Nonbacterial Food Poisoning

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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.

Gastrointestinal: Rapid Onset

Many mushrooms from various genera produce local gastrointestinal manifestations. The causative toxins are diverse and largely unknown. Within 1 h of ingestion, patients experience acute abdominal pain, nausea, vomiting, and diarrhea. Symptoms may last from hours to days, depending on the species of mushroom.

Treatment is mainly supportive. Children with large fluid losses may require parenteral fluid therapy. It is imperative to differentiate ingestion of mushrooms of this class from ingestion of Amanita and Galerina species containing cyclopeptide toxins.

Bibliography

Bedry R, Baudrimont I, Deffieux G, et al. Brief report: wild mushroom intoxication as a cause of rhabdomyolysis. N Engl J Med. 2001;345:798-804.

Berger KJ, Guss DA. Mycotoxins revisited: part I. J Emerg Med. 2005;28:53-62.

Berger KJ, Guss DA. Mycotoxins revisited: part II. J Emerg Med. 2005;28:175-183.

Diaz JH. Evolving global epidemiology, syndromic classification, general management, and prevention of unknown mushroom poisonings. Crit Care Med. 2005;33:419-426.

Diaz JH. Syndromic diagnosis and management of confirmed mushroom poisonings. Crit Care Med. 2005;33:427-436.

Klein AS, Hart J, Brems JJ, et al. Amanita poisoning: treatment and the role of liver transplantation. Am J Med. 1989;86:187-193.

Maeta K, Ochi T, Tokimoto K, et al. Rapid species identification of cooked poisonous mushrooms by using real-time PCR. Appl Environ Microbiol. 2008;74:3306-3309.

McDonald A. Mushrooms and madness: hallucinogenic mushrooms and some psychopharmacological implications. Can J Psychiatry. 1980;25:586-594.

Pradhan SC, Girish C. Hepatoprotective herbal drug, silymarin from experimental pharmacology to clinical medicine. Indian J Med Res. 2006;124:491-504.

703.2 Solanine Poisoning

Denise A. Salerno, Stephen C. Aronoff

Solanine is a mixture of several related toxins found in greened and sprouted potatoes. Potatoes exposed to light and allowed to sprout produce a number of alkaloid glycosides containing the cholesterol derivative solanidine. Two of these glycosides, α-solanine and α-chaconine, are found in highest concentration in the peels of greened potatoes and in the sprouts. Some solanine can be removed by boiling but not by baking. The major effect of α-solanine and α-chaconine is inhibition of cholinesterase. Cardiotoxic and teratogenic effects have also been reported.

Clinical manifestations of solanine and chaconine poisoning intoxication occur within 7-19 hr after ingestion. The most common symptoms are vomiting, abdominal pain, and diarrhea; in more severe instances of poisoning neurologic symptoms, including drowsiness, apathy, confusion, weakness, and vision disturbances, are rarely followed by coma or death.

Treatment of solanine poisoning is largely supportive. In the most severe cases, symptoms resolve within 11 days. Atropine treatment has not been evaluated.

Bibliography

Korpan YI, Nazarenko EA, Skryshevskaya IV, et al. Potato glycoalkaloids: true safety or false sense of security? Trends Biotechnol. 2004;22:147-151.

McMillan M, Thompson JC. An outbreak of suspected solanine poisoning in school boys: examination of criteria of solanine poisoning. Q J Med. 1979;48:227-243.

Ruprich J, Rehurkova I, Boon PE, et al. Probabilistic modelling of exposure doses and implications for health risk characterization: glycoalkaloids from potatoes. Food Chem Toxicol. 2009;47:2899-2905.

703.3 Seafood Poisoning

Denise A. Salerno, Stephen C. Aronoff

Ciguatera Fish Poisoning

Ciguatera fish poisoning is the most frequently reported seafood-toxin illness in the world. Major outbreaks of ciguatera fish poisoning have been reported in Florida, Hawaii, French Polynesia, the Marshall Islands, the Caribbean, the South Pacific, and the Virgin Islands. With modern methods of transportation, the illness now occurs worldwide. Grouper is the most commonly identified source of the toxin, followed by snapper, kingfish, amberjack, dolphin, eel, and barracuda. Poisoning has also been associated with farm-raised salmon.

The dinoflagellate Gambierdiscus toxicus, a microscopic unicellular organism found along coral reefs, produces high concentrations of ciguatoxin and maitotoxin. The toxins are passed along the food chain from small herbivorous fish that consume the dinoflagellate to larger predatory fish and then to humans. These toxins are harmless in fish but produce distinct clinical symptoms in humans.

