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Toxin Latent Period <3 hr After Ingestion of Mushrooms


Cecil F. Brownie

, DVM, PhD, DABVT, DABFE, DABFM, FACFEI, College of Veterinary Medicine, North Carolina State University

Last full review/revision Aug 2014 | Content last modified Aug 2014
Topic Resources

Clitocybe dealbata, C dilatata, and Inocybe spp

Clitocybe are fleshy, small mushrooms with white-tan-grey caps, gills that are attached and that descend the stalk, and white spore print. They are widely distributed and usually grow on the ground in open woods, parks, and lawns. Inocybe are small, brown mushrooms that grow on conifers or broad-leafed trees and oak woods (mycorrhizal). They have a cap with a knob, ringless stalk, veil covered immature gills, no remnant of universal veil, and a spore print that is bright rust/orange-brown or gray-brown.

The toxin in these mushrooms is muscarine, a quaternary ammonium compound that is poorly absorbed orally and does not cross the blood-brain barrier. Its cholinergic effects are therefore peripheral. The absorbed portion is quickly distributed throughout the body and undergoes urinary excretion. Muscarine is structurally similar to acetylcholine, a cholinergic neurotransmitter. Whereas the acetylcholine-muscarine receptor complex is susceptible to acetycholinesterase inactivation, the muscarine-muscarine receptor complex is not. Muscarine competes with acetylcholine at cholinergic receptor binding sites, leading to excessive stimulation of postganglionic cholinergic fibers and the subsequent observed clinical signs (cholinergic excess).

Clinical Findings:

Within 30–120 min of ingestion, there is mild to excessive cholinergic stimulation—ataxia, vomiting, abdominal pain, salivation, lacrimation, watery diarrhea, miosis, bronchoconstriction, bradycardia, arrhythmias, hypotension/hypertension, and shock.


Diagnosis may be based on a history of mushroom ingestion, identification of suspected mushroom and consistent clinical signs, response to supportive care, and atropine therapy. Tests used to evaluate fluid and electrolyte status in severe gastroenteritis cases, together with a liver profile, may be useful.


Other than offering supportive care (fluid and electrolyte replacement), treatment is unnecessary in most cases. In life-threatening cases, atropine therapy (0.2–2 mg/kg, a portion of the calculated dose given IV and the remaining portion IM or SC), repeated as necessary, is the treatment of choice. Efficacy of treatment should be based on lack of respiratory difficulties and respiratory secretions and not on mydriasis. Excessive atropine therapy can lead to anticholinergic effects (eg, tachycardia, GI stasis, behavioral changes, and hyperthermia); therefore, animals should be monitored.

Amanita muscaria and A pantherina

Amanita muscaria have an orange-red cap with distinctive white to yellow warts, gills that are somewhat attached, white spore print, ring stalk, and bulbous base (cup). A pantherina have a tan to yellow-brown/dark brown cap with white patches, a ringed stalk with basal bulb, and white spore print. Both of these mushrooms are found in coniferous and deciduous forests of the Pacific northwest.

The toxins in these mushrooms are isoxazole derivatives: ibotenic acid, which is structurally similar to the stimulatory neurotransmitter glutamic acid, and its decarboxylated metabolite muscimol, which is stereochemically similar to the inhibitory neurotransmitter γ-aminobutyric acid (GABA). They both cross the blood-brain barrier and effect functional changes within the CNS. The toxic dose of ibotenic acid is reported to be 30–60 mg, and that of muscimol is 6 mg (ingestion of more than two mushrooms).

Ibotenic acid undergoes spontaneous decarboxylation (stomach, liver, and brain), forming muscimol, which is a GABA-receptor agonist. Both are analogues of γ-aminobutyric acid and act as weak, noncompetitive inhibitors of GABA (inhibits neuronal and glial GABA uptake). This reduces the inhibitory effect of the Purkinje cells in the cerebellum, increases brain serotonin, and decreases catecholamine levels.

Clinical Findings:

Both compounds are rapidly absorbed from the GI tract. The onset of clinical signs (tachycardia, hypotension, ataxia, seizures, hyperthermia, vomiting, muscle fasciculation, mydriasis, incoordination, hyperactivity [paddling, chewing movements], opisthotonos, respiratory depression, coma, and death) are reportedly seen within 30–120 min after ingestion. Duration of signs is ~24 hr.


Diagnosis is based on a history of ingestion, clinical presentation, and response to treatment (symptomatic, supportive, and specific drugs, eg, benzodiazepine).


