Ackee Fruit Toxicity 

Updated: Feb 16, 2019
Author: Dave A Holson, MD, MBBS, MPH; Chief Editor: Stephen L Thornton, MD 

Overview

Practice Essentials

Ackee, the national fruit of Jamaica, is a food staple in many Jamaican diets. The fruit is rich in essential fatty acids, vitamin A, zinc, and protein.[1, 2]  Consumption of unripe ackee fruit, however, can lead to potentially fatal toxicity, known as Jamaican vomiting sickness.

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 three glassy black seeds surrounded by a thick, oily, yellow aril. (See the images below.) The fruit should be allowed to open and ripen naturally on the tree.

Differentiating ripe versus unripe ackee fruit is necessary to prevent any potential adverse health effects. Unripe fruit is green to yellow and has a closed appearance and seeds are difficult to visualize. Cooking an unripe fruit does not reduce its toxicity. The seeds remain toxic and should not be ingested. Risk factors for ackee fruit toxicity include eating an unripe Ackee and reusing water used to cook unripe Ackee.[3]

Freshly picked Ackee fruit Freshly picked Ackee fruit
Black seeds surrounded by a thick, oily, yellow ar Black seeds surrounded by a thick, oily, yellow aril (edible portion).

Awareness of the potential toxicity of unripe Ackee fruit is necessary for early diagnosis and timely management. Public health education on the proper preparation of Ackee fruit in endemic areas may further decrease rates of toxicity.[3]

Background

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.[4]

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, Hassal et al were the first to isolate two 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-α -amino-β -[methylene cyclopropyl]propionic acid. Hypoglycin B is a γ -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.

Etiology

Potential risk behaviors for ackee poisoning include consumption of unripe fruit or ackee that has been forcibly opened and 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.

Epidemiology

The epidemiology of ackee poisoning has not been well characterized, and the true incidence and mortality rate are believed to be underreported.  The FDA regulates the importation of ackee fruit to the United States, allowing only up to 100 ppm of hypoglycin A content in cans of ackee fruit[5] ; 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.[6] The second was in Connecticut in a young Jamaican man who presented with cholestatic jaundice secondary to the chronic ingestion of ackee fruit.[7]

Since 1976, over 500 poisonings have been linked to ackee fruit in Jamaica and other countries.[8]  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.[9, 10]  More than 100 cases of acute illness and death were reported.

From 1998-2001, reports detailed 16 deaths of children in Surinam along the River Maroni, which separates Surinam and French Guyana. The deaths were subsequently linked to ackee fruit poisoning as result of the misuse of the plant by Maroon witch doctors to "cure" some pathologies especially acute forms of diarrhea in children.[8]  In 2015, ackee fruit poisoning was reported in 8 Nigerian siblings resulting in one death.[11]

Ackee is consumed mostly in West Africa and Jamaica; therefore, most cases have occurred in blacks. No difference in the sex distribution is noted. 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.

Prognosis

Before treatments were developed, the mortality rate was as high as 80%. With treatment most patients make a full recovery. If untreated, disease progression includes profound hypoglycemia, acidosis, hypovolemia, seizures, coma, and death. The onset of hypoglycemia is delayed for a few hours, but once present rapidly progresses. Deaths have been reported within 12 to 48 hours.[3]  

Patient Education

Patients should be educated about the danger of eating unripe or forcibly opened ackee fruit. Instruct patients to discard the water in which the fruit was prepared. Inform patients about the symptoms and signs of ackee fruit poisoning and the importance of immediately seeking medical attention.

 

Presentation

History

The clinical syndrome induced by the consumption of the unripe ackee fruit is known in Jamaica as "Jamaican vomiting sickness" or "ackee poisoning." The symptoms are similar to Reye syndrome. 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, generalized weakness, paresthesia, and disturbed mental states. 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. Death is more common in children than in adults.

  • 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.

 

Physical Examination

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)

 

DDx

 

Workup

Laboratory Studies

In patients with suspected ackee fruit poisoning, immediately order a fingerstick glucose test; do not wait for the serum glucose result. Profound hypoglycemia with blood glucose levels as low as 3 mg/dL has been documented.[12]

Obtain a serum chemical test to exclude electrolyte abnormalities as a consequence of the intractable vomiting. Elevated ammonia levels have also been reported.

Liver function tests demonstrate increased hepatic transaminases.

Obtain a urinalysis. In ackee fruit poisoning, results show acidosis but no ketosis. 

Imaging Studies

Nonenhanced head CT scanning may be indicated for the exclusion of structural intracranial pathology in patients with altered mental status or new-onset seizures. Patients with hypoglycemia may present with a focal neurologic deficit. In other patients, head CT scan findings should be normal.

