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Chemical food poisoning is caused by eating plants or animals that contain a naturally occurring toxin.

Chemical food poisoning often involves mushrooms, poisonous plants, or marine animals. Activated charcoal may be useful. Complications (eg, gastroenteritis, dehydration, renal or hepatic failure, respiratory insufficiency) are treated supportively.

Mushrooms: Numerous species when ingested cause toxicity. Differentiating them in the wild is difficult, even for highly knowledgeable people; folklore rules for differentiating toxic and nontoxic species are unreliable. If patients have eaten an unidentified mushroom, identifying the species can help determine specific treatment. However, because an experienced mycologist is seldom available for immediate consultation, treatment of patients who become ill after mushroom ingestion is usually guided by symptoms. If a sample of the mushroom, uningested or from the patient's emesis, is available, it can be sent to a mycologist for analysis.

All toxic mushrooms cause vomiting and abdominal pain; other manifestations vary significantly by mushroom type. Generally, mushrooms that cause symptoms early (within 2 h) are less dangerous than those that cause symptoms later (usually after 6 h).

Mushrooms that cause early GI symptoms (eg, Chlorophyllum molybdites, the little brown mushrooms that often grow in lawns) cause gastroenteritis, sometimes with headaches or myalgias. Diarrhea is occasionally bloody. Symptoms usually resolve within 24 h.

Mushrooms that cause early neurologic symptoms include hallucinogenic mushrooms, which are usually ingested recreationally because they contain psilocybin, a hallucinogen. The most common are members of the Psilocybe genus, but some other genera contain psilocybin. Symptoms begin within 15 to 30 min and include euphoria, enhanced imagination, and hallucinations. Tachycardia and hypertension are common, and hyperpyrexia occurs in some children; however, serious consequences are rare. Treatment occasionally involves sedation (eg, with benzodiazepines).

Mushrooms that cause early muscarinic symptoms include members of the Inocybe and Clitocybe genera. Symptoms may include the SLUDGE syndrome (see Table 2: Poisoning: Common Toxic Syndromes (Toxidromes)), miosis, bronchorrhea, bradycardia, diaphoresis, wheezing, and fasciculations. Symptoms are usually mild, begin within 30 min, and resolve within 12 h. Atropine Some Trade Names
ATROPEN
ATROPINE-CARE
SAL-TROPINE
Click for Drug Monograph
may be given to treat severe muscarinic symptoms (eg, wheezing, bradycardia).

Mushrooms that cause delayed GI symptoms include members of the Amanita, Gyromitra, and Cortinarius genera. The most toxic Amanita mushroom is Amanita phalloides, which causes 95% of mushroom poisoning deaths. Initial gastroenteritis, which may occur 6 to 12 h after ingestion, can be severe; hypoglycemia can occur. Initial symptoms abate for a few days; then, hepatic and sometimes renal failure develops. Initial care involves close monitoring for hypoglycemia and possibly repeated doses of activated charcoal. Treatment of hepatic failure may require liver transplantation; other specific treatments (eg, N- acetylcysteine Some Trade Names
MUCOMYST
Click for Drug Monograph
, high-dose penicillin, silibinin) are unproven.

Gyromitra mushrooms can cause hypoglycemia simultaneously with or shortly after gastroenteritis. Other manifestations may include CNS toxicity (eg, seizures) and, after a few days, hepatorenal syndrome. Initial care involves close monitoring for hypoglycemia and possibly repeated doses of activated charcoal. Neurologic symptoms are treated with pyridoxine 25 mg/kg (maximum daily dose of 25 g); hepatic failure is treated supportively.

Most Cortinarius mushrooms are endogenous to Europe. Gastroenteritis may last for 3 days. Renal failure, with symptoms of flank pain and decreased urine output, may occur 3 to 20 days after ingestion. Renal failure often resolves spontaneously.

Poisonous plants: A few commonly grown plants are poisonous. Highly toxic and potentially fatal plants include castor bean, jequirity bean, poison hemlock, and water hemlock, as well as oleander and foxglove, which contain digitalis glycosides (see Table 6: Poisoning: Moderately Poisonous Plants). Few plant poisonings have specific antidotes.

