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Sorghum The
Cyanide Killer
By Utpal Sachanka Boro
Regd no. 2016-VL-27
Lakhimpur College of Veterinary Science
AAU, Joyhing
Contents
 Introduction
 Susceptible Animals
 Lethal dose
 Factors affecting Cyanide Poisoning
 Mechanism of Toxicity
 Clinical signs
 Post mortem lesions
 Diagnosis
 Treatment
Introduction
• Taxonomic Classification
Kingdom : Plantae
Order : Poales
Family : Poaceae
Sub family : Panicoideae
Genus : Sorghum
Species : Sorghum vulgare
• Common name: Jowar, Durra,
great millet,
milo
• Cyanogenetic plants: Those plants or crops which
contain Hydrocyanic acid (HCN) or cyanogenetic
glycosides are called Cyanogenic or cyanogenetic
plants.
• HCN owes its toxicity to Cyanide.
• Exampless of cyanogenetic plants include Sorghum,
maize, etc.
• Most common source of cyanogenetic plant poisoning in
Indian livestock is feeding of Sorghum fodder, especially
immature and young shoots.
• Sorghum, Cyanide is persent in two forms:
a free form as HCN and
a bound form as Cyanogenic glycoside ( dhurrin)
• Free HCN is released from the glycoside by physical
disruption (mastication), stress( draught, frost) or
action of enzyme (Beta glycosides, hydroxynitrile
lyase) which may be present in the same plant or in
bacteria of GIT of man and animals.
Susceptibility
 Most susceptible: Cattle, Buffaloes (large
Ruminants)
 Less susceptible: Sheep and Goat ( small
Ruminants)
 Monogastric animals are relatively resistant to
Cyanogenic plant poisoning due to destruction of
glycoside by the gastric acdity.
eg. Pig, Horse, etc.
I’m okay
Lethal Dose
 Plants containing More than 20mg HCN/100 grams
are toxic to animals.
 Miminum lethal dose of Cyanide for Cattle and
sheep 2mg/kg body weight.
Factors Affecting Cyanide Poisoning
1. Stage of growth: Young, immature or plants growing after draught
have higher level of HCN.
2. Climate: During draught years, Cyanogenic glycoside contents are
highest in plants.
3. Soil: High soil content of Nitrogen and Low Phosphorus promotes
high HCN of plants.
4. Fertilizer and weedicides: Nitrate fertilizer and weedicides (2,4-D)
enhance the HCN content of plants.
5. Processing of plants: Drying of plants or Silage making reduces
Cyanide content of plant.
Mechanism of Toxicity
 HCN Binds to heme iron (Fe3+) of cytochrome oxidase
(a-a3) ( has high affinity for Fe3+) forming CN-
cytochrome oxidase complex.
 CN-cytochrome oxidase complex inhibits the final
step in Oxidative phosphorylation where Oxygen is
used for producing ATP.
 This results in cellular anoxia leading to death( if not
treated).
 Note: In cyanogenetic plant poisoning, Oxygen is
retained in blood due to failure of its exchange &
utilisation by tissues.
Clincal Signs
 In Acute Cases: Animals die in10 to 25 minutes
following ingestion of large amount of Sorghum
 Exicetment
 Staggering gait
 Muscle tremor
 Dyspnea
 Dialated pupils
 Nystagmus ( uncontrolled eye movement)
 Convulsions
 Congested mucosa
Clincal Signs
 In Chronic cases: seen in Horses, Cattle and Sheep
 Urinary incontinence
 Loss of hair
 Arthrogryposis ( Congenital deformity of joints and
muscles in newborn)
 Abortion in late pregnancy
Post Mortem Lesions
 Congestion and haemorrhage in abomasum, small
intestine, trachea, lungs & Heart.
 Blood remains unclotted and bright red in colour.
 When stomach/ rumen is opened, a smell of 'bitter
almond’ is sensed.
Diagnosis
 History of sudden death following grazing near
suspected plant.
 Acute Anoxic syndrome.
 Bright red blood and mucous membrane.
 On basis of post mortem lesions.
 Detection of HCN in the suspected plant materials
or ruminal/ stomach contents by Picrate Paper
Test.
Treatment
 NaNO2 (sodium nitrite) i.v. immediately followed by sodium thiosulfate p.o. or intra
ruminally plus artificial respiration with Oxygen.
