrooms)", section on 'Erythromelalgia'.)

Delayed encephalopathy — Two rare scenarios have been associated with delayed encephalopathy after mushroom consumption [3]:

Patients with chronic renal failure, especially those receiving hemodialysis, who ingest Pleurocybella porrigens may develop delayed severe encephalopathy with altered mental status, seizures and respiratory failure from one to several days after consumption [47]. This mushroom is found in North America, northern Europe, and Japan, where it is sometimes added to miso soup. Boiling the mushroom appears to extract the toxin.

Case series describe delayed encephalopathy with ataxia after consumption of the mushrooms Hapalopilus rutilans [48,49]. The patients presented with decreased visual acuity, diplopia, nystagmus, lethargy, and weakness and were also noted to have elevated aminotransferase levels and creatinine concentrations in association with purple colored urine. Polyporic acid was identified as the likely toxin in one group of patients [48].

Immune-mediated hemolytic anemia — Consumption of Paxillus involutus has been associated with an auto-immune hemolytic anemia hemoglobinuria, and acute kidney injury [3,50-53]. Deaths in patients who developed diffuse intravascular hemolysis, hemorrhagic gastroenteritis, and renal or liver failure have been described [52]. Production of immune complexes with mushroom components that bind to red blood cells and cause complement-mediated hemolysis is the suspected pathophysiology; this etiology is supported by the identification of specific IgG antibodies in one affected patient [53]. In addition, the anti-erythrocytic antibody, auto-anti e, and prior history of hepatitis C were determined to be risk factors for the syndrome in two other patients [52].

Allergic bronchioalveolitis — Inhalation of spores from the puffball mushrooms (Lycoperdon species) has produced a diffuse pneumonitis called lycoperdonosis, which occasionally progresses to reticulonodular infiltrates and respiratory failure [3,54]. The type of exposure that produces lycoperdonosis is typically intense including placement of the mushroom in the nose to stop epistaxis, intentional insufflation, and aerosolizing large amounts of the spores by stomping on the mushrooms [54,55]. Treatment consists of the administration of corticosteroids and systemic antifungal agents.

Shiitake dermatitis — Shiitake dermatitis occurs after ingestion of raw or undercooked shiitake mushrooms [56,57]. Dermatitis is associated with the ingestion of lentinan, a polysaccharide component of shiitake species that is destabilized by heat. While classically associated with dermatitis in Japan, China and Korea, dermatitis is increasingly reported outside of Asia as cultivation and ingestion of shiitake mushrooms has increased worldwide.

Shiitake dermatitis may result from mushroom ingestion or from handling the shiitakes, which can cause an allergic contact dermatitis. Dermatitis is characterized by pruritic, erythematous, flagellate eruptions on either the trunk or the extremities (picture 9) and may appear from two hours to five days after consumption and last up to three weeks [57]. Treatment is supportive. Corticosteroids and antihistamines can be used in severe cases.

EVALUATION — Signs and symptoms may point to a specific type of mushroom poisoning (table 1). A regional poison control center should be contacted to discuss likely mushroom species ingested based upon clinical findings, identification of any mushrooms available for analysis, and treatment of specific toxic effects. Most poison control centers maintain active call lists of mycologists who are knowledgeable concerning local prevalence of mushroom genera and species and can assist in mushroom identification. (See 'Regional poison control centers' below.)

History — Key elements of the patient’s history may help determine which species of mushroom was ingested as well as guide therapy. Important questions include:

Were the mushrooms collected in a field, a pasture, or along or underneath trees? – Many of the major toxic mushrooms (eg, Amanita phalloides (picture 3), Amanita bisporigera (picture 4), Gyromitra esculenta (picture 5), Cortinarius species) tend to grow in woodlands and are often found in deciduous forests [58]. Growing season as well as geographic variation may help an expert identify particular mushrooms [34,36].

What type of tree, if any, was the mushroom on or near, and was the tree living or dead? Many mushrooms with a variety of toxicities grow on dead stumps. Amanita species, in particular Amanita phalloides, may grow under or near oak or pine trees.

Was more than one type of mushroom collected?

