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¶ What is Prussic Acid Toxicity?
The term “prussic acid” refers to hydrocyanic acid or hydrogen cyanide (HCN). Certain forage plants, notably the sorghums, can produce cyanide under certain growing conditions. Animals consuming forages with high HCN levels may die from cyanide poisoning.
Sorghums used as a forage source are most likely to cause cyanide poisoning, but other plants also have toxicity potential. Table 1 contains a list of common sorghum forages and their relative potential to accumulate cyanide. Other plants, like Indiangrass, black cherry, and chokecherries, have potential to cause cyanide poisoning under the right conditions.
Cyanogenic glucosides are cyanide-producing sugar compounds that are found in the outer leaf tissue (epidermal cells). These glucosides can break down into glucose sugars and release cyanide while doing so.
“Dhurrin” is the major cyanogenic glucoside found in sorghum. Dhurrin is non-toxic in the intact cells of healthy leaf tissue because the cyanide is bonded within the glucoside.
If the leaves are damaged, the ruptured cells release an enzyme called “emulsin” found in the internal leaf tissue (mesophyll). The ruptured cells allow the dhurrin and emulsin to mix, freeing the cyanide from its chemical bond, and releasing it.
Anything that damages plant cells - allowing the dhurrin and the emulsin to combine - will produce HCN. Cutting, wilting, freezing, drought, crushing, trampling, chewing, or chopping can all rupture plant cells. Even digestive juices may cause chemical hydrolysis and release HCN.
¶ Toxicity Symptoms
Once the HCN is released and consumed by an animal, it is absorbed directly into the bloodstream. There it combines with hemoglobin in the blood cells to form a cyanide complex called “cyanoglobin”. This complex prevents hemoglobin from transferring oxygen to individual cells, so the animal’s body tissues are without oxygen. If enough cyanide is present, the animal dies quickly from asphyxiation - often within 15 to 20 minutes.
Prussic acid poisoning symptoms are similar to nitrate toxicity symptoms. Symptoms include excess salivation, foaming at the mouth, difficult breathing or gasping, staggering, convulsions or spasms, and collapse. Blood may pass from the nostrils or mouth. Animals with cyanide poisoning have bright red blood that clots slowly, while animals poisoned with nitrate have dark, chocolate-colored blood. The smell of bitter almonds is often detected in animals poisoned with cyanide (see Figure 1).
Non-ruminant, like horses and hogs, have only one stomach which is strongly acidic. The stomach acid (hydrochloric acid) reacts with the liberated HCN to form much less toxic substances.
Ruminants (cattle and sheep) are more prone to prussic acid poisoning. The rumen is neither strongly acid nor alkaline, so detoxification is limited. Cud chewing and the rumen bacteria provide excellent conditons for hydrolyzing the glucoside and releasing HCN - which is then rapidly absorbed into the blood.
A single dose of HCN as small as 1 gram has been shown to kill a 1,000-pound cow. That same cow should be able to detoxify HCN at a rate of about 0.5 gram per hour. Thus, cattle or sheep could consume low-HCN forages without ill effects or signs of cyanide poisoning because the glucosides are eliminated before the concentration becomes harmful. Fatal poisoning occurs if the HCN enters the blood stream at a rate faster than the detoxifying rate of the animal.
¶ Toxicity Treatment
Prussic acid poisoning can be treated with simultaneous injections of sodium nitrate and sodium thiosulfate. Sodium nitrate releases the cyanide from the cell, which then binds with the sodium thiosulfate to form a nontoxic complex that is excreted. Treated animals remaining alive one to two hours after the onset of visible signs of toxicity usually recover.
¶ Plant Age and Condition
Prussic acid levels are normally higher in leaf blades than leaf sheaths or stems. Upper leaves contain more prussic acid than lower leaves. Young, rapidly growing plants are likely to contain high levels of prussic acid. Older plants have lower prussic acid levels than younger plants because of greater stem content.
Prussic acid levels generally increase within forage plants under any stress that retards normal plant growth or development. For example, rapid sorghum regrowth following drought, wilting, or frost injury may increase prussic acid in plants that would have otherwise been non-toxic. If favorable growing weather follows a killing frost, the regrowing shoots (i.e., “suckers” or tillers are likely to be very high in prussic acid.
Drought and frost are the most common stresses that trigger HCN accumulations, but soil nutrient stress may be common. Sorghums are often planted in marginal soils because of their ability to handle stress and limited water. Soils in these situations may have soil phosphorus, potassium, and zinc levels below critical thresholds. Using fertilizer nitrogen alone can help stimulate growth to a point, but limited supplies of other nutrients can limit growth. Applying fertilizer nutrients and lime based on soil analysis improves overall growth and forage quality.
Refer to Crop File 6.05.032, “Sampling and testing forages for prussic acid toxicity”, for potentially harmful HCN levels in forage samples.
¶ Table 1. Generalizing Ranking of Forage Types in Their Potential HCN Accumulations |
|
| Grain sorghum | high to very high |
| Forage sorghum, Sorgo varieties | intermediate to high |
| Sudangrass X sudangrass varieties | low to intermediate |
| Piper sudan | low |
| Sudangrass hybrids | intermediate |
| Sorghum-sudan hybrids | intermediate to high |
| Johnsongrass | high to very high |
| Shattercane | high |
| Pearl or foxtail millet | very low |
| Sorghum almum (Columbus grass) | generally high |
| Indiangrass seedlings | high |
¶ Figure 1. Cyanide vs Nitrate Poisoning
¶ References
Fjell, D., D Blasi, and G. Towne. 1991. Nitrate and Prussic Acid Toxicity in Forage: Causes, Prevention, and Feeding Management. MF-1018. Agronomy and Animal Science Extension, Kansas State Univ., Manhattan. 4 pg.
Stanton, T.L. and J. Whittier. 2006. Prussic acid poisoning. Fact Sheet No. 1.612. Colorado State University Extension, Fort Collins CO. 2 pg.
Vough, L. 1978. Preventing Prussic Acid Poisoning of Livestock. Ext. Circular NO. 950. Oregon State Univ., Ext. Serv., Corvallis OR. http://forages.oregonstate.edu/fi/topics/pasturesa...grazin gsystemdesign/preventingprussicacidpoisening accessed on 07/19/11
Stoltenow, C. and G. Lardy. 1998. Prussic Acid Poisoning. Pub. No. V-1150. NDSU Coop Ext. Svc., North Dakota State Univ., Fargo ND. http://www.ag.ndsu.edu/pubs/ansci/livestoc/v1150w.htm accessed 07/19/2011