Histologic Findings

Liver biopsy reveals depleted glycogen stores. Postmortem examination reveals the absence of liver glycogen and the fatty metamorphosis of the liver, kidney, and other organs.

 

Treatment

Approach Considerations

Traditionally, care in ackee fruit poisoning has been focused on relieving symptoms and providing supportive care with restoration of fluid, electrolyte, glucose, and pH balance. Patients with the following symptoms should be admitted to the hospital:

  • Severe and persistent hypoglycemia

  • Intractable vomiting

  • Seizures

  • Altered mental status

  • Hypotension

Consultation with a medical toxicologist through the local Poison Control Center is needed.

Medical Care

Administer a bolus of hypertonic dextrose solution followed by an infusion of 10% dextrose solution. Resuscitate volume-depleted patients with dextrose in normal saline.

Administer activated charcoal, which absorbs 100-1000 mg of poison per gram of carbon, 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. Decontamination with activated charcoal is contraindicated in patients with active emesis and risk of seizure.

Manage vomiting with antiemetics and seizures with benzodiazepines. Patients sometime require intubation and ventilatory support. Administer thiamine to the patient who is alcoholic or malnourished.

Animal studies have shown early glucose infusion with methylene blue reduces mortality associated with unripe ackee ingestion. Further testing in humans is needed.[13]

 

 

 

 

 

 

Medication

Medication Summary

The mainstay of treatment in ackee fruit poisoning is to maintain a normal blood glucose level. Antiemetics are usually indicated to control the vomiting. Administer activated charcoal as soon as possible after ingestion. Treat convulsions with benzodiazepines.

Antidote, Adsorbent

Class Summary

Consider activated charcoal decontamination in any patient who presents within 4 hours of ingestion. Activated charcoal is used for drug absorption and may be all that is required in mild-to-moderate toxicity. Activated charcoal is not absorbed and is excreted entirely through the GI tract.

Activated charcoal (Actidose-Aqua, Liqui-Char)

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal absorbs 100-1000 mg of drug per g of charcoal. Prevents absorption by adsorbing drug in the intestine. Multidose charcoal may interrupt enterohepatic recirculation and enhance elimination by enterocapillary exsorption. Theoretically, by constantly bathing the GI tract with charcoal, the intestinal lumen serves as a dialysis membrane for reverse absorption of drug from intestinal villous capillary blood into intestine. Does not dissolve in water.

Dextrose and glucose stimulators

Class Summary

Prompt gluconeogenesis is achieved with glucagon. Emergent blood glucose elevation requires the intravenous administration of dextrose.

Dextrose (D-glucose)

Used to promptly increase serum glucose level. Monosaccharide absorbed from intestine and distributed, stored, and used by tissues. Patients may recover if IV dextrose is administered before permanent damage due to low blood glucose levels occurs.

Glucagon

Polypeptide hormone identical to human glucagon; acts only on liver glycogen, converting it to glucose; do not use as empiric therapy because patients tend to be glycogen-depleted and may not improve; may be used temporarily until IV access obtained.

Antiemetics

Class Summary

These agents are used to control vomiting associated with ackee fruit poisoning.

Prochlorperazine (Compazine)

A phenothiazine derivative. May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors with its anticholinergic effects and by depressing reticular activating system.

Promethazine (Phenergan)

Phenothiazine derivative. Has antihistaminic, sedative, anti–motion sickness, antiemetic, and anticholinergic effects.

Metoclopramide (Reglan)

Stimulates motility of upper GI tract. Dopamine antagonist that stimulates acetylcholine release in myenteric plexus. Acts centrally on chemoreceptor triggers in floor of fourth ventricle, providing important antiemetic activity.

Benzodiazepines

Class Summary

These act in the GABA-benzodiazepine receptor complex and are used to control seizures.

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. May depress all levels of CNS, including limbic and reticular formation, by increasing action of GABA (major inhibitory neurotransmitter in brain).

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Insulin Secretion–inhibitors

Class Summary

Insulin secretion may be altered by various mechanisms.[14] Diazoxide inhibits pancreatic secretion of insulin, stimulates glucose release from the liver, and stimulates catecholamine release, which elevates blood glucose levels. Octreotide is a peptide with pharmacologic action similar to that of somatostatin, which inhibits insulin secretion.

Diazoxide (Hyperstat IV)

Reserved for severe persistent hypoglycemia. Increases blood glucose by inhibiting pancreatic insulin release, possibly through an extrapancreatic effect.

Octreotide (Sandostatin)

Acts primarily on somatostatin receptor subtypes II and V. Inhibits GH secretion and has multiple endocrine and nonendocrine effects, including inhibition of glucagon, VIP, and GI peptides. Highly effective in treatment of hypoglycemia caused by sulfonylurea overdose. Despite lack of published descriptions of its use in Jamaican vomiting sickness, may be useful in this setting.