Jamaican vomiting sickness is a disorder caused by the consumption of the unripe ackee fruit.
The symptoms of this illness are similar to that of Reye’s syndrome. The patient initially complains of severe epigastric pain for 2-6 hours which begins after consuming a meal of ackee fruits followed by an onset of sudden vomiting . Once the sickness begins, the progression is rapid. The symptoms patients experience are as follows: increased sweating, tachypnea, tachycardia, headache, generalized weakness, paresthesia, and disturbed mental state.
After a period of complete prostration which may last as long as 18 hours, a second bout of vomiting may occur . Unless this present condition is treated soon enough, this episode is usually followed by convulsions, coma, and death.
Death is more common in children than in adults. The average time of death is 12.5 hours. The other symptoms that come up in some cases are as follows: tonic-clonic convulsions in 25% of the patients, seizures occur in 85% of all fatal cases and fatty degeneration of the liver. Symptoms of this illness do not include fever or diarrhoea.
Jamaican vomiting sickness comes with its fair share of complications as well. These include: profound hypoglycaemia which may lead to coma and eventually death. There could also be acidosis, hypovolaemia and seizures .
Jamaican vomiting sickness is usually diagnosed by conducting the following tests: a finger prick glucose test in patients with suspected ackee poisoning, a serum chemical test to exclude electrolyte abnormalities which are likely to arise due to vomiting.
Liver function tests to demonstrate an increase in hepatic transaminases is also an indicator for the illness. Elevated levels of ammonia have been reported in cases of Jamaican vomiting sickness .
CT scan of the head may be indicated to exclude the possibility of structural intracranial pathology in patients with an altered mental status. A patient already suffering from hypoglycaemia may present with a focal neurologic deficit.
A liver biopsy may reveal depleted glycogen stores.
There is no standard method of treating Jamaican vomiting sickness. Care has been focused on relieving symptoms and providing supportive care. The traditional way of treating a bout of vomiting would always be to replenish the lost fluids in order to achieve an electrolyte, glucose and pH balance. However, here the mainstay of treatment would be to maintain a normal blood glucose level. It is advisable to administer a bolus of hypertonic dextrose solution followed by an infusion of 10% dextrose solution.
Activated charcoal is usually administered if the patient presents within 4 hours of ingestion. If mental status is altered, consideration should be given to airway protection prior to charcoal use.
Vomiting must be taken care of with antiemetics. Seizures could be managed with benzodiazepines . Some patients may require intubation and ventilator support as well.
The administration of riboflavin and glycine has also been reported to antagonize the effects of hypoglycinA intoxication. It is believed that riboflavin stimulates the de novo synthesis of acyl-CoA dehydrogenases while glycine conjugates with excess dicarboxylic acids produced due to impaired lipid metabolism.
Before various treatments came into picture, the mortality rate was 80%. However, with the introduction of various diagnostic techniques and treatment options available, the patients now have a full recovery.
There were several difficulties encountered by researchers in identifying the causative factor of the illness. The ackee fruit is eaten by many without ill effects. It was therefore not thought to be the likely source of the illness. Hypoglycin A is found predominantly in the immature fruit. The illness is caused due to the consumption of the unripe fruit or consumption of a forcibly opened fruit.
Besides this, consuming water in which an unripe ackee has been cooked also leads to the onset of an acute attack. Undernutrition in an individual also increases the susceptibility towards developing the symptoms of the disease.
The epidemiology of ackee poisoning has not really been understood well and the true incidence and mortality rate are believed to be under-reported. This problem is endemic in Jamaica. In Jamaica, the annual rate of ackee poisoning is 2 cases per 100,000 persons younger than 15 years of age and 0.4 cases per 100,000 persons older than 15 years. It is also frequent in certain other countries in the Caribbean and Western Africa. In contrast, it is rare in France and other Western countries. As ackee is consumed mostly in West Africa and Jamaica; therefore, most cases have occurred in those areas only.
