Cyanogenetic plants 

Plants that have cyanogenetic glycosides include: Acacia leucophloea, Lotus sp. Nerium oleander, Sorghum vulgare, Sorghum halepense etc.

Factors affecting toxicity:

Poisoning in ruminants depends upon

o the quantity of the plant ingested

o the previous diet of the animal

o the pH of the stomach contents

o the percentage of total hydrocyanic acid present in the free state in the plant

o the concentration of cyanide liberating enzyme present in the plant and o the total hydrocyanic acid content of the plant.

• Ruminants are more susceptible to poisoning by cyanogenetic plants than horses and pigs, since the enzyme concerned in the release of hydrocyanic acid are destroyed by the gastric hydrochloric acid.

Kinetics:

• HCN is rapidly absorbed from the intestinal tract and via the lungs.
• The gas is irritant to the mucous membrane.
• Some cyanide is also eliminated through the lungs, the exhaled air having a characteristic ‘Bitter almond’ smell.
• Cyanide is metabolized by rhodanase in the liver to thiocyanate. This reaction complexes cyanide with endogenous sulfur or sulfur supplied from the sodium thiosulfate antidote. Once thiocyanate is formed it is excreted mainly in the urine.
• Half-life for the metabolism of cyanide to thiocyanate is 20 min to 1 h. In animals, the dose of cyanide that produces signs is very close to the lethal dose and death can occur within seconds to minutes.

Mechanism of toxicity:

• Excess cyanide in blood and tissues bind to ferric iron of cytochrome oxidase and prevent the transfer of electrons.

 o Cyanide ion reacts with Fe +3 (ferric) ion of cytochrome oxidase to form a stable complex.

 o Conversion of Fe +3 to Fe +2 is thereby prevented so that electron transport and cellular respiration are stopped. The blood is oxygenated, but cannot be utilized by the cells

. o The lack of O 2 utilization in chemoreceptors and/or neurons of the brain triggers increased respiratory efforts and the blood becomes hyperoxygenated (“bright red”).

 o End result is a functional tissue anoxia.

• Cells die from lack of usable oxygen. This results in tissue anoxia with serious effects in the brain.
• In the brain, cyanide decreases oxidative metabolism,increases glycolysis, and inhibits brain glutamic acid decarboxylase, thereby decreasing gamma aminobutyric acid (GABA).
• The corpus callosum, hippocampus, corpora striata, and substantia nigra are commonly damaged in cyanide poisoning.
• Death in acute cases occurs within a few seconds.

Clinical symptoms:

 o Animals may be found dead.

o The animal looses consciousness and stops breathing, but the heart continues to beat.

o Symptoms of poisoning include panting, gasping and behavioural abnormalities, salivation, muscle tremor, urination, defecation, colic, emesis, prostration, bright red mucous membrane, clonic convulsions, mydriasis and death.

• PM lesions

 o Cherry red or bright red blood that does not clot, congestion in the gastrointestinal tract and lungs and peticheal haemorrhage.

 o Bitter almond smell will be experienced on opening the stomach/rumen.

Diagnosis:

• Clinical symptoms and lesions are not characteristic.
• Examination of stomach contents is useful.
• Rumen contents may not give a clear indication because HCN is frequently found in the rumen of animals died of other causes and in the case of cyanogenetic plants a great amount of HCN may be released after death.
• 1% mecuric chloride is suggested as a preservative for sending the stomach and ruminal contents for analysis.

Treatment:

• The treatment of cyanide poisoning needs to be undertaken very rapidly if it is to be successful.
• The approach consists of administration of sodium nitrite and sodium thiosulphate.
• Sodium nitrite administered intravenously converts haemoglobin to methaemoglobin.
• Ferric iron of methaemoglobin complexes with cyanide to form cyanmethaemoglobin and thus reactivates cytochrome oxidase.
• Sodium thiosulphate detoxifies cyanmethaemoglobin by converting cyanide moiety to thiocyanate, which is non toxic.
• Sodium nitrite treatment should not be repeated, as there is danger of producing nitrite poisoning.
• In horses and cattle 10ml of a 20% solution of sodium nitrite intravenously followed immediately with 50 ml of 20% solution of sodium thiosulphate.
• In sheep 10ml of 10% sodium nitrite and 10% of 20ml sodium thiosulphate should be given. In dogs 20mg/kg as 1% solution of sodium nitrite and 1g/kg of 25% solution sodium thiosulphate should be administered.
• All injections should be given slowly.
• Hydroxycobalamine and other compounds of cobalt have also been shown to be of value.