Cyanide Poisoning

A number of common plants may accumulate large quantities of cyanogenic compounds. Sorghums and related species readily accumulate these compounds. These cyanogenic compounds are in epidermal cells (outer tissue) of the plant, while the enzymes that enable cyanide production are in the mesophyll cells (leaf tissue).

Any event that causes the plant cell to rupture, allowing the cyanogenic compound and the enzyme to combine, will produce cyanide. Plant cells can be ruptured by cutting, wilting, freezing, drought, crushing, trampling, chewing or chopping.

Once plants containing cyanide have been consumed, the toxin rapidly enters the blood stream and is transported throughout the body of the animal. Cyanide inhibits oxygen utilization by the cells in the animal’s body. In essence, the animal suffocates.

Ruminant animals (cattle and sheep) are more susceptible to cyanide poisoning than nonruminant animals because the ruminal microorganisms have enzymes that will release cyanide in the animal’s digestive tract.

Cyanide is a potent, rapidly acting poison. Signs of cyanide poisoning can occur within 15 to 20 minutes to a few hours after animals consume the toxic forage. Animals often are found dead.

Clinical signs, when noticed, occur in rapid succession. Excitement, rapid pulse and generalized muscle tremors occur initially, followed by rapid and labored breathing, staggering and collapse. Signs also may include salivation (drooling), lacrimation (runny eyes), and voiding of urine and feces. The mucous membranes are usually bright pink, and the blood will be a characteristic bright cherry red.

When livestock losses occur and cyanide poisoning is suspected:

• Contact your veterinarian.
• Send the suspect forage to the diagnostic laboratory for analysis. Do not send grains, stomach contents or blood samples.
• Change forages or remove animals from suspected pastures until results of the analysis are returned.

The treatment for cyanide poisoning consists of re-establishing oxygen transport at the cellular level. Your veterinarian is the only qualified individual to institute this treatment.

Sodium nitrite is injected intravenously to convert hemoglobin to methemoglobin, which reacts with cyanide from the cyanide-cytochrome complex to form cyanmethemoglobin. A simultaneous injection of sodium thiosulfate provides sulfur to convert cyanmethemoglogin to the less toxic thiocyanate, which is excreted in the urine. The remaining methemoglobin is converted by other enzymes to hemoglobin, which then is available to transport oxygen normally.

Caution: Clinical signs of cyanide poisoning and nitrate poisoning are quite similar. Be certain nitrates are not a problem before administering sodium nitrite. An injection of sodium nitrite into an animal already suffering from nitrate poisoning would be disastrous.

The blood of animals affected with nitrate poisoning will be chocolate brown, compared with the cherry red of blood from prussic acid poisoning.

Sodium thiosulfate, alone, is also an effective antidotal therapy for cyanide poisoning.

Cyanide poisoning most often is associated with sorghums and sudangrass. However, a number of other plants can be cyanogenic. A list of these plants is found in Table 1.

Leaves usually produce two to 25 times more cyanide than do stems in forage grasses; seeds contain no cyanide. Young, upper leaves have more cyanide than lower leaves. New shoots often contain high concentrations of cyanide. New shoots produced after frost can be especially hazardous.

Cyanide content appears to be higher in plants grown in soils high in nitrogen and low in phosphorus. When fertilizing forage ground, use split nitrogen (N) applications when the total amount exceeds 60 pounds of N per acre to decrease the risk of cyanide toxicity.

Herbicides such as 2,4-D can increase cyanide concentrations in forage for several weeks after application. Plan grazing rotations accordingly.

Drought increases the chance for high levels of cyanide in plants. This may be because the plants have not been able to mature and contain mostly leaves, which have a higher in cyanide content. In general, any stress condition that retards plant growth can result in higher than normal levels of cyanide.

Frost or freezing causes plant cells to rupture, allowing cyanide to be released. If the potential for poisoning is great before freezing (high concentrations of cyanide-containing compounds are present), then the danger of poisoning is even greater while the plant is frozen and for several days following a frost.

Do not graze frosted summer annuals until the regrowth of shoots is 15 to 18 inches tall, or until several days after the entire plant and shoots are killed by a subsequent frost.

nide toxicity.