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<br />Mozambique in 1981 from adrought-stricken cas-
<br />save staple area; from Zaire in 1928, 1932, 1937,
<br />and again in 1978-81; in Nigeria; and in the
<br />United Republic of Tanzania. The mean serum
<br />thiocyanate level in patients with Mantakassa is
<br />2.6 times higher than in non-Mantakassa patients
<br />in Nigeria, and 3.5 times higher Lhan in Tanzanian
<br />patients. Pesticides, infection, viruses, and con-
<br />sumption of food other than cassava were elimi-
<br />nated as possible causative agents in Mantakassa
<br />disease. Still unresolved is whether the disease is
<br />triggered when a threshold level of thiocyanate is
<br />reached, or when a critical combination of cyanide
<br />intoxication plus nutritional deficiency occurs
<br />(Cliff et al. 1984).
<br />Routes of administration other than dietary
<br />ingestion should not be discounted. Livestock
<br />found dead near a cyanide dispose] site had been
<br />drinking surface water runoff from the area that
<br />contained up to 365 mg HCN/L (EPA 1980). The
<br />use of cyanide fumigant powder formulations ma}'
<br />be hazardous b}' contact of the powder with moist
<br />or abraded skin, contact with the eye, swallowing,
<br />and inhalation of evolved HCN (Ballantyne 1988).
<br />In rabbits, lethal systemic toxicity was produced
<br />by contamination ofthe eye, moist skin, or abraded
<br />skin (but not dry skin) with cyanide powder formu-
<br />lations (40`%NaCN plus 607. kaolin) administered
<br />at 1-5 g powder per cubic meter (Ballantyne 19881.
<br />Hydrogen c}'anide in the liquid slate can readily
<br />penetrate the skin, and skin ulceration has been
<br />reported from splash contact with cyanides among
<br />workers in the electroplating and gold extraction
<br />industries-although effects in those instances
<br />were more like]}' due to the alkalinity' of the aque-
<br />ous solutions (Homan 1987). In one case, liquid
<br />HCA' ran over the bare hand of a worker wearing a
<br />fresh air respirator; he collapsed into unconscious-
<br />ness in :~ min, but ultimately recovered (EPA
<br />1980).
<br />Use of poisons in livestock collars is both spe-
<br />cific and selective for animals causing depreda-
<br />tions, as is the case for c}•anide collars to protect
<br />sheep against coyotes (Sterner 1979; Table 5).
<br />These collars contain a 33~ 1~'aCN solution and are
<br />usually' effective against coyotes. However, Feld
<br />results indicate that some coyotes kill b}' means
<br />other than neck attack, and some exhibit great
<br />wariness in attacking collared sheep (Savarie and
<br />Sterner 1979).
<br />Calcium c}•anide in (lake form w'as used in the
<br />1920~s to kill black-tailed prairie dogs and pocket
<br />gophers (Geom}•s bursoriusl in fiansas, and vari-
<br />ous other species of rodents in Nova Scotia (Wade
<br />C]'AN IDE 35
<br />1924). For prairie dog control, the usual practice
<br />was to place 43-56 g of calcium c}'snide 0.3-0.7 m
<br />below the rim of the burrow and to close the en-
<br />trances. The moisture in the air liberated HCN
<br />gas, which remained in the burrow for several
<br />hours, producing 100~~ kill. A lower dose of28 g per
<br />burrow was about 90~7r eflective (Wade 1924). Con-
<br />trol of prairie dogs with cyanide sometimes re-
<br />sulted inthe death of burrowing owls that lived in
<br />the prairie dog burrows (Wade 1924).
<br />Clinical signs of acute cyanide poisoning in
<br />mammals last only a few minutes after ingestion
<br />and include rapid and labored breathing, ataxia,
<br />cardiac irregularities, dilated pupv7s, convulsions,
<br />coma, respiratory failure, and rapid death
<br />(Egekeze and Oehme 1980; Ballantyne 1983). Cya-
<br />nide poisoning causes cardiovascular changes as
<br />well as its better known effects on cellular respira-
<br />tion. Cyanide increases cerebral blood flow in rab-
<br />bits and cats, and disrupts systemic arterial
<br />pressure in dogs (Robinson et a1. 1985). C--yanide af-
<br />fects mammalian behavior, most}y motor func-
<br />tions, although these effects have not been
<br />quantified. Cyanide-induced motor alterations ob-
<br />served in rats and guinea pigs include muscular
<br />incoordination, increased whole-body locomotion,
<br />disrupted swimming performance, and altered
<br />conditioned avoidance responses 6D'Mello 1987).
<br />As a consequence of the cytotoxic hypoxia in acute
<br />cyanide poisoning, there is a shift from aerobic to
<br />anaerobic metabolism, and the devClopment of lac-
<br />tate acidosis. A combination of rapid breathing,
<br />convulsions, and lactate acidosis its strongl}• sug-
<br />gestive of acute cyanide poisoning (Ballantye
<br />19831. As with other chemical asphyxiants, the
<br />critical organs that are most sensutive to oxygen
<br />depletion are the brain and heart (Egekeze and
<br />Oehme 19801. The only' consistent postmortem
<br />changes found in animals poisoned b}' cyanid!' are
<br />those re] sting to oxygenation of the blood. Because
<br />oxygen cannot be utilized. venous blood has a
<br />bright-red color and is slow to clot (Egekeze and
<br />Oehme 1980). Bright-red venous blood is not a reli-
<br />able indicator of cause of death, however, because
<br />it is also associated With chemicals other than cya-
<br />nide (Ballantyne 19831.
<br />Cyanide poisoning is associated with changes
<br />in various physiological and bioch@mical parame-
<br />ters. The earliest effect of cyanide intoxication in
<br />mice seems u• be inhibition of hepatic rhodanese
<br />activity, due to either blockage by excess binding to
<br />the active site or to depletion of the sulfane-sulfur
<br />pool. These changes do not seem to occur in blood,
<br />where rhodanese functions at its maximal rate,
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