The lipid ciguatoxin-1 is odorless, colorless, and tasteless and is not destroyed by cooking or freezing. Ciguatoxin-1 increases the sodium ion permeability of excitable membranes and depolarizes nerve cells, actions that are inhibited by calcium and tetrodotoxin.

Between 2 and 30 hr after ingestion, ciguatoxin poisoning typically produces a biphasic illness. The initial symptoms are not specific and of gastrointestinal origin (diarrhea, vomiting, nausea, and abdominal pain). The second phase occurs within a few days of ingestion and consists of intense itching, anxiety, myalgias, painful intercourse, and rash on palms and soles; the neurologic symptoms of circumoral or extremity dysesthesias (characterized by reversal of hot and cold sensation) are characteristic of this disease and may last for months. Tachycardia, bradycardia, hypotension, and death occur infrequently. Eating fish organs, roe, or viscera is associated with greater symptom severity. The diagnosis of ciguatera fish poisoning is based on clinical presentation and a compatible epidemiologic history; the diagnosis is confirmed by testing the ingested fish for toxin. Currently, there is no human biomarker to confirm ciguatera fish poisoning.

Treatment

Treatment of ciguatera fish poisoning is supportive. Gastric lavage is recommended to remove any remaining toxin. Intravenous fluids may be required for severe diarrhea, and parenteral administration of calcium can be used to treat hypotension. Once adequate hydration is established, mannitol (0.5-1.0 g/kg, IV over 30-45 min) given within 48-72 hr of the toxic fish ingestion is recommended for reduction of acute symptoms (especially neurologic) and possible prevention of chronic neurologic symptoms. Various other medications and herbal remedies have been tried, with variable results. Most cases are self-limited, and death occurs in less than 0.1% of cases.

Scombroid (Pseudoallergic) Fish Poisoning

Epidemic outbreaks have been linked with ingestion of members of the Scombresocidae and Scombridae families, including albacore, mackerel, tuna, bonita, and kingfish. Nonscombroid fish and marine mammals, such as mahi-mahi (dolphin) and bluefish, also have been associated with poisoning.

Scombrotoxin, either histamine or the product of the action of the toxin on fish flesh, is responsible for the clinical syndrome. Histidine is found in high concentrations in the flesh of scombroid fish; the action of bacterial decarboxylases during putrification converts the histidine to histamine. Fish containing more than 20 mg of histamine per 100 g of flesh are toxic. In patients receiving isoniazid, a potent histaminase blocker, ingestion of fish flesh containing a lower concentration of histamine may be toxic.

The onset of clinical manifestations is acute and occurs within 10 min to 2 hr of ingestion. The most common symptoms and signs are diarrhea, flushing, diaphoresis, urticaria, nausea, and headache. Abdominal pain, tachycardia, oral burning, dizziness, respiratory distress, and facial swelling also occur. The illness is usually self-limited, terminating within 8-10 hr.

Treatment

Treatment is mainly supportive. Gastric lavage decreases continued absorption of histamine. With severe diarrhea, fluid replacement may be necessary. Antihistamines have been variably successful. Four patients with severe toxicity treated with cimetidine (a histamine blocker) showed rapid response. Because data on these possible treatments are limited, cimetidine or ranitidine should be reserved for severe cases.

Paralytic Shellfish Poisoning

Mussels, clams, oysters, scallops, and other filter-feeding mollusks may become contaminated during dinoflagellate blooms or “red tides.” During periods of contamination, water in coastal areas can be colored red by the algae, thus the term “red tide.” (Such discoloration does not necessarily indicate the presence of toxin, and toxin may be present in high quantities without discoloration. Nonetheless, discolored water should be regarded with suspicion.) The dinoflagellates Alexandrium spp. and Gymnodinium catenatum often are responsible for these red tides and contain several potent neurotoxins. Paralytic shellfish poisoning is a distinctive neurologic illness caused by 20 closely related heat-stable paralytic shellfish toxins. Saxitoxin is the most potent of the neurotoxins responsible for paralytic shellfish poisoning. This toxin prevents nerve conduction by inhibiting the sodium-potassium pump. Other toxins may be bioconverted to less toxic compounds. Consumption of bivalves, such as mussels, scallops, and clams, is the usual pathway of intoxication, although crustaceans and fish have been implicated as well.

