Hydrocyanic acid (HCN)

CYNOGENETIC PLANTS  

  • The plants which contain hydrocyanic acid (HCN) or cyanogenic glycosides or cyanogenetic glycosides are called as cyanogenetic plants or cyanogenic plants.
  • HCN owes its toxicity to cyanide. In plants, cyanide is present in tow forms viz. a free form as HCN and a bound form as cyanogenic glycoside.
  • Free HCN is released from the glycoside by physical disruption (mastication, trampling), strees (drought, frost) or the action of an enzyme (beta glycosidase and hydroxynitrile lyase), which may be present in the same plant or other plants or in bacteria in the gastrointestinal tract of man and animals.
  • In ruminants, the hydrolyzing enzymes present in ruminal microflora liberate free HCN from the glycoside.
  • Poisoning may also occur due to accidental ingestion of potassium cyanide or malicious poisoning of man and animals.
  • Cyanogentic plant poisoning is one of the most common plant poisonings among the grazing livestock.
  • Cattle and Buffaloes are the most susceptible species.
  • Sheep and Goats are relatively less susceptible compared to cattle and buffaloes due to differences in the enzyme systems in the fore stomachs of these species.
  • Monogastric animals (pig and horse) are relatively resistant to cyanogenic plant poisoning due to destruction of the glycoside by the gastric acidity.
  • Cyanogenic plant poisoning usually occurs in animals when HCN content in the plants is high and when the animals ingest large amounts of the plant in relatively short period of time.
  • Starved or underfed animals when let loose for grazing ingest large amounts of the toxic plants within a short period and succumb to toxicity.
  • There have been instances of poisoning in starved sheep fed on linseed meal.

Sources

  • There are more than 120 plants containing sufficient quantities of cyanogenetic glycosides and responsible for poisoning in animals, however, some of the most commonly occurring cyanogenetic plants are listed in Table.

Table: Some of the commonly available cyanogenetic plants

Acacia leucophloea

Lotus sp.

Sorghum vulgare

Andrachne cordifolia

Nerium oleander

Sorghum halepense

Cynodon sp.

Neyraudia medagascariensis

Sorghum sudanensis

Eucalyptus sp.

Phaseolus luntus

Kalanchoe integra

Euphorbia sp.

Prunus sp.

Zea mays

Linum usitatissimum

Sugarcane leaves/tops

Triglochin maritime

  • In India, the most common source of cyanogenic plant poisoning in livestock is feeding of green Sorghum fodder, particularly immature plants or young shoots and also accidental ingestion of the pods or leaves of Acacia leucophloea by Sheep and Goats.
  • The HCN or the glycoside content of the plants varies based on several factors.

Mechanism of toxicity

  • Acute cyanogenetic plant poisoning causes cytotoxic anoxia which is the actual cause of death.
  • Toxic effects of HCN are due to its affinity towards, cytochrome oxidase.

Clinical signs

  • Under field conditions most of the recognized cases of cyanogenic plant poisoning are of acute nature.
  • The affected animals die suddenly (within 10 to 25 min) following ingestion of large quantities of the plant material without premonitory signs.
  • Acute ingestion of HCN or KCN results in death of animals within a few minutes.
  • The onset of symptoms depends upon the quantity of plant material ingested and also the rate of liberation of HCN from the glycoside.
  • If animal consumes large amounts of the plant it dies within a few minutes without showing much clinical symptoms except, dyspnoea, anxiety, restlessness, stumbling gait, tremors, recumbency, terminal clonic convulsions and death in per-acute cases.
  • In acute cases, clinical manifestations such as excitement, staggering, muscle tremors, dyspnoea, hyperaesthesia, lacrimation, hypersalivation, bright red mucosa, dilatation of pupil, nystagmus and terminal convulsions are seen.
  • The mucosae appear congested and cyanotic in terminal stages.
  • Chronic toxicity is believed to be sometimes observed in horses, cattle and sheep.
  • Clinical signs are urinary incontinence, loss of hair and arthrogryposis but not proved.

Post-mortem lesions

  • Congestion and / or haemorrhages in abomasum, small intestines, trachea, lungs and heart.
  • Blood remains unclotted and bright red in colour.
  • When the stomach/rumen is opened a smell of bitter almonds’ is felt.
  • Laboratory analysis of stomach or ruminal contents, liver and muscle reveals presence of HCN
  • If postmortem is delayed for 1 or 2 days, muscle tissue must be sent for laboratory analysis.

Diagnosis

  • History of sudden death following grazing in the vicinity or near the suspected plants.
  • Acute anoxic syndrome.
  • Bright red coloured blood and mucous membranes.
  • Post-mortem lesions
  • Detection of HCN in the suspected plant material or ruminal/stomach contents by picrate paper test.
Last modified: Friday, 23 March 2012, 8:47 AM