Nonbacterial Food Poisoning

Published on 22/03/2015 by admin

Filed under Pediatrics

Last modified 22/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 3 (2 votes)

This article have been viewed 4147 times

Chapter 703 Nonbacterial Food Poisoning

703.1 Mushroom Poisoning

Denise A. Salerno, Stephen C. Aronoff

Mushrooms are a great source of nutrition. They are low in calories, fat free, and high in protein, making them an ideal food except for the fact that some are highly toxic if ingested. Picking and consumption of wild mushrooms are increasingly popular in the USA. This rise in popularity has led to increased reports of severe and fatal mushroom poisonings.

The clinical syndromes produced by mushroom poisoning are divided according to the rapidity of onset of symptoms and the predominant system involved. The symptoms are due to the principal toxin present in the ingested mushrooms. The eight major toxins produced by mushrooms are categorized as cyclopeptides, monomethylhydrazine, muscarine, hallucinogenic indoles, isoxazole, coprine (disulfiram-like reaction), orellanine, and gastrointestinal tract–specific irritants. In addition, the edible wild mushroom Tricholoma equestre has been associated with delayed rhabdomyolysis, and Clitocybe amoenolens and Clitocybe acromelalgia have been reported to cause erythromelalgia. The toxins responsible for these effects are unknown. Rapid tests are becoming available to permit timely identification of specific toxins.

Gastrointestinal: Delayed Onset

Amanita Poisoning

Poisonings by species of Amanita and Galerina account for 95% of the fatalities due to mushroom intoxication; the mortality rate for this group is 5-10%. Most species produce two classes of cyclopeptide toxins: (1) phallotoxins, which are heptapeptides believed to be responsible for the early symptoms of Amanita poisoning, and (2) amanitotoxin, an octapeptide that inhibits RNA polymerase and subsequent production of messenger RNA. Cells with high turnover rates, such as those in the gastrointestinal mucosa, kidneys, and liver, are the most severely affected.

Amanita poisoning causes cellular necrosis, which may occur throughout the gastrointestinal tract, the most heavily exposed site. Acute yellow atrophy of the liver and necrosis of the proximal renal tubules are found in lethal cases.

The clinical course of poisoning with Amanita or Galerina species is biphasic. Nausea, vomiting, and severe abdominal pain ensue 6-24 hr after ingestion. Profuse watery diarrhea follows shortly thereafter and may last for 12-24 hr. During this time, as much as 9 L of fluid may be lost. From 24-48 hr after poisoning, jaundice, hypertransaminasemia (peaking at 72 to 96 h), renal failure, and coma occur. Death occurs 4-7 days after the ingestion. A prothrombin time less than 10% of control is a poor prognostic factor.

Treatment

Treatment for Amanita poisoning is both supportive and specific. Fluid loss from severe diarrhea during the early course of the illness is profound, requiring aggressive therapy for correction of this loss. In the late phase of the disease, management of renal and hepatic failure is also necessary.

Specific therapy for Amanita poisoning is designed to remove the toxin rapidly and to block binding at its target site. Oral activated charcoal and lactulose combined with fluid and electrolyte replacement are recommended as part of the initial treatment for children with Amanita poisoning. Forced diuresis should be avoided, since this increases renal exposure. Intravenous penicillin G (400,000 U/kg/24 hr) administered as a continuous infusion and silybin dihemisuccinate, the water-soluble isomer of the flavolignone silymarin (in an intravenous dosage of 20-50 mg/kg/24 hr), act synergistically to inhibit binding of both toxins, to interrupt enterohepatic recirculation of amanitotoxin, and to protect from further hepatic injury from the toxins. Hemodialysis and hemoperfusion are also recommended as part of the initial treatment for intoxicated children. Orthotopic liver transplantation is recommended for children in whom severe hepatic failure develops.

Monomethylhydrazine Intoxication

Species of Gyromitra contain monomethylhydrazine (CH3NHNH2), which inhibits central nervous system (CNS) enzymatic production of γ-aminobutyric acid (GABA). Monomethylhydrazine also oxidizes iron in hemoglobin, resulting in methemoglobinemia. Children with Gyromitra poisoning experience vomiting, diarrhea, hematochezia, and abdominal pain within 6-24 hr of ingestion of the toxin. Symptoms of CNS depression and seizures develop later in the clinical course. Hemolysis and methemoglobinemia are potential life-threatening complications of monomethylhydrazine poisoning.

