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Chapter: Modern Medical Toxicology: Food Poisons: Food Poisoning

Cyanogenic Plants - Food Poisoning

Cyanogenic plants may contain amygdalin or other glyco-sides, which on hydrolysis can release traces of cyanide.


There are a number of plants that can cause food poisoning on their own, or through inadvertent contamination/deliberate adulteration of other food products. They include cyanogenic plants, fava beans, cycads, sweet pea and prickly poppy.

Cyanogenic Plants


Cyanogenic plants may contain amygdalin or other glyco-sides, which on hydrolysis can release traces of cyanide. The following contain mostly glycosides other than amygdalin:

■■  Apple (Malus species)

■■  Bracken Fern (Pteridium aquilinum)

■■  Cassava (Manihot species)

■■  Clover (Trifolium species)

■■  Elderberry (Sambucus species)

■■  Hydrangea (Hydrangea species)

■■  Lima Beans (Phaseolus species)

■■  Linseed (Linum usitatissimum, Linum neomexicanum)

■■  Pear (Pyrus species)

■■  Rush (Juncus species)

■■  Sedges (Carex species).


The botanical name of cassava is Manihot esculenta. Cassava root is said to be the second largest carbohydrate crop in the world, and constitutes a staple diet for millions of people. It is popular in several Indian states, especially in the deep South.

The edible part of manihot is the root, which is commonly referred to as cassava. If this is properly processed before consumption, it causes no harm. However, insufficiently processed cassava liberates cyanide in the gut from the ingested cyanogenic glycoside linamarin. This is normally converted to the less toxic thiocyanate by the enzyme rhodanese. The substrate for this reaction is sulfur originating from proteins in the diet. When dietary protein intake is low, signs of toxicity begin to manifest. The following conditions may occur:

·      Tropical ataxic neuropathy (TAN): More common in males.Main feature is posterior column sensory loss with ataxic gait. Optic atrophy and perceptive deafness have also been reported. Optic neuropathy results in decreased visual acuity, abnormal pupil size or an afferent pupillary defect, pigment disturbance and clumping beneath the macula, and loss of foveal reflex, associated with pallor and/or atrophy of a sector of the disc opposite the macula. When visual field defects are present the predominant defects are central and centro-cecal scotomas. Colour testing may reveal generalised dyschromatopsia, red-green and/or blue-yellow colour blindness.

·      Epidemic spastic paraparesis (ESP): More common infemales and children. Main feature is spastic paralysis of lower limbs. One variety of spastic paresis is called Konzo. It is characterised by bilateral, symmetrical involvement of the pyramidal tracts affecting the lower extremities resulting in spastic gait, paraplegia, extensor plantar responses, spastic bladder, constipation and impotence. Sometimes there is visual impairment. Epidemics of spastic paraparesis have been described in many areas of the world where cassava with high cyanogenic glycosides content is consumed as a significant proportion of the diet. Pancreatitis and endemic goitre have also been reported in patients from cassava-consuming areas.

Administration of cassava or Laetrile® in animal studies have resulted in limb defects, open eye defects, microcephaly, and foetal growth retardation. Sodium thiosulfate administra-tion protected the foetus from such teratogenic effects. Acute toxicity is rare. However, there is one report of deaths of three patients after a single meal of cassava. Cyanide levels in the blood averaged 1.12 mg/L; urinary levels averaged 0.54 mg/L.

Treatment involves symptomatic and supportive measures.

Amygdalin-containing Plants

The common sources of naturally occurring amygdalin are mentioned below. Amygdalin is the cyanogenic diglucoside D-mandelonitrile-beta-D-gentiobioside, and is not toxic until it is metabolised by the enzyme emulsin which is present in the seeds of these plants. Synthetic amygdalin (laetrile) has been tried without significant success, in the treatment of cancer.

Overdose of amygdalin can produce manifestations of cyanide poisoning.

1.  Almond (Prunus dulcis var amara)

2.  Apricot (Prunus armeniaca)

3.  Cherry Laurel (Prunus caroliniana & Prunus laurceroasus)

4.  Choke Cherry (Prunus virginiana & Prunus melanocarpa)

5.  Peach (Prunus persica)

6.  Plum (Prunus domestica)

7.  Wild Cherry (Prunus serotina).

Crushed seeds of some of the mentioned varieties are marketed as health foods. They are also marketed and sold as cancer remedies or vitamin supplements. Some examples include Laetrile®, Bee Seventeen®, and Aprikern.

One of the richest sources of amygdalin is the bitter almond and it has been established that 40 to 60 seeds, yielding 70 mg of hydrocyanic acid would result in severe toxicity or death.

Acute toxicity results in dyspnoea, weakness, dizziness, sweating, vomiting, disorientation, convulsions, paralysis, cyanosis, coma, and cardiovascular collapse. Cherry red blood colouration is rarely seen, but has been reported. In most cases, symptoms are mild.

Mild to moderate toxicity requires only decontamination and supportive measures. Severe poisoning must be treated on the same lines as for cyanide poisoning. The usual antidotes (nitrites and thiosulfate) should be administered in patients who are clinically symptomatic (unstable vital signs, acidosis, impaired consciousness, seizures, or coma). The goal of nitrite therapy has been to achieve a methaemoglobin level of 20–30%. Administer 100% humidified supplemental oxygen with assisted ventilation as required. Hyperbaric oxygen has been recommended as being more efficacious. Crystalloids and vasopressors can be given for hypotension. Administer sodium bicarbonate if required.


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