Symptomatic and supportive treatment includes maintaining hydration (IV fluids), keeping airways free of respiratory secretions, and frequent positional changes. Seizures may be controlled with diazepam (0.5 mg/kg, IV to effect; repeated as needed), phenobarbital (6 mg/kg, IV), or pentobarbital (5–15 mg/kg, IV). Benzodiazepines and barbiturates are GABA-receptor agonists and may potentiate CNS and respiratory depression. Muscarine concentrations in A muscaria are very low, and peripheral effects are more anticholinergic than cholinergic. Therefore, atropine therapy is contraindicated.

Chlorophyllum molybdites and Russula emetica

Chlorophyllum molybdites mushrooms have caps that are large, white to brown, egg-shaped, convex knobbed to flat, with numerous cinnamon or buff scales. They have unattached white gills, green or grayish-olive spores, and a ring on the stalk. They are common in the southern and central USA. Russula emetica mushrooms have a reddish, slimy cap with short whitish stalk and gills; no veils; and a white to yellowish-white spore print. They grow singly or in a group and are found throughout the USA. The toxins in these mushrooms are varied and unknown GI irritants that are thought to be high-molecular-weight proteins found throughout the mushroom.

Clinical Findings:

Within minutes to hours (0.5–3 hr) after exposure, clinical signs become evident. These include vomiting, bloody diarrhea, abdominal pain, muscle cramps, liver injury, and circulatory disturbances that are self-limiting. Although recovery generally occurs within 6–24 hr, it could be prolonged or become life threatening (rare) in cases of hypovolemic shock, oliguria, and/or transient increased BUN secondary to dehydration. Death is rare.


A tentative diagnosis may be based on history and early onset of reported clinical signs (gastroenteritis—vomiting and bloody diarrhea). Except for dehydration, there are no systemic signs. If the mushroom is available, the gills (light green) and spore print (green) color may be used to distinguish C molybdites, the most common GI irritant mushroom species, from others.


There are no specific antidotes. Dehydration and electrolyte imbalance should be addressed. Gastric lavage and activated charcoal therapy may be considered. Analgesics are useful in some cases, but caution should be exercised in administering acetaminophen (inherently hepatotoxic) to hepatic insult cases. Phenothiazines interact adversely with toxins to induce CNS and/or GI effects. Fluids and vasopressors should be administered in hypovolemic shock cases. Liver and kidney functions should be monitored.

Psilocybe cubensis, Conocybe cyanopus, Gymnopilus spectabilis, and Panaeolus subbalteatus

Psilocybe cubensis are small, brown, slender-stalked mushrooms. They commonly grow in piles of dung and fertilized grasses in moist areas throughout the USA, especially in the southeastern and northwest regions. The mushrooms develop a blue-green color in handled and injured areas. They have yellowish, sticky to moist caps with brown gills; a persistent ring on the stalk; and a purple-brown spore print. Conocybe cyanopus are small and fragile, with brown caps, brown gills, and a large ring midway down the long, thin stalk. The spore print is cinnamon brown. They are widely distributed in North America. Gymnopilus spectabilis are large yellow-orange mushrooms with an orange to rust orange spore print. They are found in clusters on wood, stumps, or on the ground over buried wood. Panaeolus subbalteatus have broadly conical to flat caps with a dark belt around margin, brown gills, hairy reddish stalks, and a blackish spore print. They are widely distributed in North America.

These hallucinogenic mushrooms contain psilocybin and psilocin, which are indole alkaloids similar to lysergic acid diethylamide (LSD). Psilocybin undergoes rapid dephosphorylation (plasma, kidneys, and liver), forming psilocin, which is structurally similar to serotonin (stimulatory to serotonin receptors in the central and peripheral nervous systems). Metabolites cross the blood-brain barrier and concentrate in brain tissue. Growth conditions, geographic location, storage conditions, and mushroom species are factors that influence toxin concentrations. Ingestion of five or six dried mushroom caps is reported to be toxic.

Clinical Findings:

Clinical signs occur within 0.5–1 hr; they are rarely delayed as long as 3 hr after ingestion. Signs include vocalization, aggression, nystagmus, ataxia, tachycardia, vomiting, urinary incontinence, dyspnea, mydriasis, weakness, hyperthermia, mild methemoglobinemia, and hallucination, with recovery within 6 hr of observed clinical signs.


A history of mushroom ingestion, identification of suspected mushroom(s), consistent clinical presentation, and response to supportive and symptomatic care are critical for diagnosis. With isoxazole-induced toxicity, coma is distinctly expressed; however, the opposite is true in psilocin-induced toxicity. Tests detecting psilocin and its glucuronide metabolite in urine, serum, and blood, although confirmatory, are not widely available clinically.


Treatment is primarily symptomatic and supportive. Diazepam (0.5–1 mg/kg, IV, with incremental dose increase of 5–10 mg to effect) or phenobarbital (6 mg/kg to effect) may be given. Body temperature should be monitored. In some cases, leaving the animal untreated in a quiet, dark environment might be all that is necessary.

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