BLOOD TEST
Note the bright red color of the sample on the left indicative of
cyanogenic toxicosis.
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Toxic
principle: cyanogenic
glycosides or cyanogens (amygdalin, prunasin, dhurrin, linamarin)
Hydrogen
cyanide (HCN) is formed when the glycosides are hydrolyzed by enzymes in plants
or by rumen microorganisms:
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β - glucosidase |
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Cyanogenic
glycosides ® sugar +
aglycone |
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Aglycone
® HCN + aldehyde or ketone |
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Hydroxynitrile lyase |
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The
glycosides occur in vacuoles in plant tissue while the enzymes are found in the
cytosol. Damage to the plant from
wilting, trampling, mastication, frost, drought, bruising etc. results in the
enzymes and glycosides coming together causing hydrogen cyanide to be formed.
b-glycosideases
are also produced by rumen microorganisms.
The optimal pH for enzyme activity is near neutrality, so release of HCN
is more rapid in the rumen than in the highly acid stomach of monogastrics.
For this reason, ruminants are more sensitive to cyanogens than
nonruminants.
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Toxicity:
Cyanide is lethal at dosages of 0.5 to
3 mg/kg b.w. Ingestion of 100 g of
wild cherry leaves with ~ 200 mg CN per 100 grams would be lethal to a 100 lb.
animal.
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Once
free cyanide is released from the plant tissue and is absorbed it reacts with
ferric iron (+3) in cytochrome oxidase which halts cellular respiration.
Oxyhemoglobin cannot release oxygen for electron transport in the
cytochrome system since the cyanide – cytochrome oxidase will not function in
electron transport. |
Diagnosis
Clinical signs:
ü
Animals
are commonly found dead due to rapidity of cyanide’s effects
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When
observed, signs may include excitement, general muscle tremors, dyspnea,
salivation, defecation, urination followed by clonic convulsions and death.
Laboratory
diagnosis:
Measurement of cyanide in GI contents.
Lesions: bright red color to blood and mucous membranes, detection of
plant material in GI tract.
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Treatment:
General: remove from source
Specific:
sodium nitrite at 10 to 20 mg/kg with 500 mg/kg sodium thiosulfate as
needed. The treatment is directed
at breaking the cyanide – cytochrome bond with the nitrite forming
methemoglobin. Methemoglobin has a
greater affinity for cyanide than does cytochrome oxidase, so it strips cyanide
from the enzyme. The thiosulfate
then reacts with the cyanide via the enzyme rhodanase forming thiocyanate which
is readily excreted in the urine.
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Prevention: Test forage prior to feeding. Cyanide
is volatile, so opening bales of hay
24 hours before feeding allows the cyanide to dissipate.
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