The onset of clinical manifestations of paralytic shellfish poisoning occurs rapidly, 30 min to 2 hr after ingestion. Abdominal pain and nausea are common. Paresthesias are common and occur circumorally, in a stocking-glove distribution, or both. Perioral numbness or tingling, diplopia, ataxia, dysarthria, and the sensation of floating are seen less commonly. Hot-cold reversal in temperature sensation is not unusual. In severe cases, respiratory failure from diaphragmatic paralysis may result. Swimming in the water during a red tide episode does not appear to have neurologic sequalae, although skin or mucosal irritation may result.

Treatment

No antidote for paralytic shellfish poisoning is known. Supportive care, including mechanical ventilation, may be needed. Although the symptoms are usually self-limited and short-lived, weakness and malaise may persist for weeks after ingestion.

Neurotoxic Shellfish Poisoning

Neurotoxic shellfish poisoning is a rare disease caused by molluscan shellfish contaminated with brevetoxins. Shellfish harvested along the Gulf of Mexico during or right after a red tide are at risk of contamination with brevetoxins produced by the dinoflagellate Karenia brevis. There has also been recent evidence of brevetoxin production by raphidophytes (Chattonella spp.). Brevetoxins are a group of more than ten lipid-soluble neurotoxins that activate sodium ion channels, causing nerve membrane depolarization. Shellfish are not affected by the brevetoxins. Rinsing, cleaning, cooking, and freezing do not destroy the toxins. Consumption of contaminated shellfish goes unnoticed since the brevetoxins cannot be detected by taste or smell.

The onset of clinical manifestations of neurotoxic shellfish poisoning occurs from within a few minutes up to 18 hr after consumption. The majority of symptoms are gastrointestinal (nausea, vomiting, and diarrhea) or neurologic (numbness and tingling of the lips, mouth, face, and extremities, ataxia, partial limb paralysis, reversal of hot and cold sensation, slurred speech, headache, and fatigue). Neurotoxic shellfish poisoning is similar to a mild case of paralytic shellfish poisoning.

Treatment

There are no specific antidotes for brevetoxins. Treatment involves mostly supportive care. Brevenal, a natural antagonist of brevetoxin produced by Karenia brevis may be used as a form of treatment in the future.

Diarrhetic Shellfish Poisoning

Several outbreaks of diarrhetic shellfish poisoning have been reported in Europe after consumption of mussels, cockles, and other shellfish. The dinoflagellates Dinophysis and Prorocentrum produce okadaic acid and its derivatives, the dinophysistoxins. These compounds inhibit protein phosphatases. The intracellular accumulation of phosphorylated proteins causes increased fluid secretion by gut cells via calcium influx, which is mediated by cyclic adenosine monophosphate and prostaglandins.

Patients have severe diarrhea. Care is supportive and directed at rehydration. The illness is self-limited, and recovery occurs in 3-4 days; few patients require hospitalization.

Amnesic Shellfish Poisoning

Amnesic shellfish poisoning was first reported in 1987 in Canada when a group of people demonstrated severe gastroenteritis as well as neurologic symptoms, including memory loss, after eating mussels from Prince Edward Island. Subsequent cases have been identified after consumption of shellfish from the USA, Spain, and the United Kingdom. The responsible toxin, domoic acid, comes from a diatom, Pseudonitzschia multiseries, and is a potent glutamate agonist, disrupting neurochemical transmission in the brain. It also binds to glutamate receptors, which increase calcium influx, producing neuronal swelling in the hippocampal area of the brain and death.

The initial clinical manifestations are gastrointestinal. Memory loss is closely related to advanced age. Those patients younger than 40 yr are more likely to suffer only from diarrhea, whereas those older than 50 yr suffer from short-term memory loss lasting months to years.

Azaspiracid Poisoning

The azaspiracids are a class of algal toxins. Azaspiracid poisoning results from ingestion of contaminated shellfish, especially mussels. Azaspiracid toxins are distributed throughout the muscle tissue in the shellfish. Symptoms start 6-18 hr after ingestion and include nausea, vomiting, severe stomach cramps, and diarrhea, which often persist up to 5 days.

Bibliography

Ciguatera Fish Poisoning

Caplan CE. Ciguatera fish poisoning. CMAJ. 1998;159:1394.

CDC. Cluster of ciguatera fish poisoning—North Carolina, 2007. MMWR Morb Mortal Wkly Rep. 2009;58:283-285.

DiNubile MJ, Hokama Y. The ciguatera poisoning syndrome from farm-raised salmon. Ann Intern Med. 1995;122:113-114.

Friedman MA, Fleming LE, Fernandez M, et al. Ciguatera fish poisoning: treatment, prevention and management. Mar Drugs. 2008;6:456-479.

