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Acute ackee fruit intoxication

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Other Names: Ackee poisoning; Jamaican vomiting sickness

A rare disease caused by the ingestion of unripe Blighia sapida fruits. It is a serious intoxication that is frequent in certain countries in the Caribbean and Western Africa. In contrast, it is rare in France and other Western countries. Intoxication leads to toxic hypoglycaemia and inhibition of neoglucogenesis. The hypoglycaemia is caused by the effect of hypoglycin A, which is found in the arils.

Ripe ackee fruit in Jamaica. The white flesh is eaten cooked for breakfast, with salt fish or the like. (33317955982).jpg
Ackee 001.jpg


The Blighia sapida tree is native to West Africa. In 1778, it was imported to Jamaica where it has remained the national fruit of the country and an essential part of the Jamaican diet. The epidemiology of the disease has not been well established in Jamaica, but mortality and morbidity are thought to be underreported. There are more cases of the illness in during Jamaican winter months when the fruit is not yet ripe. Blighia sapida also is found in southern Florida, several Caribbean countries, and Cental America. Ackee imported into the United States is regulated by the Food and Drug Administration (FDA) to limit products containing dangerous amounts of the toxin, hypoglycin A. Only a few cases of toxicity have been reported within the United States. Pediatric patients and the malnourished are at greatest risk for toxicity.


The Ackee fruit matures into three sections, each consisting of a large black seed and a fleshy yellow aril. The aril, the edible portion of the fruit, initially contains high levels of the toxin, hypoglycin. However, over time, as the fruit ripens, the hypoglycin levels drop to ranges allowing for safe human consumption. Toxicity only occurs with ingestion of the unripe Ackee fruit.

Differentiating ripe versus unripe Ackee fruit is necessary to prevent any potential adverse health effects. Ripe Ackee fruit may be identified by a yellow-red to red color and wide-open appearance (seeds easily visible). Unripe fruit is green to yellow and has a closed appearance (seeds are difficult to visualize). Cooking an unripe fruit does not reduce its potential for toxicity. The seeds remain toxic and should not be ingested. Risk factors for Ackee fruit toxicity include eating an unripe Ackee, purchasing tampered Ackee, or the reusing of water that has been previously used to cook unripe Ackee.

Signs and symptoms

The clinical manifestations are severe (coma, convulsions, delirium, toxic hepatitis, acute dehydration and a state of shock) and may lead to death.


Patients with clinical suspicion for Jamaican vomiting sickness should be evaluated in a hospital and admitted for observation. Intravenous access should be obtained to administer fluids and dextrose if needed.

Diagnostic evaluation should include blood glucose, serum electrolytes, liver function tests, renal function, lactate, ketones, and blood gasses. Symptomatic patients will require close monitoring of laboratory tests, especially glucose and serum electrolytes. An early ECG may show evidence of electrolyte abnormalities before laboratory diagnostic results. Hypoglycin and its metabolite MCPA may be tested for in blood and urine; however, they may be undetectable secondary to rapid elimination. Other diagnostic tests that help confirm the diagnosis include elevated serum/urine carnitine concentrations and elevated concentrations of urinary dicarboxylic acid.


Treatment is primarily supportive as no current antidote for hypoglycin A exists. Patients require close monitoring for hypoglycemia and should be treated with dextrose. Boluses of dextrose may be given initially followed by an infusion which may be titrated to maintain euglycemia. Intravenous fluids should be provided to prevent dehydration and antiemetics to alleviate symptoms.

Vomiting and dehydration may lead to electrolyte abnormalities which should be repleted. Benzodiazepines may be used for the treatment of seizures, but again it is prudent to rule out hypoglycemia as the cause of the seizures. GI decontamination, including activated charcoal and gastric lavage, may be considered if there is a concern for potential toxicity if the patient presents within a few hours of ingestion. There is not sufficient evidence to suggest GI decontamination consistently improves patient outcomes. There id no role for syrup of ipecac following acute ingestions.

Riboflavin and glycine have been used for treatment as they are thought to antagonize hypoglycin A. Methylene blue has also been proposed as a treatment option for potentially fatal encephalopathy. True efficacy of these supplements is unknown. A medical toxicologist may assist in providing management and may be reached through the local Poison Control Center.

Patients with persistent hypoglycemia, seizures, metabolic acidosis, altered mental status, or poor perfusion will most likely require admission to an intensive care unit (ICU).

Education focusing on the health hazards of eating unripe Ackee fruits may decrease the future incidence of the disease.

NIH genetic and rare disease info

Acute ackee fruit intoxication is a rare disease.

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