How long after ingestion did symptoms develop? – Symptoms that develop more than six hours after ingestion indicate poisoning with potentially lethal mushroom toxins (eg, amatoxin (picture 3 and picture 4), gyromitrin (picture 5), or orellanine). Three caveats must be understood in relation to the six-hour timeframe as follows:

Amatoxin-containing mushrooms can cause symptoms before six hours, albeit rarely.

Mushroom foragers often collect more than one type of mushroom and symptom onset before six hours does not rule out concurrent ingestion of a more dangerous mushroom.

In the United States Pacific Northwest, Amanita smithiana poisoning may produce gastroenteritis symptoms before six hours.

How much was eaten? – Information about the amount of mushrooms ingested may be useful in predicting the course and degree of poisoning once the patient becomes symptomatic.

Were the mushrooms ingested for recreational hallucinatory effects (eg, mushrooms containing psilocybin or muscimol and ibotenic acid)?

Were the mushrooms eaten at more than one meal? – Symptoms may be the result of an earlier ingestion rather than the most recent ingestion which increases the likelihood of life-threatening poisoning.

What did the mushroom look like? – If no sample is available for identification, then a description may suggest the potential for serious, life-threatening toxicity. For example, mature amatoxin-containing mushrooms tend to be large and white (eg, Amanita bisporigera (picture 4), virosa or verna) or greenish-white (eg, Amanita phalloides (picture 3)) with a large bulb on the end of the stalk or ring around the middle of the stalk. Gyromitrin-containing mushrooms have a brain-like appearance and are often confused with morels (Morchella esculenta) (picture 5).

Was any ethanol ingested with the mushroom? – Certain mushroom species (eg, Coprinus) can cause a disulfiram-like reaction when ethanol is ingested with or up to 48 hours after Coprinus mushroom consumption.

Is everyone who ate the mushrooms ill? Is anyone who did not eat the mushrooms ill? – These questions help differentiate mushroom poisoning from other types of food poisoning. However, due to variations in amount ingested and possible types of mushrooms ingested (if more than one mushroom was present at the meal), not all persons who ingest toxic mushrooms may become poisoned.

Other individuals who ate mushrooms along with the patient should be contacted. Symptomatic patients and any asymptomatic person who might be at risk for life-threatening toxicity (eg, amatoxin-, gyromitrin-, orellanine-containing mushrooms) warrant emergent medical evaluation.

Physical examination — Classification of poisoning based upon clinical presentation (eg, gastroenteritis, liver failure, seizures, cholinergic poisoning, hallucinations, renal failure (table 1)) is most helpful in guiding further treatment and more quickly arrives at the type of mushroom ingested in most instances. (See 'Mushroom poisoning syndromes' above.)

Consultation with a medical toxicologist is advised when evaluating patients with suspected mushroom poisoning since signs and symptoms of mushroom poisoning (eg, vomiting and diarrhea) may occur in more than one mushroom poisoning syndrome as well as with other toxic exposures (eg, food poisoning, botulism). (See 'Regional poison control centers' below.)

Ancillary studies — Specific testing to identify mushrooms and their toxins is discussed separately. (See 'Mushroom identification' below.)

Acute testing in patients with mushroom exposures is guided by the clinical presentation:

Asymptomatic individuals with ingestions that are unlikely to be toxic may be observed without any testing.

Asymptomatic patients with ingestion of potentially lethal mushrooms should undergo baseline assessment of the following:

Serum electrolytes, calcium, and phosphate

Blood urea nitrogen and serum creatinine

Urinalysis

Serum creatine kinase

Liver studies (eg, aspartate aminotransferase [AST], alanine aminotransferase [ALT], total protein, albumin, total and direct bilirubin)

Prothrombin time (PT), partial thromboplastin time (PTT)

Complete blood count with platelets

Symptomatic patients should undergo testing as described for asymptomatic patients with potentially lethal mushroom ingestion. In addition, they may warrant other studies based upon their clinical findings as follows:

Fulminant hepatic failure – Serum glucose, blood gas determination, serum lactate, blood ammonia, and serum lactate dehydrogenase (LDH)

Altered mental status – Rapid blood glucose, blood gas determination, and, if hepatic encephalopathy is suspected or the patient shows signs of increased intracranial pressure, neuroimaging (eg, computed tomography of the brain) to assess for cerebral edema

Cyanosis not responsive to oxygen therapy or ingestion of mushrooms containing gyromitrin toxin – Methemoglobin level

Hypoxia or respiratory distress – Blood gas determination, pulse oximetry, chest radiography

Interpretation of results — Electrolyte abnormalities are often associated with gastrointestinal symptoms (eg, vomiting, abdominal pain, and diarrhea), are nonspecific and occur commonly in patients with mushroom poisoning.