Lange WR. Ciguatera fish poisoning. Am Fam Physician. 1994;50:579-584.

Palafox NA, Jain LG, Pinano AZ, et al. Successful treatment of ciguatera fish poisoning with intravenous mannitol. JAMA. 1988;259:2740-2742.

Scombroid Fish Poisoning

Gilbert RJ, Hobbs G, Murray CK, et al. Scombrotoxic fish poisoning: features of the first 50 incidents to be reported in Britain (1976–9). BMJ. 1980;281:71-72.

Hughes JM, Potter ME. Scombroid fish poisoning: from pathogenesis to prevention. N Engl J Med. 1991;324:766-768.

Wu SF, Chen W. An outbreak of scombroid fish poisoning in a kindergarten. Acta Paediatr Taiwan. 2003;44:297-299.

Shellfish Poisoning

Gessner BD, Middaugh JP. Paralytic shellfish poisoning in Alaska: a 20-year retrospective analysis. Am J Epidemiol. 1995;141:766-770.

Isbister GK, Kiernan MC. Neurotoxic marine poisoning. Lancet Neurol. 2005;4:219-228.

Kite-Powell HL, Fleming LE, Backer LC, et al. Linking the oceans to public health: current efforts and future directions. Environ Health. 2008;7(Suppl 2):56-70.

Morris PD, Campbell DS, Taylor TJ, et al. Clinical and epidemiological features of neurotoxic shellfish poisoning in North Carolina. Am J Public Health. 1991;81:471-474.

Shimizu Y, Yoshioka M. Transformation of paralytic shellfish toxins as demonstrated in scallop homogenates. Science. 1981;212:547-549.

Watkins SM, Reich A, Fleming LE, et al. Neurotoxic shellfish poisoning. Mar Drugs. 2008;6:431-455.

Whittle K, Gallacher S. Marine toxins. BMJ. 2000;56:236-253.

Fish Poisoning

Bret MM. Food poisoning associated with biotoxins in fish and shellfish. Curr Opin Infect Dis. 2003;16:461-465.

703.4 Melamine Poisoning

Denise A. Salerno, Stephen C. Aronoff

Melamine (1,3,5-triazine-2,4,6-triamine, or C3H6N6), a compound developed in the 1830s, is found in many plastics, adhesives, laminated products, cement, cleansers, fire retardant paint, and more. Melamine poisoning from food products was unheard of until 2007, when melamine-tainted pet food caused the death of many dogs and cats in the USA. In 2008, feeding of melamine-tainted infant formula to more than 300,000 children resulted in kidney injuries, 50,000 hospitalizations, and 6 deaths in China. This was the first reported epidemic of melamine-tainted milk products.

Melamine contains 66% nitrogen by mass. The addition of melamine to infant formula can give the formula a milky appearance and falsely raise the protein content as measured by nitrogen testing.

Melamine, combined with cyanuric acid, forms cyanurate crystals in the kidneys. Along with protein, uric acid, and phosphate, Melamine forms renal calculi.

Clinical manifestations are initially subtle and nonspecific. Severity is dose related. The first symptoms in affected infants are unexplained crying (especially when urinating), vomiting, and discolored urine caused by the formation of stones and gravel in the urinary tract. Urinary obstruction and acute renal failure follow. In the absence of a specific diagnosis, death due to renal failure occurs. Whether children with melamine-induced renal failure will have chronic sequelae is currently unknown.

The melamine stones and gravel can be treated with hydration, alkalinization, or lithotripsy. Acute renal failure requires supportive care and dialysis if needed.

Bibliography

Coulombier D, Heppner C, Fabiansson S, et al. Melamine contamination of dairy products in China—public health impact on citizens of the European Union. Eurosurveillance. 2008;13:1-2.

Ingelfinger JR. Melamine and the global implications of food contamination. N Engl J Med. 2008;359:2745-2748.

Lam HS, Ng PC, Chu WC, et al. Renal screening in children after exposure to low dose melamine in Hong Kong: cross sectional study. BMJ. 2008;337:a2991.

2009 Melamine and food safety in China [editorial]. Lancet. 2009;373:353.

2008 Melamine-tainted milk product (MTMP) renal stone outbreak in humans [editorial]. Hong Kong Med J. 2008;14:424-426.

2008 Melamine and cyanuric acid: toxicity, preliminary risk assessment and guidance on levels in food: WHO preliminary guidance. Geneva: World Health Organization, 2008.

Yang VL, Battle D. Acute renal failure from adulteration of milk with melamine. ScientificWorldJournal. 2008;8:974-975.

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