It is a beautiful tree with smooth grey bark. It grows to 10-12 metres. The tree grows well in tropical to subtropical areas and can grow up to 900 metres above sea level. The leaves are composite, and are 15 to 30 cm long. They are shiny on the upper side and lightly hairy on the underside. The small bisexual and male flowers form pleasant-smelling white flower clusters 7-17 cm across. The fruit is pear-shaped with three distinct lobes. The fruit is 7-10 cm across. The unripe fruit is green and the seed mantle is closed. When the fruit is ripe it opens spontaneously, showing the black, shiny seeds, each surrounded by a cream-coloured seed mantle. They are similar to their distant relatives, the lychee and rambutan. Normally there are three seeds, but in 30-50% of fruits 1 or 2 of the seeds are very small or absent. The base of each seed mantle (syn. aril) is attached on the stalk side by a pinkish orange membrane. When the fruit ripens it become yellow, then red. The fruit is eaten fresh, baked, boiled in milk or soup or processed into preserves.

The fruit of the tree is rightly infamous. The seeds and the membrane at the base of the seed mantle are always poisonous. Only when the fruit ripens and opens naturally on the tree may the fruit be eaten. The membrane at the base should be removed. The seed mantle of unripe fruits contains the toxic constituents hypoglycin A and B. The gamma-glutamyl derivative of hypoglycin A is known as hypoglycin B. It is a water-soluble liver toxin. The poison limits the availability of various cofactors such as coenzyme A and carnitine. Hypoglycaemia results (disturbed gluconeogenesis), together with microvesicular steatosis of the liver (accumulation of lipid vesicles in the liver), hyperammonaemia (disturbed urea cycle) and metabolic acidosis.

When food is scarce and people eat the unripe fruits, there may be epidemics of hypoglycaemia. Uninformed young children may accidentally eat unripe fruits. Most cases of poisoning do in fact occur in young children (2-6 years). It is thus chiefly in the paediatric department that problems are seen. Sometimes more than one family member is affected, e.g. when several people have eaten unripe fruit or if water in which ackee fruit has been cooked, is re-used in the kitchen. Since the condition is well known in Jamaica, the disorder is sometimes described as "vomiting sickness of Jamaica". This does not mean that there are not regularly cases in West Africa and in countries other than Jamaica. In Jamaica, the problem occurs principally during the cooler months, from November to April.

Ackee poisoning produces nausea and acute vomiting without diarrhoea, followed by dizziness, slight fever, convulsions, coma and death. There is extreme hypoglycaemia which can be corrected by IV glucose. The symptoms begin 2-3 hours after the meal, although the incubation time is sometimes shorter. The patient has intense thirst. There is pronounced sweating, tachypnoea and tachycardia, headache, general weakness and hypotonia. The child is confused or stuporous. Tonic-clonic convulsions occur in one quarter of patients. Fatty degeneration of the liver, similar to Reye’s syndrome, is seen. Death may follow within 12 hours.

The glycaemia should be determined in the laboratory as quickly as possible. It is wise to follow blood electrolytes, renal function, liver function, ammonaemia, coagulation tests, lactate and arterial pH (for the evaluation of acidosis). A CT-scan of the brain is normal in ackee poisoning. Gas chromatography of the urine shows an excess of medium-chain fatty acids. At autopsy massive liver steatosis is observed.

The patient is treated with IV fluids containing glucose. Benzodiazepines are given in case of convulsions (also given as preventive). If possible intubate and give artificial respiration. Give activated charcoal PO, e.g. via nasogastric tube. The very large surface of the activated charcoal particles absorbs 100-1000 mg of poison per gram of carbon. Activated charcoal is not soluble in water. It is administered at 1 gram per kilogram of body weight. Do not mix activated charcoal with milk. In theory glycine, riboflavin and carnitine may be beneficial, but this has not yet been proven in clinical practice. The estimated useful dose of carnitine is 1-3 g per day PO or 50 mg/kg IV over 2-3 minutes.

In diabetic hyperglycaemic coma and in delirium tremens, administration of glucose without thiamine may be dangerous. In people with thiamine deficiency (e.g. alcoholics), administration of glucose may trigger overt clinical symptoms of vitamin B1 deficiency. Acute beriberi may follow.

Patients and their families should be informed of the risk of unripe ackee fruit. Eating unripe fruit and re-using water in which ackee fruit have been cooked in the kitchen, must be avoided. Malnutrition is a risk factor for severe poisoning. An information campaign should be organised for the general population at regular intervals.