Liver studies are typically normal in most acute mushroom exposures, but following ingestion of mushrooms containing amatoxin or gyromitrin toxins (eg, Amanita virosa, Amanita phalloides, Gyromitra esculenta), liver enzymes will begin to rise on reassessment approximately 24 to 36 hours after ingestion [1]. Thrombocytopenia, coagulopathy, hyperbilirubinemia, or hyperammonemia with encephalopathy indicates progressive toxicity in such patients and may be associated with gastrointestinal bleeding. Acidosis, hypoglycemia, and renal failure signifying hepatorenal syndrome are markers for poor prognosis.

Acutely, renal insufficiency may occur as a nonspecific result of hypovolemic shock due to vomiting and diarrhea or may indicate ingestion of norleucine toxin (Amanita smithiana) [29]. Renal insufficiency occurring days to weeks after mushroom ingestion is characteristic of orellanine toxicity (Cortinarius mushroom species) [38].

Ingestion of gyromitrin-containing mushrooms (eg, Gyromitra esculenta) may cause methemoglobinemia. Hemolysis indicated by anemia, red blood cell fragments on blood smear, and hemoglobinuria may also occur or may indicate immune-mediated hemolytic anemia caused by Paxillus involutus [35,51].

Elevated creatine kinase occurring one to three days after mushroom ingestion suggests rhabdomyolysis induced by mushrooms, such as Tricholoma equestre or Russula species (eg, Russula emetica) [41].

Inhalational "puffball" exposure (eg, Lycoperdon species) may cause respiratory symptoms in association with bilateral reticulonodular infiltrates (allergic bronchoalveolitis) seen on chest radiograph [55].

Mushroom identification — Mushroom identification is usually not readily available during the acute phase of care, and most mushrooms causing toxicity are never correctly identified [4]. However, if possible, determination of the specific type of mushroom ingested can be helpful for treatment recommendations and prognosis. Consultation with a medical toxicologist and professional mycologist is advised when attempting mushroom identification (see 'Regional poison control centers' below). We recommend that clinicians NOT attempt to use the internet to identify mushrooms.

Whenever possible, samples of all ingested mushrooms should be obtained for potential identification by a professional mycologist [3]. Whole mushrooms are preferred, but identification can be made on parts of the mushroom, especially the cap. Storage is facilitated by wrapping the mushrooms in wax paper, placing it in a paper bag, and refrigerating the sample [1]. Storage in plastic bags should be avoided. Digital photographs of whole mushrooms can be immediately sent to a mycologist for inspection. Although they are insufficient to make a definitive diagnosis, photographs have been used successfully to exclude ingestion of a seriously toxic mushroom in time to assist with treatment decisions [59].

Unfortunately, patients often ingest multiple mushrooms and have cooked, or otherwise damaged the fungi they have ingested, making direct identification difficult or impossible. In these situations, a centrifuged gastric aspirate may be obtained for microscopic evaluation of spores by a professional mycologist [1].

Testing methods vary depending upon the mushroom sample available and include:

Spore print analysis – Spore prints can successfully identify mushrooms with high specificity (picture 10). However, this procedure is typically not useful for patient management in the acute phase of mushroom poisoning, because it requires fresh, intact, and carefully preserved mushroom caps, several hours to obtain the print, and a professional mycologist to perform the spore print correctly and interpret the results.

