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 may contain
amygdalin or other glyco-sides, which on hydrolysis can release traces of
cyanide. The following contain mostly glycosides other than amygdalin:
Fern (Pteridium aquilinum)
Beans (Phaseolus species)
(Linum usitatissimum, Linum neomexicanum)
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
Treatment involves symptomatic and
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.
of amygdalin can produce manifestations of cyanide poisoning.
1. Almond (Prunus dulcis var amara)
2. Apricot (Prunus armeniaca)
3. Cherry Laurel (Prunus caroliniana &
4. Choke Cherry (Prunus virginiana & Prunus
5. Peach (Prunus persica)
6. Plum (Prunus domestica)
7. Wild Cherry (Prunus serotina).
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.
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.
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.
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.