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Toxicity, Plants - Ackee Fruit
Updated: Apr 20, 2009
Introduction
Background
Ackee, the national fruit of Jamaica, is a food staple in many Jamaican diets. The word "ackee" originated from the Twi language. The ackee tree is a tropical evergreen tree that can grow as tall as 40 feet. Its leaves are broad and pinnate; its approximately 10-cm wide, 100-g fruit may be colored anywhere from straw to bright red. The fruit splits open while still on the tree to reveal 3 glassy black seeds surrounded by a thick, oily, yellow aril. The fruit should be allowed to open and ripen naturally on the tree. The fruit is rich in essential fatty acids, vitamin A, zinc, and protein.1
Freshly picked Ackee fruit
Black seeds surrounded by a thick, oily, yellow aril (edible portion).
The ackee tree is indigenous to West Africa, where it is called ankye or ishin. Thomas Clarke, Jamaica's first botanist, introduced the plant to the island in 1778. However, the ackee tree, Blighia sapida, was named after the infamous Captain William Bligh who took the breadfruit tree to the West Indies. The tree also grows in other West Indian Islands such as Cuba, Haiti and Barbados, in Central America, and in Southern Florida.
An association between ackee poisoning and Jamaican vomiting sickness was first noted in 1875 and documented in 1904. In 1937, Jordan and Burrows found a water-soluble toxic material in the seed and pods of the ackee fruit. In 1954, Hass et al were the first to isolate 2 toxic compounds in their crystalline form. These compounds were called hypoglycin A and hypoglycin B because of their hypoglycemic activity.
Pathophysiology
Two toxic water-soluble substances can be extracted from the fruit. The first toxin, hypoglycin A, is L-a -amino-b -[methylene cyclopropyl]propionic acid. Hypoglycin B is a g -L-glutamyl derivative of hypoglycin A and is less toxic than hypoglycin A. Hypoglycin A, but not hypoglycin B, can be found in the aril of the fruit. The unripe fruit has a much higher concentration of hypoglycin A (approximately 20 times) than that of the ripe aril. Both components are found in the seeds. Therefore, the seeds and the membrane at the base of the seed mantle are always poisonous.
Hypoglycin A, which is now simply called hypoglycin, is metabolized by means of transamination and oxidative decarboxylation to methylene cyclopropyl acetic acid (MCPA). MCPA forms nonmetabolizable carnitine and coenzyme A (CoA) esters, thereby depressing tissue levels of these cofactors and making them less available for other biochemical reactions. Hypoglycemia results because both CoA and carnitine are necessary cofactors for long-chain fatty acid oxidation and because oxidation is a requisite for active gluconeogenesis. MCPA also inhibits the dehydrogenation of several acyl-CoA dehydrogenases, including butyryl CoA, glutaryl CoA, and isovaleryl CoA. As a result of the inhibition of butyryl CoA dehydrogenase, the oxidation of long-chain fatty acids stops at the level of hexanoyl CoA and butyryl CoA. This effect leads to the decreased production of nicotinamide adenine dinucleotide (NADH) and acetyl CoA.
Because NADH and acetyl CoA are required as a cofactor of 3-phosphoglyceraldehyde phosphate dehydrogenase and as an activator of pyruvate carboxylase, respectively, their diminished concentration contributes to the inhibition of gluconeogenesis. The inhibition of glutaryl CoA dehydrogenase results in the accumulation of glutaryl CoA, which could inhibit transmitochondrial malate transport, a rate-limiting step in the early phase of gluconeogenesis, and consequently suppress gluconeogenesis. Altered levels of circulating insulin do not cause hypoglycemia associated with hypoglycin action.
Frequency
United States
Ackee is illegal in the United States; therefore, underreporting may occur. To date, 2 cases of ackee poisoning have been reported in the United States. The first was in Ohio in a Jamaican woman who presented with Jamaican vomiting sickness after a meal of ackee fruit. The second was in Connecticut in a young Jamaican man who presented with cholestatic jaundice secondary to the chronic ingestion of ackee fruit.
International
The epidemiology of ackee poisoning has not been well characterized, and the true incidence and mortality rate are believed to be underreported. At the request of the Jamaican Ministry of Health (JMH), the Centers for Disease Control and Prevention (CDC) identified 38 cases of Jamaican vomiting sickness and 6 deaths from 1989-1991. This problem is endemic in Jamaica; 271 cases have been reported to the JMH since 1980.
In 1998, an unexplained outbreak of epidemic fatal encephalopathy (EFE) occurred in Burkina Faso in West Africa. The only factor associated with EFE was the presence of ackee trees within 100 m of the households. The consumption of unripe ackee fruit possibly caused this epidemic.
In late 2000, the CDC provided technical support to the Ministry of Health in Haiti during an outbreak of ackee poisoning in the northern region of that country.2,3 More than 100 cases of acute illness and death were reported.
Mortality/Morbidity
Before treatments were developed, the mortality rate was as high as 80%. No deaths from ackee fruit poisoning have been reported in the United States. In Jamaica, 6 deaths were reported in 1989-1991. A link between ackee fruit poisoning and unexplained deaths of preschool children in West Africa has been postulated.
Race
Ackee is consumed mostly in Africa and Jamaica; therefore, the most cases have occurred in blacks.
Sex
No difference in the sex distribution is noted.
Age
In Jamaica, the annual rate of ackee poisoning is 2 cases per 100,000 persons younger than 15 years and 0.4 case per 100,000 persons older than 15 years.