Treatment

Hypovolemia due to gastrointestinal fluid losses and seizures requires supportive intervention. Pyridoxal phosphate, the coenzyme that catalyzes the production of GABA, can reverse the effects of monomethylhydrazine when administered in high doses. Pyridoxine hydrochloride (25 mg/kg) is administered intravenously at a frequency dependent on clinical improvement. Parenteral administration of methylene blue is indicated if the methemoglobin concentration exceeds 30%; severe methemoglobinemia may require dialysis. Blood transfusions may be required for significant hemolysis.

Renal: Delayed Onset

Orellanine Poisoning

Species of Cortinarius contain the heat-stable toxin bipyridyl orellanine, which causes severe nonglomerular renal injury characterized by interstitial fibrosis and acute tubular necrosis. The exact mechanism of injury is unknown. Cortinarius poisoning is characterized by nausea, vomiting, and diarrhea that manifest 36-48 hr after ingestion. Although the initial symptoms may be trivial, more serious renal toxicity occurs in several days. Acute renal failure occurs in 30-50% of those affected, beginning with polyuria and progressing to renal failure.

Treatment

Treatment for orellanine poisoning is supportive. Early presentation, within 4-6 hr after ingestion, can be treated with activated charcoal and gastric lavage. Hemodialysis may be needed in patients suffering from renal failure. Most patients recover within 1 mo but chronic renal insufficiency develops in one third to one half of patients.

Autonomic Nervous System: Rapid Onset

Muscarine Poisoning

Mushrooms of the genera Inocybe and, to a lesser degree, Clitocybe contain muscarine or muscarine-related compounds. These quaternary ammonium derivatives bind to postsynaptic receptors, producing an exaggerated cholinergic response.

The onset of symptoms is rapid (30 min to 2 hr after consumption) and the disease spectrum is characterized by the following hypercholinergic response diaphoresis, excessive lacrimation, salivation, miosis, urinary and fecal incontinence, and vomiting. Respiratory distress caused by bronchospasm and increased bronchopulmonary secretions is the most serious complication. The symptoms subside spontaneously within 6-24 hr.

Treatment

Atropine sulfate, the specific antidote, is administered intravenously (0.01 mg/kg; max 2 mg). This is repeated until the pulmonary symptoms resolve or the patient becomes overtly tachycardic.

Coprine Ingestion

Coprinus atramentarius and Clitocybe clavipes contain coprine. Like disulfiram (Antabuse; Odyssey Pharmaceuticals, Inc.), coprine inhibits the metabolism of acetaldehyde after ethanol ingestion. The clinical manifestations result from accumulation of acetaldehyde.

Coprine intoxication becomes apparent after ethanol ingestion and may occur up to 5 days after consumption of the mushroom. Hyperemia of the face and trunk, tingling of the hands, metallic taste, tachycardia, and vomiting occur acutely. Hypotension may result from intense peripheral vasodilation.

The syndrome typically is self-limited and lasts only several hours. No specific antidote is available. If hypotension is severe, vascular reexpansion with isotonic parenteral solutions may be required. Small oral doses of propranolol have also been suggested.

Central Nervous System: Rapid Onset

Isoxazole Intoxication

Although Amanita muscaria and Amanita pantherina may contain muscarine, the toxins responsible for the CNS symptoms after ingestion of these mushrooms are muscimol and ibotenic acid, the heat-stable derivatives of the isoxazoles. Muscimol, a hallucinogen, and ibotenic acid, an insecticide, have anticholinergic effects. From 30 min to 3 hr after ingestion, CNS symptoms appear: obtundation, alternating lethargy and agitation, and, occasionally, seizures. Nausea and vomiting are uncommon. If large amounts of muscarine are contained in the mushroom, symptoms of cholinergic crisis also may occur.

Specific therapy must be carefully selected. If an exaggerated cholinergic response is observed, atropine should be administered. Because ingestions of A. muscaria often are associated with anticholinergic findings, the acetylcholinesterase inhibitor physostigmine is often used to reverse the delirium and coma. Benzodiazepines also are used for the agitation and delirium. Seizures can be controlled with diazepam. In most cases, however, early treatment with ipecac (if the patient is conscious) and close observation are all that is required.

Indole Intoxication

Mushrooms belonging to the genus Psilocybe (“magic mushrooms”) contain psilocybin and psilocin, two psychotropic compounds. Within 30 min after ingestion, patients experience euphoria and hallucinations, often accompanied by tachycardia and mydriasis. Fever and seizures have also been observed in children with psilocybin poisoning. These symptoms are short-lived, usually lasting for 6 hr after consumption of the mushroom. Severely agitated patients may show response to diazepam.

Buy Membership for Pediatrics Category to continue reading. Learn more here

Related posts:

Disorders of the Complement System Default ThumbnailGynecologic Care for Girls with Special Needs Cardiac Development Hypothyroidism Cystic Diseases of the Biliary Tract and Liver Vesicoureteral Reflux