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<br />34 BIOLOGtCnL RerottT 85(1.23)
<br />soning occurs when animals are exposed to chemi-
<br />cals used for fumigation or as a fertilizer (Webber
<br />et a1.1984),butthereisgeneralagreementthatin-
<br />gestion of plants containing high levels of
<br />cyanogenic glycosides is the most frequent cause of
<br />c}'anide poisoning in livestock.
<br />Cassava, also known as manioc, tapioca, yuca,
<br />or guacamate, is one of the very few-and, by far,
<br />the most important-food crops in which the cya-
<br />nide content creates toxic problems (Cooke and
<br />Coursey 1981). Cassava is a major energy' source
<br />for people and livestock in many parts of the world;
<br />it accounts for an average of 404 of the human ca-
<br />]oricintake inAfrica {Casadei et al. 1984), to more
<br />than 70°'e in some African diets (Way 1984). In
<br />comparison to other tropical crops it produces the
<br />highest yield )per hectare (Okeke et al. 1985). Cas-
<br />sava is native to tropical America from southern
<br />Mexico to northern Argentina and probably has
<br />been under cultivation there for 4,000-5,000
<br />years. It has been introduced to east Africa, Indian
<br />Ocean islands, southern India, and the Far East
<br />(Cooke and Coursey 19811. The global production
<br />ofcassava roots was estimated at50 million tons in
<br />1950, and 100 million tons in 1980; about 44.2 mil-
<br />]iontons are grown annually in Africa, 32.7 million
<br />tons in tropical America, and 32.9 million tons in
<br />Asia (Cooke and Coursey 1981). Linamurin is the
<br />principal cyanogenic glycoside in cassava; its toxic-
<br />ity isdue to hydrolysis by intestinal microflora re-
<br />leasing free cyanide (Padmaja and Panikkar
<br />1989 ). Rabbits (Oryctolagus cuniculus) fed 1.43 mg
<br />linamurin per kilogram BW daily (10 mg/kg BW
<br />weekly) for 24 weeks showed effects similar to
<br />those of rabbits tad 0.3 mg KCN/kg BW weekly.
<br />Specific effects produced by linamurin and KCN
<br />included elevated lactic acid in heart, brain, and
<br />liver; reduced glycogen in liver and brain; and
<br />marked depletion in brain phospholipids (Pad-
<br />maja and Panikkar 1989).
<br />The use ofcassava in animal feed presents two
<br />major problems: the presence of cyanogenic
<br />glycosides in the tuber, and the remarkably ]ow
<br />protein levels in fresh and dried cassava. Pigs fed
<br />low-protein cassava diets for 8 weeks had reduced
<br />food consumption and lowered liver weight; addi-
<br />tion of protein supplement to the diet reversed
<br />these trends (Tewe 19826). Removal of cyanogenic
<br />glycosides from cassava tubers, mash, peels, and
<br />root meal is accomplished with several techniques.
<br />Usually', the cassava root is dried in the sun for sev-
<br />eral weeks, and this process removes most of the
<br />cyanogenic glycosides; however, under conditions
<br />of famine or food shortage, this process cannot be
<br />carried out properly !Cliff et al. 1984). Long fer-
<br />mentation periods, especially under conditions of
<br />high moisture content, may be effective in sub-
<br />stantial detoxification of cassava mash (Ukhun
<br />and Dibie 1989). Cassava peels contajningas much
<br />as 1,061 mg HCN/I:g FW can be rendered suitable
<br />for feeding to livestock (4-625 mg/kg) by boiling for
<br />7 min, roasting for 30 min, soaking far 15 h, or dry-
<br />ing inthe sun for 7.6 days (Okeke et al. 1985). Cas-
<br />sava root meal (up to 400 of cassava meal) is
<br />satisfactory as a diet supplement for domestic pigs,
<br />provided cyanide content is <100 mg/kg ration
<br />(Gomez et al. 1983).
<br />Neuropathies associated with cassava inges-
<br />tion (i.e., cyanide intoxication) can develop into a
<br />syndrome in humans and domestic animals, char-
<br />acterized by nerve deafness, optic atrophy, and an
<br />involvement of the sensory spinal ner~ a that pro-
<br />duces ataxia, Other symptoms include stomatitis,
<br />glossitis, and scrotal dermatitis (Way 1981). Po-
<br />tentiallymore serious are long-term ¢ffects such as
<br />ataxic neuropath}', goiter, and cretinism, which
<br />have been attributed to high cassava content in di-
<br />ets. Thiocyanate~ne of the detoxification prod-
<br />ucts-inhibits iodine absorption and promotes
<br />goiter, a common ailment in trop~ca] countries
<br />(Cooke and Course}' 1981). At high dietary cyanide
<br />intakes there is an association with diabetes and
<br />cancer (Cliff et al. 1984), but this requires verifica-
<br />tion. The first case of cassava toxicity occurred al-
<br />most 400 years ago (Cooke and Coursey 1981). The
<br />toxic principle was later identified as a cyanogenic
<br />glycoside, shown Lo be identical with flax
<br />]inamurin (2-(beta-D-glucopyranasyloxy)-isobu-
<br />tyronitrile). All pans of the plant, except possibly
<br />the seeds, contain the glycoside tog¢ther with the
<br />enzyme linamarase. This enzyme effects hydroly-
<br />sis ofthe nitrile to free HCN when the tissue cellu-
<br />lar structure is damaged (Cooke and Coursey
<br />1981). Mantakassa disease is related to chronic
<br />cyanide intoxication associated with a dietconsist-
<br />ing almost exclusively of cassava; in times of fam-
<br />ineand sulfur-poor diets, Mantakassa effects were
<br />more pronounced (Casadei et al. 19$4). Symptoms
<br />of Mantakassa disease include the sudden onset of
<br />difficulty in walking, increased kne¢ and ankle re-
<br />flexes, elevated serum thiocyanatB levels, fever,
<br />pain, headache, slurred speech, dizziness, and
<br />vomiting. Vvomen of reproductive afle and children
<br />were the most seriously affected. Symptoms per-
<br />sisted for up to 4 months after treatment with
<br />hydroxycobalamin, vitamin supplements, and a
<br />high protein, energy-rich diet (C]itT et al. 1984).
<br />Mantakassa w'as reported in 1,102 victims in
<br />~~i
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