Cyanide Toxicosis
Basic Information 
Clinical Presentation
Etiology and Pathophysiology
• Cyanide reversibly inhibits mitochondrial cytochrome oxidase and blocks electron transport, resulting in decreased oxidative metabolism and oxygen utilization.
• Plant-associated cyanide toxicity depends on enzymatic hydrolysis of cyanogenic glycosides that liberates the toxic cyanide ion responsible for toxicity. Plants do not contain free HCN because the cyanogenic glycosides and the hydrolyzing enzymes are compartmentalized in the plant.
• Damage to the plant cell compartments is necessary to start the hydrolytic process. Optimally, this occurs at a pH greater than 4 or when the plants are damaged as a result of drought, wilting, freezing, or crushing.
• Plant-induced acute cyanide poisoning in horses is poorly documented in the literature, but cyanide poisoning in ruminants is well documented. This species difference is related to the ability of rumenal digestive microflora to rapidly hydrolyze cyanogenic glycosides and the low pH of the horse’s stomach in contrast to the more alkaline pH of the rumen.
• Plant cyanide-producing potential is highest in new growth and declines significantly as leaves mature.

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