Table 6
Moderately Poisonous Plants Plant Symptoms Treatment Aloe spp Gastroenteritis, nephritis, skin irritation Supportive care and irrigation with soap and water Azalea Cholinergic symptoms Supportive care and atropine Some Trade Names ATROPEN ATROPINE-CARE SAL-TROPINE Click for Drug Monograph Cactus spp Infection, granuloma formation Removal of spines Caladium spp Oral mucosal damage due to Ca oxalate crystals in leaves Supportive care and demulsification (eg, with milk or ice cream) Capsicum spp (peppers) Mucous membrane irritation and swelling Supportive care, irrigation, and possibly demulsification Colchicine Some Trade Names No US trade name Click for Drug Monograph (autumn crocus, meadow saffron, glory lily) Delayed gastroenteritis, multiple organ failure Supportive care and colchicine Some Trade Names No US trade name Click for Drug Monograph -specific Fab fragments* Deadly nightshade Anticholinergic symptoms, hallucinations Supportive care; for severe hyperthermia or seizures, possibly physostigmine Some Trade Names No US trade name Click for Drug Monograph Dumbcane (dieffenbachia) Oral mucosal damage due to Ca oxalate crystals in leaves Supportive care and demulsification (eg, with milk or ice cream) Fava beans In patients with G6PD deficiency, gastroenteritis, fever, headache, hemolytic anemia Supportive care; for severe anemia and poisoning, consideration of exchange transfusion Green potato and potato sprout Gastroenteritis, hallucinations, delirium Supportive care Holly berries Gastroenteritis Supportive care Jimsonweed Anticholinergic symptoms, hallucinations Supportive care; for severe hyperthermia or seizures, possibly physostigmine Some Trade Names No US trade name Click for Drug Monograph Lily of the valley Hyperkalemia, arrhythmias See discussion of digitalis preparations on see Heart Failure: Digitalis preparations Mistletoe Gastroenteritis Supportive care Nettle Local stinging and burning Supportive care Nightshade, common or woody Gastroenteritis, hallucinations, delirium Supportive care Philodendron spp Oral mucosal damage due to Ca oxalate crystals in leaves Supportive care and demulsification (eg, with milk or ice cream) Poinsettia Minor mucous membrane irritation Unnecessary Poison ivy Dermatitis See Dermatitis Pokeweed Mucous membrane irritation, gastroenteritis Supportive care Pothos Oral mucosal damage due to Ca oxalate crystals in leaves Supportive care and demulsification (eg, with milk or ice cream) Yew Gastroenteritis; rarely, seizures, arrhythmias, coma Supportive care *Not available outside France. Fab = fractionated antibodies.

Castor bean contains ricin, an extremely concentrated poison, but in a relatively impervious shell; thus, the bean must be chewed to release the toxin. Jequirity bean also has a concentrated cellular poison, which can cause death after swallowing or, in children, after chewing only 1 bean. Symptoms of either poisoning may include delayed gastroenteritis, sometimes severe and hemorrhagic, followed by delirium, seizures, coma, and death. Whole-bowel irrigation should be considered; it aims to remove all beans ingested.

Oleander, foxglove, and the similar but less toxic lily of the valley can cause gastroenteritis, confusion, hyperkalemia, and arrhythmias. The serum digoxin Some Trade Names
DIGITEK
LANOXIN
Click for Drug Monograph
level can confirm ingestion but is not useful as quantitative information. K levels are closely monitored. Hyperkalemia may respond only to hemodialysis. Ca is not recommended for arrhythmias. Digoxin Some Trade Names
DIGITEK
LANOXIN
Click for Drug Monograph
-specific Fab (fractionated antibody) fragments have been used to treat ventricular arrhythmias.

Hemlock poisoning can cause symptoms within 15 min. Poison hemlock has nicotinic effects, beginning with dry mouth and progressing to tachycardia, tremors, diaphoresis, mydriasis, seizures, and muscle paresis. Rhabdomyolysis and bradycardia may occur. Water hemlock appears to enhance γ−aminobutyric acid (GABA) activity. Symptoms may include gastroenteritis, delirium, refractory seizures, and coma.

Fish: There are 3 common types of fish poisoning.

Ciguatera poisoning may result from eating any of > 400 species of fish from the tropical reefs of Florida, the West Indies, or the Pacific, where a dinoflagellate produces a toxin that accumulates in the flesh of the fish. Older fish and large fish (eg, grouper, snapper, kingfish) contain more toxin. No known processing procedures, including cooking, are protective, and flavor is unaffected. Symptoms may begin 2 to 8 h after eating. Abdominal cramps, nausea, vomiting, and diarrhea last 6 to 17 h; then, pruritus, paresthesias, headache, myalgia, reversal of hot and cold sensation, and face pain may occur. For months afterward, unusual sensory phenomena and nervousness may cause debilitation. IV mannitol Some Trade Names
OSMITROL
RESECTISOL
Click for Drug Monograph
has been suggested as a treatment, but no clear benefit has been shown.

Scombroid poisoning is caused by high histamine levels in fish flesh due to bacterial decomposition after the fish is caught. Commonly affected species include tuna, mackerel, bonito, skipjack, and mahimahi. The fish may taste peppery or bitter. Facial flushing and possibly nausea, vomiting, epigastric pain, and urticaria occur within a few minutes of eating and resolve within 24 h. Symptoms are often mistaken for those of a seafood allergy. Unlike other fish poisonings, this poisoning can be prevented by properly storing the fish after it is caught. Treatment may include H₁ and H₂ blockers.

Tetrodotoxin poisoning is most commonly due to eating the puffer fish (fugu), a sushi delicacy, but > 100 fresh and salt water species contain tetrodotoxin. Symptoms are similar to those of ciguatera poisoning; potentially fatal respiratory paralysis can also occur. The toxin cannot be destroyed by cooking or freezing.

Shellfish: Paralytic shellfish poisoning can occur from June to October, especially on the Pacific and New England coasts, when mussels, clams, oysters, and scallops are contaminated by the poisonous dinoflagellate responsible for red tide. This dinoflagellate produces the neurotoxin saxitoxin, which is resistant to cooking. Circumoral paresthesias occur 5 to 30 min after eating. Nausea, vomiting, and abdominal cramps then develop, followed by muscle weakness. Untreated respiratory paralysis may be fatal; for survivors, recovery is usually complete.

Last full review/revision November 2005

Content last modified November 2005