Before treatments were developed, the mortality rate was as high as 80%. In recent years, there have been reported incidences of this illness in Burkina Faso, The Ivory Coast, Togo and Benin. Lethality was 100% in the Burkina Faso epidemic and victims of the illness were all children . Deaths were linked to ackee intoxication due to enhanced concentrations of dicarboxylic acids in the urine of the victims. Suggestions have been made that the ingestion of unripe ackee fruits may be responsible for a substantial number of unexplained deaths in preschool children in West Africa.
Two water-soluble toxins can be extracted from the fruit namely: hypoglycin A and hypoglycin B. Hypoglycin A is found in the aril of the fruit and is also more toxic than hypoglycin B . The unripe fruit contains 20 times more hypoglycin A than a ripe fruit. Both the components are found in the seeds. Hence, the seeds and the membrane covering the base of the seeds are considered poisonous.
The consumption of the ackee fruit leads to toxic hypoglycaemia and inhibition of neoglucogenesis. The hypoglycaemia is caused by the effect of hypoglycin A which is metabolized by means of transamination and oxidative decarboxylation to methylene cyclopropyl acetic acid (MCPA). MCPA forms non-metabolizable carnitine and coenzyme A (CoA) esters. MCPA inhibits beta-oxidation of fatty acids in two ways. Firstly, it interferes with the transport of long chain fatty acids into the mitochondria. Also, it inhibits acyl- CoA dehydrogenases so that only unsaturated fatty acids can be fully oxidized. Therefore, fatty acids accumulate in the liver in a microvesicular pattern. Hence, in the absence of fatty acid metabolism, the body becomes dependent on glucose and glycogen for energy. Hypoglycaemia thus results because both CoA and carnitine are necessary co-factors for long chain fatty acid oxidation and oxidation is a primary requisite for active gluconogeneis  . Once the glycogen stores are depleted, the body cannot synthesize glucose and severe hypoglycemia results.
Children are most susceptible to this illness and there appears to be ignorance with regards to the toxic nature of the unripe fruit. Ongoing educational campaigns are of utmost importance for the prevention and total eradication of this deadly syndrome.
The best way to prevent an attack of this illness is to avoid eating the unripe ackee fruit, avoid eating fruit that has been forcibly opened and totally avoid consuming water in which the ackee fruit has been boiled. It is best to discard such water.
Jamaican vomiting sickness (acute ackee fruit intoxication) is an acute illness caused due to the consumption of the unripe ackee fruit. The ackee fruit is the national fruit of Jamaica and is an integral part of many Jamaican diets.
In 1955 the causative factor of Jamaican vomiting sickness was isolated, a non proteinogenic amino acid, hypoglycin A, so named due to its ability to induce severe hypoglycaemia. Its chemical structure was elucidated in 1958 and scientifically it is referred to as L-alpha-amino-beta-methylene cyclopropane propionic acid.
Jamaican vomiting sickness is characterized by a sudden onset of vomiting which follows epigastric discomfort starting 2-6 hours after the consumption of a meal containing ackee .
Jamaican vomiting sickness is an acute illness characterized by the consumption of the unripe ackee fruit that is native to Jamaica. It is also caused by consuming an ackee fruit which has been forcibly opened, or drinking the water in which it has been boiled. Because of the prevalence of this illness more in the Caribbean, it is a must to educate the people about the dangers associated with the consumption of the unripe fruit.
The unripe fruit contains a much higher level of a toxin (hypoglycin A) than the ripe one. The concentration of the toxin is highest in the seeds and the membrane covering them.
A patient suffering with this illness will complain of severe epigastric pain which continues for hours followed by vomiting, convulsions or seizures    . The patient will also present with increased sweating, increased heart rate and pulse rate. There will be profound weakness and fatigue as well. The major complication associated with this illness is that of hypoglycaemia because the toxin interferes with the fatty acid metabolism thus utilizing the glycogen stores from the liver. This results in fatty degeneration of the liver as well. There are some cases which lead to coma and eventually death.
Death is mainly recorded in school children. However, with the introduction of various modes of treatment, the mortality rate has reduced considerable.
It is important to seek medical attention at the right time to prevent complications such as coma and death.