CYANIDE TOXICITY IN CATTLE

CYANIDE TOXICITY IN CATTLE

Abhishek Pathak¹, Renu Yadav²

¹Department of Veterinary Pharmacology and Toxicology, ²Department of Veterinary Anatomy, C.V.A.Sc. G.B. Pant University of Agriculture & Technology,

Pantnagar, Uttarakhand- 263145

Introduction

One of the poisons that affects the cow population most quickly is cyanide. Prussic acid and hydrocyanic acid are other names for it. Because of its acidic character, hydrogen cyanide (HCN), commonly known as “prussic acid,” was originally extracted from the blue dye (Prussian blue) A colorless, odorless gas with a bitter almond scent is hydrocyanic acid. The cyanogenic glycosides are found in more than 2000 plant species. The most common sources of prussic acid are tar and sorghum and these plants are typically to blame for poisoning. Although cyanide is utilized in manure, cloth, paint, herbicides and insecticides, plants are the main cause of cyanide poisoning in animals. Cyanide is also present in bitter almond, cherry, peach and plum. Cherry kernels and bitter almond pulp each contain about 170 and 250 mg of cyano-glycoside, respectively, per 100g. Excessive cyanide exposure can be lethal [1, 2].

Etiopathology

As cyanogenic glycosides, cyanogenic plants contain cyanide. These glycosides are normally non-toxic, but when they are hydrolyzed, they become poisonous to both humans and animals. According to reports, injured plant cells can release enzymes in their vacuoles after being frozen, cut or chewed. These enzymes and cyan-glycosides may then interact to form cyanure.  The rumen microflora of cattle has bacteria that may manufacture the same enzymes and transform cyanogenic glycosides into cyanure gas. As the most prevalent glycosides in cyanogenic plants, Amygdalin, Lotaustralyn, Vicianyn, Proteacyn, Prunacin, Linamaryn, Dhurryn, Taxiphylyn, and Gynocardyn have been identified. According to reports, ingesting high amounts of cyanogenic plants, ruminal pH and microbiota, cyanogenic glycoside content or free HCN content can all raise the level of toxicity. Older plants and leaves contain less cyanogenic glycoside, which reduces the risk of poisoning. It has been demonstrated that some herbicides, such as 2,4-Dichlorophenoxyacetic acid, can potentially make plants more hazardous following application [3,4].

According to research, having too much nitrogen and not enough phosphorus in the soil might make plants more poisonous. The degree of poisoning is increased by high ruminal and abomasal pH. However, poisoning does not happen if the pH is less than 5.0 because the enzymes that separate the glycosides from the cyano get denatured. For sheep and cattle, the fatal dose of HCN is around 2 mg/kg of body weight. If the plants have more than 200 ppm of these glycosides, they are regarded as dangerous. Upon entering the body, cyanide is quickly absorbed, circulated and combined with methemoglobin to create cyano-methemoglobin. By attaching to the ferric (Fe⁺⁺⁺) iron present in the cytochrome oxidase enzyme, the circulating cyanide renders it inactive. Normally, the final stage of oxidative phosphorylation is catalyzed by the cytochrome oxidase enzyme. This function cannot be carried out because of the enzyme-cyanide complex. This prevents the enzyme from combining with oxygen and inhibits electron transport. Since the patient is unable to use caloric oxygen, cellular respiration instantly stops. Histotoxic anoxia results from this mechanism, which results in death [5,6].

Clinical signs

Cyanure is one of the most potent toxins and can quickly result in death. Affected animals quickly start to exhibit toxication signs; the severity of the poisoning relies on the amount of cyanogenic structure consumed and the pace of consumption. According to Arnold and Gaskill, toxication symptoms might appear anywhere between five minutes to a few hours following cyanogenic structure consumption, however patients typically don’t survive past two hours. Clinical symptoms in affected animals include dyspnea, laborious breathing, restlessness, tremors, moaning, terminal clonic convulsions and opisthotonos. Because blood contains a surplus of oxygen while tissues can’t utilize it, mucous membranes first seem brilliant and cherry-red. Mucous membranes turn cyanotic when a patient is hypoxic. Symptoms of poisoning do not appear when the intracellular cyanide content is less than 0.2 g/ ml. Between 0.5 and 1 g/ml of cyanide, skin hyperemia and tachycardia are observed, while between 1 and 2.5 g/ml, excitement and unconsciousness are noted. Patients at the levels above will quickly go into a coma and eventually die. Hypoxia can cause poisoning symptoms. Arthrogryposis can be shown in the calves that eat sorghum in cases of chronic poisoning. In some situations, myelomalacia and urine incontinence can develop. Patients may exhibit pawning in the posterior extremities, ataxia, head shaking and lack of coordination. Such patients may also have a decrease in production, difficulties getting pregnant and abortion [6,7].

