Cassava Cyanide Diseases & Neurolathyrism Network (CCDNN)
Towards the elimination of cyanide poisoning, konzo, tropical ataxic neuropathy (TAN) and neurolathyrism


Konzo, TAN, cyanide poisoning and other cyanide diseases from cassava

Konzo 


In East and Central Africa excessive cyanide intake of bitter cassava and its products causes konzo which was first described in 1928 in the Democratic Republic of Congo (DRC). Konzo is an irreversible paralysis of the legs which affects mainly children and women of child bearing age. Konzo is an upper motor neuron disease and about one half of those with konzo need assistance with sticks or from another person in order to stand or walk. Konzo occurs in DRC, Mozambique, Tanzania, Cameroon, Central African Republic and was recently reported in Angola. The geographic spread of konzo is increasing within Mozambique (Cliff et al.,2011) and Tanzania (Mlingi et al., 2011) due to droughts and in DRC due to civil war (Chabwine et al.,CCDN News No 14, p 6). It has recently appeared in Angola and will continue to spread due to increased production of cassava in Africa (because of population pressure), its introduction into new areas where there is little or no experience of correct methods of processing and more frequent incidences of drought due to climate change (Nhassico et al., 2008).

Total reported konzo cases up to 2009 are 6788 (Cliff, CCDN News No 15, p 4), but in DRC alone there has been an estimate of 100,000 cases due to the prolonged war. Many cases are not reported since konzo often occurs during war and in isolated areas. In Mozambique and Tanzania recent outbreaks have been due to drought, which causes the cassava plant to produce much more cyanogens than normal. In 2004 we developed a simple wetting method that reduces the cyanide content of cassava flour 3-6 fold (see Wetting method to remove cyanide from cassava flour). This method has now been used successfully in a konzo village in DRC to prevent the occurrence of new cases of konzo (see Prevention of konzo using wetting method in a village in DRC).

Tropical ataxic neuropathy (TAN) and konzo 


TAN is a condition that has been known for more than a century and occurs in many countries of Africa, the West Indies and India (see Madhusudanan et al., CCDN News No 11, p3). It is a chronic condition of gradual or insidious onset, which is commonest amongst poor people in their 50's and 60's and is rare in children under 10. Patients are usually poor and consume a monotonous cassava diet. Symptoms include loss of sensation in hands, a sensation of something smeared on the soles of the feet which cannot be removed by trying to wipe it off, loss of vision, ataxia of gait, deafness, weakness and thinning of the legs. The disease is persistent in Nigeria and its incidence can be up to 18-26 persons per 1000 in villages where the diet is nearly all cassava. By comparison in yam-eating villages there is no incidence of TAN. It was considered that TAN was due solely to chronic cyanide intoxication but studies by Rosling and coworkers have shown that the situation may be more complex. By contrast konzo is due to acute cyanide exposure and levels of blood cyanide in konzo patients were found to be about 20 times as high as those in TAN patients. The onset of TAN is usually slow over months or years, whereas the onset of konzo is abrupt and its course is non-progressive. The mean age of people affected by TAN is greater than 40 years whereas konzo is primarily a disease of children and young women.

Cyanide poisoning

Cyanide is very poisonous because it binds to an enzyme called cytochrome oxidase and stops its action in respiration, which is the key energy conversion process in the body. The lethal dose of cyanide for an adult depends on body weight and is between 30 and 210 mg of hydrogen cyanide. Sometimes these limits are exceeded by persons eating a cassava meal and deaths occur due to cyanide poisoning. Smaller (non-fatal) amounts of cyanide cause acute intoxication with symptoms of dizziness, headache, nausea, stomach pains, vomiting and diarrhea.

Goitre and cretinism

Low dietary intake of iodine causes insufficient production of iodine-containing hormones in the thyroid gland and this produces goitre (enlargement of the thyroid gland) and cretinism (shortness of stature and severe mental impairment). Iodine deficiency disorders including goitre and cretinism are a major global health problem which affects about 500 million people. Ingested cyanide from cassava consumption is converted in the body to thiocyanate which is removed in the urine. The thiocyanate is a goitrogen, because it inhibits the uptake of iodine by the thyroid gland. Cyanide intake from cassava consumption thereby aggravates goitre and cretinism, but only if the iodine supply is below the recommended daily intake. Thus the effect of cassava in exacerbating goitre and cretinism may be corrected by increasing the intake of iodine.

Stunting of Children


Children in the DRC who ingested large amounts of cyanide from cassava were found to be stunted. The body converts cyanide into thiocyanate by a reaction that uses up S-containing amino acids that can only be obtained from food consumed (Cardoso et al., 2004). This priority removal of S-containing amino acids to detoxify cyanide, may lead to a shortfall of these amino acids in the diet which would limit protein synthesis and cause stunting.


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