Clinical
History
Jamaican vomiting sickness is characterized by a sudden onset of vomiting that is preceded by generalized epigastric discomfort starting 2-6 hours after the ingestion of a meal containing ackee. Once the sickness begins, symptom progression is rapid. Patients experience pronounced diaphoresis, tachypnea, tachycardia, headache, and generalized weakness. After a period of prostration, which may last as long as 18 hours, a second bout of vomiting may occur. Unless treatment is given, this episode is usually followed by convulsions, coma, and death.
- Tonic-clonic convulsions occur in 25% of the patients.
- Seizures occur in 85% of all fatal cases.
- Fatty degeneration of the liver similar to Reye syndrome also occurs.
- The average time to death is 12.5 hours.
- Symptoms of the disease do not include fever or diarrhea.
Guidelines for the diagnosis and management of other foodborne illnesses have been established by the American Medical Association, American Nurses Association, American Nurses Foundation, Centers for Disease Control and Prevention, Center for Food Safety and Applied Nutrition, US Food and Drug Administration, Food Safety and Inspection Service, and US Department of Agriculture.4
Physical
The general physical examination is important in deciding how aggressively to resuscitate the patient. Observed clinical manifestations, listed by degree of severity, are as follows:
- I - Asymptomatic with normal vital signs
- II -Dehydration and hypotension as a result of the intense vomiting
- III - Delirium or coma
- IV - Seizure (an ominous sign)
Causes
- Potential risk behaviors for ackee poisoning include the following:
- Consumption of unripe ackee fruit
- Consumption of ackee that has been forcibly opened
- Reuse of the water in which an unripe ackee has been cooked
- Undernutrition is also thought to be associated with individualized susceptibility to Jamaican vomiting sickness and the severity of the disease.
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References
Sharma S, Yacavone MM, Cao X, Samuda PM, Cade J, Cruickshank K. Nutritional composition of commonly consumed composite dishes for Afro-Caribbeans (mainly Jamaicans) in the United Kingdom. Int J Food Sci Nutr. Apr 1 2009;1-11. [Medline].
Joskow R, Belson M, Vesper H, et al. Ackee fruit poisoning: an outbreak investigation in Haiti 2000-2001 and review of the literature. Clin Toxicol (Phila). 2006;44 (3):267-73.
Moya J. Ackee (Blighia sapida) poisoning in the Nothern Province, Haiti, 2001. Epidemiol Bull. June 2006;22 (2):8-9.
American Medical Association; American Nurses Association-American Nurses Foundation; Centers for Disease Control and Prevention; Center for Food Safety and Applied Nutrition, Food and Drug Administration; Food Safety and Inspection Service, US Department of Agriculture. Diagnosis and management of foodborne illnesses: a primer for physicians and other health care professionals. MMWR Recomm Rep. Apr 16 2004;53:1-33. [Medline].
[Best Evidence] Vlasselaers D, Milants I, Desmet L, et al. Intensive insulin therapy for patients in paediatric intensive care: a prospective, randomised controlled study. Lancet. Feb 14 2009;373(9663):547-56. [Medline].
Addae JI, Melville GN. A re-examination of the mechanism of ackee-induced vomiting sickness. West Indian Med J. Mar 1988;37(1):6-8. [Medline].
Barennes, H, Valea, I, Boudat AM, et al. Early glucose and methylene blue are effective against unripe ackee apple poisoning in mice. Food and Chemical Toxicology. 2004;42(5):809-815. [Medline].
Bressler R, Corredor C, Brendel K. Hypoglycin and hypoglycin-like compounds. Pharmacol Rev. Jun 1969;21(2):105-30. [Medline].
CDC. Toxic hypoglycemic syndrome--Jamaica, 1989-1991. MMWR Morb Mortal Wkly Rep. Jan 31 1992;41(4):53-5. [Medline].
Eddleston M, Persson H. Acute plant poisoning and antitoxin antibodies. J Toxicol Clin Toxicol. 2003;41(3):309-15. [Medline].
Kean EA. Commentary on a review on the mechanism of ackee-induced vomiting sickness. West Indian Med J. Sep 1988;37(3):139-42. [Medline].
Larson J, Vender R, Camuto P. Cholestatic jaundice due to ackee fruit poisoning. Am J Gastroenterol. Sep 1994;89(9):1577-8. [Medline].
McTague JA, Forney R Jr. Jamaican vomiting sickness in Toledo, Ohio. Ann Emerg Med. May 1994;23(5):1116-8. [Medline].
Mills J, Melville GN, Bennett C, et al. Effect of hypoglycin A on insulin release. Biochem Pharmacol. Feb 15 1987;36(4):495-7. [Medline].
Tanaka K, Kean EA, Johnson B. Jamaican vomiting sickness. Biochemical investigation of two cases. N Engl J Med. Aug 26 1976;295(9):461-7. [Medline].
Further Reading
Keywords
ackee fruit, Blighia sapida, akee fruit, unripe akee fruit, unripe ackee fruit, Jamaican vomiting sickness, ackee fruit poisoning, akee fruit poisoning, toxic hypoglycemic syndrome, THS, Ankye, lshin, hypoglycin A, hypoglycin B, hypoglycin, ackee ingestion, unripe ackee ingestion, ackee poisoning, hypoglycemia, cholestatic jaundice, epidemic fatal encephalopathy, tonic-clonic convulsions, seizures, dehydration, hypotension