Diagnosis

For the diagnosis, cyanide analysis must be done on suspicious foods, plants or cattle rumen content. Examples of cyanide detection using sodium picrate test can be found and commercial test kits are also offered. Collection of instances is crucial for carrying out an accurate analysis that results in a correct diagnosis. The sample must be kept fresh; if it is allowed to dry, prussic acid will be lost. According to reports, samples must be frozen, stored in a container that may be tightly sealed and moved in a cold chain in order to be collected and sent [9,11]. Early death attendance formation might be seen during necropsy. Because oxygen couldn’t be retained and was consumed by tissues, blood appears red. The mouth and stomach exhibit red and orange coloring. Rumen and internal organs might smell like bitter almonds. All cases had subendocardial and sub pericardial hemorrhages [8, 9].

The difficulties in diagnosing acute cyanide poisoning might result from early, non-specific toxicity symptoms such weakness, disorientation, hyperpnea, and laborious breathing. Patients who exhibit these symptoms may actually have sulphur, organophosphorus, or nitrate poisoning. Because the majority of the clinical indications of prussic acid poisoning resemble those of other poisonings, a precise diagnosis is crucial. To distinguish cyanide poisoning from other incidents, there are some telltale signs. The animal’s blood turns a vivid cherry red when exposed to prussic acid, although this won’t always happen. In contrast to prussic acid poisoning, giving sodium nitrite to animals with nitrate poisoning may make their condition worse. In the necropsy, cyanide poisoning is indicated by findings including a bitter almond odour and an early onset of death [10, 11].

Treatment

Although early-discovered instances can sometimes be treated, treatment is frequently too late and most cases end in death. However, sick cattle should be quickly given intravenous doses of sodium nitrate and sodium thiosulfate. The rumen contents of the patient should be changed for those of a healthy animal. To guarantee that all cyanogenetic material has been removed completely, this technique should be done right away. The specific antidotes for cyanide poisoning are sodium nitrite and sodium thiosulphate. Animals can receive an intravenous injection of a 20% sodium nitrate and 20% sodium thiosulphate combination. Following the therapy, the cattle’s respiration rate slowed and they appeared to be in a more relaxed state. Patients must be positioned in sternal recumbency and an effort must be made to get them to stand up right away [12, 13].

Prevention

When they are young, sorghum and Sudan grass should not be grazed. Before grazing, they must be given time for these forages to grow to a height of 15 to 18 inches. When choosing seed, new sudan grass and sorghum varieties with decreased prussic acid contents should be taken into account. It is necessary to prevent animals from accessing the wild cherry leaves. When growth is drastically decreased during droughts or the plant is wilted or bent, it must not be grazed. Animals must have had enough food, such as hay, so they won’t be starving when they move to other pastures. As a result, the animal will ingest less prussic acid and have more time to detoxify low amounts of HCN. Cattle must not have been fed green chop if excessive cyanide levels at the forages are detected. Conclusion One of the most significant poisonings in animals is cyanide poisoning. The ability of animals to pica made it more hazardous. The goal of this review is to focus on cyanide poisoning [14].

References

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10. Morocco AP (2005) Cyanides. Crit Care Clin 21(4): 691-705.
11. Nobrega JR, Escariao da J, Franklin RC, Rosary MT (2006) Poisoning by Sorghum halepense (Poaceae) in cattle in the Brezilian semiraid. Resq Vet Bra 26(4): 201-204.
12. Harshad PB, Shailesh NK, Chinag MM (2012) Treatment of cyanide poisoning in crossbred cows: a profile of drug synergism. IRJP 3(10): 169-170.
13. Borron SW (2006) Recognition and treatment of acute cyanide poisoning. J Emerg Nurs 32(4 Suppl): S12-S18.
14. Anonymous (2014) Prussic acid poisoning in livestock. Washington state university extension fact sheet, FS129E, pp. 1-3.

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