CYANIDE POISONINGDr. H. T. Rawte

Dy. Commissioner of A.H.Toxicology - D.I.S. (M.S.) &

Regional Disease Diagnostic Laboratory (Western India)

• Highly toxic for all animals

• Major Source of cyanide for concerned livestock is foundin some plants in form of cynogenic glycosides (non-toxic),which on enzymic or acid hydrolysis release hydrogencyanide. Such enzymes usually occur in the cynogenic plantsit self. Ruminal and intestinal micro flora also cause suchhydrolysis.

• Toxicity - About 40 enzymes of the body are alleged to beinhibited by cyanides, but 'cytochrome oxydase' is mostsensitive of all. In normal condition this enzyme isresponsible for final utilization of oxygen in the cells at theend of chain reactions for energy production. Cyanide rendersthis enzyme incapable of this function leading to tissueanoxia. Cerebral tissues show the highest sensitivity toinsufficient oxygen supply and the animal starts showingsymptoms concerned with C.N.S. derangements.

• Metabolism and detoxication - Small amounts eliminated asHCN via lungs, some cyanide excreted unchanged throughfaeces and sometimes through urine. Major portion istransformed (mainly in liver) to sulphocyanide, which isrelatively non-toxic and excreted through urine. Presence ofprecursor of vitamin B-12 helps in reducing bloodconcentration of cyanide by causing production ofcyanaocobalamine (pre cursors- hydroxicobalamine,chlorocobalamine. )

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• Lethal dose - The lethal dose of cyanogenic glycoside inplants cannot be detennined precisely since the plant contentsof cyanogenic glycoside may vary with the length of growingseason, weather, contents of nutrients of soil and with thestage of fodder. Young-growing plants contains largestamount of glycosides. The concentration still enhances if thegrowth is retarded or stopped by drought, frost, wilting ortrampling.

• Nitrate fertilization also markedly increases the content. Theeenoentration of HeN more than 20 mg. per 100 gram offodder is likely to cause toxicity.

Factors affecting toxicity

In animals the toxicity is influenced by the amount ofpoisonous plant material ingested, the activity of concernedhydrolyzing enzymes in the plant and the micro flora in theG.I.tract. Toxicity is also influenced by the previous diet and pHof rumen content and abomasum content. If the rate of intakeIJf poisonous material exceeds detoxication capacity of the bodythe toxicity occurs.

• Symptoms - Death in per acute cases. In acute casesexcitement, profuse salivation, jerky movements of eye balls,respiratory troubles, falling down, titanic spasms, opisthotonus,some tirnea vomiting, and death within few minutes. In lessa~ytQ cases, dizziness, staggering gait, vomiting followed bystages of asthma, convulsions, paralysis, asphyxia and death.In sub lethal doses, the animal shows nervous system fatigue,stupor, bloat and cessation of respiration before that ofheartbeats. In chronic cases, if the body is unable to eliminatethe sulphocyanides with sufficient rapidity, the accumulationof sulphocyanide g\styrb the synthesis of thyroid hormone andelicit typicg] ~¥'mptQIllS of hypothyroidism.

• Pf\tbQJogy ~ Congestion of blood vessels with unclotted brightred coloured blood, congestion and haemorrhage of lungs,

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reddening and congestion of mucous- membrane of stomachand gastroenteritis. In some cases characteristic smell of bitteralmond as soon as the abdomen is opened.

• Treatment - It is aimed towards -

1) Releasing the enzyme from clutch of cyanide,

2) Detoxifying cyanide by adding sulphur to it &

3) Other needful symptomatic requirements.

4) MtHb shows higher affinity for cyanide than that shown bycytochrome oxydase. MtHb in blood is produced by theaction of nitrites i.e. amyl nitrite through inhalation or i.v.administration of sodium nitrite or methylene blue or thionine.

* Doses - Slow i.v. injection of Sodium nitrite @ 5-10 mg.!kg. b.m.in 20 ml. of normal saline.

Note- Nitrite inj. Is contraindicated in equines.

In equines slow i.v. inj. Of metylene blue @ of 2-5 mg./kg.B.m. as 1-2% solution in normal saline

1) After 3-5 minutes slow i.v. injection of Sodiumthiosulphate @ 250 mg. /kg. B.m. as 25% solution innormal saline or in 25% dextrose solution.

2) Soln. Of Sodium thiosulphate need fully intra ruminally.

3) Animal charcoal orally.

4) Analeptics.

Note- Nitrite and sulphocyanide may cause hypo tension as asideeffect, which is to be taken care of.

• Samples to be sent

Unexposed rumina I contents about 1 kg., 3 intestinal loops,vital organs (each at least 250 grams),brain if possible,preferably skeletal muscles and suspected feed/fodder at least250 grams.

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P.N. - Samples be preserved in 1% solution of mercuricchloride, while sending.

References - Clinical Veterinary Toxicology - By - Lorgue,Lechenet & Riviere.

Veterinary Toxicology - By - Clark, Harvey & Humphreys.

Veterinary Toxicology - By - Bartik & Piskac.

Toxicology - By - Stewart & Stolman.

In the surveillance conducted by this institute many of theherbs are found to contain cyanide. Local names of those herbsin the concerned districts are as follows:-

A] Raigad - Ranbhend, Morga, Vavi cha pala, Burbutli,Bhambrut, Ghasri, Bivla, Pusari, Dati, Kalaki,.

B) Ratnagiri - Karad gavat, Kajra, Kadvai, Kel, Nachani chikad, Katval gavat, Bhata cha penda, Fanasa chyamula (Roots of Jack fruit tree)

C] Sindhudurg - Kajra, Nigadi, Payar, Kel, Shivan, Karad gavat,Bhata cha penda, Nachani cha penda,

D) Satara - Mokashi cha bhagad gavat, Ran kothimbir, Adalvanaspati, Ovi, Petumbali, Ghol, Nerda, Kusar, Rotad,Kevan, Vanali, Kandin.

E) Akola - Kapsa chi pane, Kapsa chya bia (saraki).

F) Solapur - Hivra chya shenga

G) Nanded - Soya husk.

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