Mushroom Toxicity Workup

Updated: May 12, 2022
  • Author: B Zane Horowitz, MD, FACMT; Chief Editor: Sage W Wiener, MD  more...
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Approach Considerations

Many patients who ingest a mushroom do not require laboratory testing. Testing should be driven by the patient's clinical condition and the most likely toxin (based on identification of the mushroom by a mycologist, location of the ingestion, and the history).

Several texts describe how to determine whether a suspect botanical contains amatoxin, a potent toxin found in some of the Amanita species. [24]  However, for symptomatic patients, identification of the mushroom by a mycologist is highly desirable.

Botanical identification remains the most reliable method of identifying the mushroom involved in the poisoning. When the mushroom specimen is available, the Meixner test is occasionally used but is unreliable when attempted by inexperienced operators. The test consists of expressing a drop of mushroom juice onto a lignin paper (newspaper) and allowing it to air-dry. A drop of hydrochloric acid (10-12N) is then placed on the same spot, and the area is observed for any color change. The presence of amatoxin is suggested by a bluish color. False-positive results may occur with psilocybin.

By far, the most reliable way to identify a mushroom is to allow examination of the mushroom by an experienced local mycologist. This may be arranged by contacting the local Poison Center (800-222-1222).


Laboratory Studies

In patients with severe diarrhea or vomiting, a basic serum metabolic profile (sodium, potassium, chlorine, carbon dioxide, creatinine, glucose, and calcium) should be obtained for evaluation of fluid and electrolyte disturbances. Electrolyte disturbances (eg, hypokalemia) may occur in patients with severe gastroenteritis. Hypocalcemia may occur with orellanine-induced renal failure and in both gyromitrin and amatoxin poisoning. Hypophosphatemia may occur with amatoxin and gyromitrin poisoning, especially in children.

Hypoglycemia may develop suddenly during the gastroenteritis phase of gyromitrin poisoning, as well as during the hepatic failure phase of both gyromitrin and amatoxin poisoning. Hypoglycemia in the setting of liver failure signals a grim prognosis.

Baseline renal function studies are indicated if nephrotoxic mushroom ingestion cannot be ruled out. Blood urea nitrogen (BUN) concentration, creatinine level, and urinalysis are used as screening tools for renal function. [27]  Renal insufficiency occurs as a result of circulatory collapse from any cause, and in the setting of amatoxin and gyromitrin toxicity, it may be part of the hepatorenal syndrome.

Orellanine is a direct nephrotoxin and may induce oliguric renal failure several days or weeks after ingestion of the toxic mushroom. Mild renal insufficiency also may be observed with intravenous (IV) injection of psilocybin.

Baseline liver function studies may be indicated if hepatotoxic mushrooms are a possibility. For example, hepatic failure is a common complication of amatoxin and gyromitrin ingestions. Biomarkers of hepatocellular necrosis include aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase, and lactic dehydrogenase (LDH). With amatoxin- and gyromitrin-induced hepatic necrosis, these biomarkers begin to rise exponentially 36-72 hours after mushroom ingestion. Bilirubin is elevated, as are the prothrombin time (PT) and activated partial thromboplastin time (aPTT).

A complete blood count (CBC) should be obtained if there is suspicion of a mushroom that causes hemolytic anemia. Anemia may be secondary to the acute blood loss associated with hemorrhagic gastroenteritis, or it may be secondary to the hemolysis observed with gyromitrin poisoning. Anemia may also be secondary to the renal failure observed in orellanine poisoning.

Methemoglobinemia may be observed with gyromitrin poisoning and occasionally after an IV injection of psilocybin.

Elevated creatine phosphokinase (CPK) levels are a manifestation of rhabdomyolysis, which may be noted with Tricholoma flavovirins and some Russula species. Evaluation for rhabdomyolysis should be considered if warranted by the signs and symptoms.

Drug screening

Urine drug screening should be considered, especially in the following situations:

  • The patient has unexplained behavioral changes
  • Suicidal intent, substance abuse, or foul play is suspected
  • Ingestion of unknown toxins is suspected

Acetaminophen and salicylate levels should be obtained for all patients with an unknown ingestion, and acetaminophen toxicity should be suspected in all patients with fulminant hepatic failure (FHF). Toxicology screening for barbiturates, benzodiazepines, opiates, and alcohol may be obtained to help differentiate the cause of coma. Screening for phencyclidine, LSD, MDMA, and cocaine may help determine the cause of hallucinations and agitation. Screening for phenothiazines may help distinguish the cause of anticholinergic toxicity.

Other tests

Enzyme-linked immunosorbent assay (ELISA) analysis of urinary amanitin appears to be efficacious in confirming amatoxin poisoning, but this is not widely available except in forensic laboratories.

Chromatographic techniques (eg, thin-layer chromatography [TLC], gas-liquid chromatography [GLC], and high-pressure liquid chromatography [HPLC]), as well as mass spectometry, have been used to detect various mushroom toxins (eg, amanitins, orellanine, muscimol and ibotenic acid, psilocybin, muscarine, and gyromitrins). [27]  However, these techniques are typically unavailable, being largely limited to research laboratories.

Hemagglutination inhibition has been used to detect anti-Paxillus immunoglobulin G (IgG).


Imaging Studies

Chest radiography, if clinically indicated, should be performed to assess for aspiration pneumonia or pulmonary edema. Bilateral reticulonodular infiltrates may be seen with puffball (Lycoperdon)-induced allergic bronchoalveolitis. Computed tomography (CT) of the brain is indicated in all patients with encephalopathy in order to rule out structural disease or cerebral edema.

Renal ultrasonography may reveal enlarged kidneys in patients with orellanine poisoning.

Electrocardiography (ECG) may be performed to evaluate the presence of atrioventricular (AV) nodal disease and heart block. ECG may reveal signs of hyperkalemia, which may complicate orellanine-induced renal failure.


Histologic Findings

At autopsy or after transplantation, histologic examination of the liver reveals diffuse hepatocellular damage with gyromitrin toxicity and fatty degeneration of the liver with extensive central zone necrosis and centrilobular hemorrhage in amatoxin poisoning. Electron microscopy reveals changes consistent with extensive lipid peroxidation of the cytoplasm as well as the nucleus, vacuolization of the mitochondria, and clumping of the nucleolar chromatin.

Renal biopsy findings may reveal interstitial nephritis in gyromitrin toxicity. Acute tubular necrosis and dedifferentiation of the proximal tubule is present with orellanine toxicity. Electron microscopy reveals vacuolization of the tubular cells with loss of the brush border.

Gastric contents may be examined, but this is usually impractical as a means of identification. By means of microscopy, a mycologist may be able to identify the spores recovered from the patient’s gastric contents.