Specific laboratory testing – Laboratory analysis in patients with mushroom exposure should be based upon their clinical presentation. Analysis for specific mycotoxins can be difficult and not usually feasible in a timeframe that is of clinical utility although later documentation of mushroom poisoning as the underlying etiology for specific clinical findings may be of prognostic importance [60]. Assays for some of the most toxic mycotoxins are available and may be important to confirm the clinical impression in a critically ill patient. The clinician should contact a poison control center to discuss appropriate testing methods, type of specimen needed, specimen handling, laboratories where testing is available, and interpretation of results (see 'Regional poison control centers' below). There are a variety of assays that have been used to detect myotoxins and a variety of matrixes (blood, urine, gastric contents, and bile) that may be analyzed [60].

Specific assays for mycotoxins include:

Enzyme-linked immunoassay (ELISA) – Urine and blood tests for amatoxins are not widely available, but sensitive tests do exist [1]. Amatoxin is rapidly cleared from the blood; urine is the matrix of choice for testing for amatoxins. ELISA assays should be interpreted in conjunction with the clinical assessment. False positives have been reported with ingestion of mushroom species that do not contain amatoxins. ELISA may be of particular use in ruling out potential exposures to amatoxin-containing mushrooms in patients who present after mixed-mushroom exposures and have early onset of gastrointestinal symptoms. ELISA assays are most useful if samples are tested early in patient presentation. The sensitivity of ELISA assays decreases substantially after 36 hours [61,62].

Radioimmunoassay (RIA) – RIA's performed on urine detected amatoxin in 100 percent of cases for assays performed within 24 hours and in 80 percent of cases within 48 hours of known cyclopeptide-containing mushroom exposures. ELISA has largely replaced RIA methodology for identifying amatoxins [61].

Gas chromatography-mass spectroscopy (GC/MS) – GC/MS has been used to confirm exposures to cyclopeptide-containing mushrooms, and it has been used to identify hydrazines found in gyromitrin-containing mushrooms. GC/MS may aid in diagnosis of exposure to other mushrooms containing toxins, such as psilocybin or psilocin and orellanine [63]. GC/MS has also been used to identify psilocin in chocolate/mushroom concoctions by the Drug Enforcement Agency [64].

High-performance liquid chromatography (HPLC) and tandem mass spectroscopy – HPLC has been used to identify a variety of mycotoxins (eg, amatoxin, acromelic acid) [1]. Typically, only research or reference laboratories will be able to perform these assays.

Polymerase chain reaction (PCR) – PCR tests have been developed for a variety of highly toxic mushrooms, including Amanita phalloides, Lepiota cristata, Lepiota brunneoincarnata, Inocybe asterospora, and toxic Japanese mushrooms (eg, Omphalotus japonicus, Clitocybe acromelalga, Tricholoma ustale, Entoloma rhodopolius) [65,66]. These tests are highly sensitive and specific and can even detect the presence of these mushrooms in difficult to use sources, such as cooked mushrooms, mushrooms mixed with pasta, and gastric aspirates.

Meixner test – We do not recommend use of the Meixner test for determining the presence of amatoxin in mushroom samples [67,68]. Although this test was used in the past as a means to identify amatoxin-containing mushrooms, it has been demonstrated to be unreliable with false positives as well as false negatives [69,70]. This test should also not be used by foragers to determine whether or not a mushroom is edible.

DIFFERENTIAL DIAGNOSIS — Food poisoning caused by bacterial toxins (eg, Staphylococcus aureus enterotoxin, Bacillus cereus emetic toxin, foodborne botulism, shiga toxin producing E. coli [hemolytic uremic syndrome]) may also cause delayed onset of nausea, vomiting, abdominal pain, and diarrhea after eating contaminated food. In most situations, the ill patient will provide a food history that implicates the typical source of food poisoning (eg, undercooked meat, eggs, rice, salads, home-canned vegetables), and mushrooms are found not to have been consumed. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-abundant settings", section on 'Clinical clues to the microbial cause'.)

However, sometimes mushrooms are coingested with the food or are the source of the contamination (eg, botulism from canned mushrooms). When differentiating mushroom poisoning from food poisoning in these situations, the clinician should monitor for specific findings that point to the underlying etiology (eg, descending paralysis [botulism], hemolytic uremic syndrome [enterohemorrhagic E. coli], liver toxicity [amatoxin mushroom poisoning]) and provide comprehensive supportive care. When botulism is suspected, administration of antitoxin may also be indicated. (See "Botulism", section on 'Treatment' and "Shiga toxin-producing Escherichia coli: Clinical manifestations, diagnosis, and treatment" and "Botulism", section on 'Clinical manifestations'.)

