Cyanide toxicity in animals

Pashu Sandesh, 06 June 2019

Dr Mamta Meena, Dr Ashok Prajapat, Dr Shikha Saini, Dr Tripti Gurjar


The plants, the most important source of cyanide toxicity in animals, which contain hydrocyanic acid (HCN) either free or in form of cyanogenic glycosides, are called as cyanogenetic plants. The glycoside itself is non-toxic, which owes its toxicity to cyanide after hydrolysis. Cyanogenetic plant toxicity is one of the most common plant poisonings among grazing livestock. Ruminants are more susceptible to poisoning by cyanogenic plants, which release hydrogen cyanide than horses and pigs due to more efficient hydrolysis of the cyanogenic glycosides. Within the group of ruminants, goats appear to be the most susceptible to cyanide.

The following intake mg hydrogen cyanide (equivalents/kg b.w. per day) seems to be tolerated by the following animal species: 


Tolerance level (mg/kg per day)









Cattle and buffaloes are also highly susceptible species. This type of toxicity usually occurs in animals when an animal ingests a large amount of immature sorghum fodder at the pre-bloomed stage. 

Rapid intake of plant equivalent to about 4 mg HCN/kg of body weight is considered to be a lethal amount of plant material. In the current trend for earning more profit, farmers are trying to cultivate more crops throughout the year, so they may cut the forage in the immature stage, which is the main source of cyanide toxicity. Generally, it happens due to lack of forage for feeding to animals because of improper forage management and also sometimes it may occur due to accidental ingestion while grazing. About 120 plant species containing cyanogenetic glycosides are found in India. The plant material containing over 20 mg HCN per 100 gm is potentially toxic to livestock. 

HCN/kg feed (ppm)

Effect of HCN on animals


Generally safe


Potentially toxic


Dangerous to cattle and usually cause death


The most common source of cyanogenic plant poisoning in livestock is feeding of green Sorghum fodder, particularly immature plant or young shoots.


Cyanide poisoning, Cyanide toxicity, Cyanide toxicosis and Formic anamminide or Formonitrile and Prussic acid poisoning


Cyanide exists in two from, free HCN and bound form. The bound form is cyanogenic glycoside, which is widely distributed in nature among 100 families of flowering plants. They are also found in some species of ferns, fungi and bacteria. It is reported that if the plant is frozen, chopped or chewed, damaged plant cells can release enzymes in their vacuoles, these enzymes and cyanoglycosides may contact with each other and produce cyanure. Cattle have bacterias that can produce the same enzymes in their rumen microflora and can convert the cyanogenic glycosides to cyanure gas. Amygdalin, Prunasin, Linamaryn, Lotaustralin, Dhurryn, Taxiphylyn, Vicianyn, Proteacyn ve Gynocardyn have been detected as most common glycosides in cyanogenic plants.

Factors that incur the likelihood of HCN poisoning from ingestion of cyanogenic plants include: 

(1) A large amount of free HCN and cyanogenic glycoside in the plant, 

(2) Rapid ingestion,

(3) Ingestion of a large amount of plant, 

(4) Ruminal pH and microflora that continue to hydrolyze glycosides to release hydrogen cyanide.

If the cyanide is taken to the body, it’s rapidly absorbed and circulated, then it’s merged with methemoglobin and forms cyanomethemoglobin. The circulating cyanide inactivates cytochrome oxidase enzyme by binding ferric (Fe+++) iron which is within this enzyme. Normally the cytochrome oxidase enzyme catalyzes the last step of oxidative phosphorylation. The enzyme-cyanide complex prevents this task from being performed. Because of that, the enzyme cannot combine with oxygen and electron transportation becomes inhibited. The patient cannot use caloric oxygen and cellular respiration stops immediately. As a result of this process, death occurs due to histotoxic anoxia.

Clinical sign:

Cyanure is one of the most vigorous toxins and can cause death in a short amount of time. The toxicity depends on the amount of ingested cyanogenic structure and ingestive rate, affected cattle rapidly begin to show toxication symptoms. Toxication symptoms may occur in 5-15 minutes to a few hours, but usually, animals do not survive 2 hours after consuming the lethal dose of cyanogenic structures. Dyspnoea, laboured breathing, restlessness, tremors, groaning, terminal clonic convulsions and opisthotonus are the clinical signs in affected animals. When the intracellular cyanide concentration is less than 0.2μg/ml, symptoms of poisoning do not occur. When the cyanide level is between 0.5 and 1μg/ml hyperemia of the skin and tachycardia and between 1-2.5μg/ml unconsciousness and excitement are seen. At the levels above, animals will easily enter a coma and die. Symptoms of poisoning occur mainly due to hypoxia. 

