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' • • i 1 dietary, industrial, and environmental factors (Way 1981, 1984; Gee 1987; Marrs and Ballantyne 1987). Chronic exposure to cyanide is correlated with specific human diseases: I~'igerian nutritional neuropathv, Leber's optical atrophy, retrobulbar neuritis, pernicious anemia, tobacco amblyopia, cretinism, and ataxic tropical neuropathy (Towill et al. 1978; Way 1981; Sprince et al. 1982; Bernin- ger et al. 1989; Ukhun and Dibie 1989 ). The effects of chronic cyanide intoxication are confounded by various nutritional Cactors, such as dietary defi- ciencies ofsulfur-containing amino acids, proteins, and water-soluble vitamins (Way 19811. Most authorities now agree on five points: (1) cyanide has low persistence in the environment and is not accumulated or stored in any mammal studied; (2) cyanide biomagnification infood webs has not been reported, possibly due to rapid detoxi- fication of sublethal doses by most species, and death at higher doses;(3)cyanide has an unusu- ally ]ow chronic toxicity, but chronic intoxication exists and, in some cases, can be incapacitating; (4 ) despite the high lethality of large single doses or acute respiratory exposures to high vapor concen- trations of cyanide, repeated sublethal doses sel- dom result in cumulative adverse effects; and (51 cyanide, in substantial but sublethal intermittent doses can be tolerated b}~ many species fur long pe- riods, perhaps indefinite]}~ (To~~ill et al. 1978; EPA 1980; V~'ay 1984; Ballantyne and Marrs 1987a; Ta- ble 5). The toxicity of cyanogenic plants is a problem for both domestic and wild ungulates. Poisoning of herbivorous ungulates is more prevalent under drought conditions, when these mammals become less selective in their choice of forage; dry growing conditions also enhance cyanogenic glycoside accu- mulations in certain plants (To~vil] et al. 1978). Animals that eat rapidly are at greatest risk, and intakes of 4 mg HCI\/kg BV.' can be lethal if con- sumed quick]}• (Egekeze and Oehme 1980). In gen- eral, cattle are most vulnerable to cyanogenic plants; sheep, horses, and pigs-in that order-are more resistant than cattle (Cade and Rubira 1982 ~. Deer IOdocoilcus sp.) and elk (Ceruus sp.) have been observed to graze on forages that contain a high content of cyanogenic glycosides; however, c}•anide poisoning has not been reported in these species (Towill et al. 1978). Ruminant and nun ruminant undulate mam- mals that consume forage with high cyanogenic glycoside content, such as sorghums, Sudan grasses, and corn, may experience toxic signs due to microbes in the gut that hydrolyze the CYANIDE 33 glycosides, releasing free hydrogen cyanide (Towill et al. 19781. Signs of acute cyanide poisoning in livestock usually occur H~ithin 10 min and include initial excitabilit}~ with muscle tremors, salivation, ]acrimation, defecation, urination, and labored breathing, followed by muscular incoordination, gasping, and convulsions; death can occur quickly depending on the dose administered (Towill et al. 1978; Cade and Rubira 1982). Thyroid dysfunction has been reported in sheep grazing on stargrass (('ynodon plectostachyus), s plant with high cyanogenic glycoside and ]ow iodine content. Sheep developed enlarged thyroids and gave birth to lambs that were stillborn or died shortly after birth (Towill et al. 1978). Cyanogeroic foods can ex- acerbate selenium deficiency, as judged by the in- creased incidence of nutritional myopathy in lambs on low-selenium diets (E1zUbier and Davis 1988a). A secondary effect fYom ingesting cyanogenic glycosides from forage is sulfur defi- ciency as a result of sulfur moliiliz~tion to detoxify the cyanide to thiocyanate (Towill et al. 1978). Cyanide poisonings of livestock b}' forage sor- ghums and other cyanogenic plantg are well docu- mented (Cade and Rubira 1982). Horses in the southwestern United States grazing on Sudan grass and sorghums developed pgsterior muscle incoordination, urinary incontinence, and spina] cord histopatholog}•; offspring of mares that had eaten Sudan grass during early pregnancy devel- oped musculoskeleta] deformities (Towill et al. 1978). Salt licks containing sulfur (8.5~i~) have been used to treat sheep after they failed to gain weight when grazing on sorghum with high HCI~' content (Towill et al. 1978). Sugar gum (Eucalyp- tus cladoca~vs) and manna gum (Eucal}~ptus uinxin.alis) contain high levels of cyanogenic glycosides, and both have been implicated as the source of fatal HCN poisoning in domestic sheep and goats that had eaten leaves from branches felled for drought feeding, or after grazing sucker shoots on lopped stumps (Webber et al. 19841. In one case, 10 goats died and 10 others were in di=_- tress within 2 h after eating ]eaves from a felled sugar gum. Dead goats had bright red blood that failed to clot and subepicardial petechia] hemor- rhages. Rumens of dead goats contained leaves of Eucalyptus spp. and smelled of bitter almonds. The 10 survivors were created intravenouslc with 3 mL of a 1-L solution made to contain 20 g of so- diumnitrite and 50 g of sodium thiosulphate: four recovered and six died. Of 50 afillcted goats, 24 died within 29 h and the remainder recovered (Webber et al. 1984. ]n rare instances HCN poi-