When evaluating patients with renal insufficiency, liver failure, or rhabdomyolysis of unknown etiology, the clinician should remember to inquire about mushroom consumption because other persons who shared in the meal may also be at risk.

ADDITIONAL RESOURCES

Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison centers".)

SUMMARY AND RECOMMENDATIONS

Epidemiology – Mushroom ingestion occurs frequently, but serious toxicity is uncommon. In most cases, the specific species of mushroom consumed is unknown. When serious mushroom poisoning does occur, it typically results from misidentification by amateur foragers. (See 'Epidemiology' above.)

Timing of symptom onset and classification of poisoning syndrome – Classification of poisoning based upon clinical presentation (table 1) and timing of onset of symptoms is most helpful in achieving a working diagnosis, assessing the clinical concern for potentially serious toxicity, and guiding further treatment. Mushrooms that only cause acute toxicity (<6 hours after ingestion) are rarely life threatening. Mushrooms that cause symptoms more than six hours after consumption are associated with serious and potentially lethal toxicity. However, early symptoms do not exclude the possibility of consumption of potentially lethal mushrooms, especially if more than one type of mushroom was eaten. (See 'Concern for serious toxicity depends on timing of symptom onset' above.)

Symptom onset <6 hours after ingestion – These rarely result in life-threatening toxicity. Many mushroom species cause acute gastroenteritis, such as the "little brown mushroom" (picture 1). Other acute-onset syndromes include hallucinations caused by Psilocybe, central nervous system excitation/depression caused by Amanita muscaria and Amanita pantherina (picture 6A-B), cholinergic excess caused by Inocybe and Clitocybe, disulfiram-like reaction caused by Coprinus atramentarius, and rhabdomyolysis caused by Russula. (See 'Acute symptom onset (<6 hours after ingestion)' above.)

Symptom onset >6 hours after ingestion – Patients who ingest potentially lethal mushrooms (eg, Amanita bisporigera (picture 4), Amanita phalloides (picture 3), Gyromitra esculenta (picture 5), Cortinarius orellanus) typically develop signs of toxicity more than six hours after ingestion. (See 'Delayed symptom onset (>6 hours after ingestion)' above.)

History – Key elements of the patient's history may help determine which species of mushroom was ingested as well as guide therapy. Important questions include (see 'History' above):

Where was the mushroom collected (field, pasture, or along or underneath trees)?

Was more than one type of mushroom collected or eaten?

Did everyone who ate the mushroom become ill, and did anyone who didn’t eat the mushrooms become ill?

How long after eating the mushroom did symptoms begin?

Were mushrooms collected and/or eaten for hallucinogenic effects?

Was any alcohol consumed after eating the mushroom?

Ancillary studies – Ancillary testing in patients with mushroom exposures is guided by the clinical presentation. Asymptomatic individuals with ingestions that are unlikely to be toxic may be observed without any testing. Symptomatic patients and asymptomatic patients with ingestion of potentially lethal mushrooms should have serum electrolytes, calcium, and phosphate, blood urea nitrogen and serum creatinine, urinalysis, serum creatine kinase, liver transaminases, coagulation profile, complete blood count, and potentially others depending on symptoms. (See 'Ancillary studies' above.)

Mushroom identification – Whenever possible, samples of all ingested mushrooms can be obtained for potential identification by a trained mycologist. Whole mushrooms are preferred, but identification can be made on parts of the mushroom, especially the cap. Further storage is facilitated by wrapping the mushrooms in wax paper, placing it in a paper bag, and refrigerating the sample. Storage in plastic bags should be avoided. (See 'Mushroom identification' above.)

Additional resources – A regional poison control center can be contacted to help determine likely mushroom species ingested based upon clinical findings, identification of any mushrooms available for analysis, and treatment of specific toxic effects. (See 'Regional poison control centers' above.)

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Topic 16135 Version 31.0

References

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