In chronic poisonings, arthrogryposis can be observed in the calves which consume sorghum. Myelomalacia and urinary incontinence can be formed in some cases. Cattle may have incoordination, ataxia, head shaking and pawning in the posterior extremities. Decrease of productivity, difficulty on conceiving and abortion can be also seen in such animals.

Postmortem findings:

Mucous membranes colour is pink in cyanide toxicity whereas venous blood is bright red which may clot slowly. Subendocardial and subepicardial petechial and ecchymotic haemorrhages typical of an agonal death may be present. A “bitter almond” or “cherry coke” odour from stomach contents may be detectable. Venous blood may not be bright red in animals dead several hours. The ability to detect the odour of bitter almonds is genetically determined, and many people cannot do so. Cyanotic mucosa, dark muscles, lung oedema and haemorrhages were observed at postmortem of died cattle. In cattle, Wallerian degeneration of the white matter of the spinal cord, cerebellar peduncles and cerebellum were reported.

Diagnosis and Differential Diagnosis

Cyanide analysis must be performed on suspected feeds and plants or cattle’s rumen content for the diagnosis. Sodium picrate test can be used for the cyanide detection in examples and commercial test kits are also available. To perform an accurate analysis that leads to a correct diagnosis, the collection of samples is very important. The sample must remain fresh if it is allowed to dry it end up with the loss of prussic acid. It is reported that for collection and transmit, samples must be placed in a container that can be tightly sealed, samples must be frozen, and they must be transported in the cold chain. 

In necropsy, the early formation of death attendance can be observed. Blood can be seen in red colour because oxygen couldn’t be kept and it’s used by tissues. Red and orange colour in the mouth and stomach can be observed. Bitter almond odour can be smelt in the rumen and internal organs. Subendocardial and subpericardial haemorrhages occur in all cases.

The challenges in recognizing acute cyanide poisoning can be originated from nonspecific early symptoms of toxicity such as dizziness, weakness, diaphoresis, hyperpnea and laboured breathing. Patients including these symptoms can be misdiagnosed with nitrate poisoning, organophosphorus poisoning and sulphur poisoning. An accurate diagnosis is essential because most of the clinical signs of prussic acid poisoning are similar to those poisonings. There are some distinguishing characteristics to eliminate cyanide poisoning from other events. Prussic acid causes the animal’s blood to turn a bright cherry red but in other events, it won’t occur. Providing sodium nitrite to animals suffering from nitrate poisoning rather than prussic acid poisoning could make these animals worse. Findings such as bitter almond odour and early formation of death attendance are characteristic to cyanide poisoning in the necropsy.


Treatment is often too late, and most cases result in death but some early noticed cases can be treated. However, sodium nitrate and sodium thiosulfate should be rapidly administered intravenously to affected cattle. Rumen content should be removed and replaced with contents from a healthy animal. This procedure should be repeated immediately to ensure complete removal of cyanogenetic material. Sodium nitrite and sodium thiosulphate are the specific antidotes for cyanide poisoning. 20% of sodium nitrate and 20% of sodium thiosulphate mixture can be applied intravenously to animals. After the treatment, the respiratory rate becomes slower and the cattle seemed to be more relaxed. 

Supportive therapy:

Oral therapy with glucose, molasses, or glyceraldehyde may provide a benefit. These products act as slow antagonists by tying up free HCN into cyanhydrin. However, due to the slow nature of this detoxification, they should not be used as a primary treatment. Saturated jaggery solution along with standard antidotal treatment was found to be synergistic for early recovery of animals.


Sorghum and sudangrasses should not be grazed when they are in an immature state. They must be allowed these forages to attain a height of 15 to 18 inches before grazing. New varieties of sudangrass and sorghum with lower prussic acid content should be considered when selecting seed. The animal's access to the wild cherry leaves must be interrupted. Plants must not be grazed during drought periods when growth is severely reduced or the plant is wilted or twisted. Animals must have been provided sufficient feed, like hay, so they will not be hungry when they enter fresh pastures. This will reduce the amount of prussic acid consumed and allow more time for the animal to detoxify low levels of HCN. If high cyanide is suspected at the forages, animals must not have been fed as green chop.


Cyanide being a potent inorganic poison and having a wide distribution in the environment causes incidences of toxicity in domestic animals. The early diagnosis and treatment with sodium thiosulphate and sodium nitrite are being used widely along with supportive therapy like oxygen therapy, cobalt salts, hydroxyl cobalamine etc. A newly developed antidote “Sulfenegen” has been proved 100 per cent effective in reducing blood cyanide level and protecting all the pig exposed to cyanide. The clinical implementation of this newly developed antidote would pave the new avenue for the treatment of cyanide toxicity. Scientific feeding and grazing management prevents the occurrence of cyanide toxicity.