 Mechanism of treatment:
NaNO2 + Hb(Fe2+) Methaemoglobin (Hb3+)
Cytochrome Fe3+ oxidase-CN complex + Methaemoglobin Cyanomethaemoglobin
+ Cytochrome oxidase
NaS2O3 + Cyanomethaemoglobin SCN (Thiocyanate)+ Hb+ Na2SO4
Thank You!

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Hydrocyanic acid or Cyanogenetic Plant Poisoning.pdf

  • 1. Sorghum The Cyanide Killer By Utpal Sachanka Boro Regd no. 2016-VL-27 Lakhimpur College of Veterinary Science AAU, Joyhing
  • 2. Contents  Introduction  Susceptible Animals  Lethal dose  Factors affecting Cyanide Poisoning  Mechanism of Toxicity  Clinical signs  Post mortem lesions  Diagnosis  Treatment
  • 3. Introduction • Taxonomic Classification Kingdom : Plantae Order : Poales Family : Poaceae Sub family : Panicoideae Genus : Sorghum Species : Sorghum vulgare • Common name: Jowar, Durra, great millet, milo
  • 4. • Cyanogenetic plants: Those plants or crops which contain Hydrocyanic acid (HCN) or cyanogenetic glycosides are called Cyanogenic or cyanogenetic plants. • HCN owes its toxicity to Cyanide. • Exampless of cyanogenetic plants include Sorghum, maize, etc. • Most common source of cyanogenetic plant poisoning in Indian livestock is feeding of Sorghum fodder, especially immature and young shoots.
  • 5. • Sorghum, Cyanide is persent in two forms: a free form as HCN and a bound form as Cyanogenic glycoside ( dhurrin) • Free HCN is released from the glycoside by physical disruption (mastication), stress( draught, frost) or action of enzyme (Beta glycosides, hydroxynitrile lyase) which may be present in the same plant or in bacteria of GIT of man and animals.
  • 6. Susceptibility  Most susceptible: Cattle, Buffaloes (large Ruminants)  Less susceptible: Sheep and Goat ( small Ruminants)  Monogastric animals are relatively resistant to Cyanogenic plant poisoning due to destruction of glycoside by the gastric acdity. eg. Pig, Horse, etc. I’m okay
  • 7. Lethal Dose  Plants containing More than 20mg HCN/100 grams are toxic to animals.  Miminum lethal dose of Cyanide for Cattle and sheep 2mg/kg body weight.
  • 8. Factors Affecting Cyanide Poisoning 1. Stage of growth: Young, immature or plants growing after draught have higher level of HCN. 2. Climate: During draught years, Cyanogenic glycoside contents are highest in plants. 3. Soil: High soil content of Nitrogen and Low Phosphorus promotes high HCN of plants. 4. Fertilizer and weedicides: Nitrate fertilizer and weedicides (2,4-D) enhance the HCN content of plants. 5. Processing of plants: Drying of plants or Silage making reduces Cyanide content of plant.
  • 9. Mechanism of Toxicity  HCN Binds to heme iron (Fe3+) of cytochrome oxidase (a-a3) ( has high affinity for Fe3+) forming CN- cytochrome oxidase complex.  CN-cytochrome oxidase complex inhibits the final step in Oxidative phosphorylation where Oxygen is used for producing ATP.  This results in cellular anoxia leading to death( if not treated).  Note: In cyanogenetic plant poisoning, Oxygen is retained in blood due to failure of its exchange & utilisation by tissues.
  • 10. Clincal Signs  In Acute Cases: Animals die in10 to 25 minutes following ingestion of large amount of Sorghum  Exicetment  Staggering gait  Muscle tremor  Dyspnea  Dialated pupils  Nystagmus ( uncontrolled eye movement)  Convulsions  Congested mucosa
  • 11. Clincal Signs  In Chronic cases: seen in Horses, Cattle and Sheep  Urinary incontinence  Loss of hair  Arthrogryposis ( Congenital deformity of joints and muscles in newborn)  Abortion in late pregnancy
  • 12. Post Mortem Lesions  Congestion and haemorrhage in abomasum, small intestine, trachea, lungs & Heart.  Blood remains unclotted and bright red in colour.  When stomach/ rumen is opened, a smell of 'bitter almond’ is sensed.
  • 13. Diagnosis  History of sudden death following grazing near suspected plant.  Acute Anoxic syndrome.  Bright red blood and mucous membrane.  On basis of post mortem lesions.  Detection of HCN in the suspected plant materials or ruminal/ stomach contents by Picrate Paper Test.
  • 14. Treatment  NaNO2 (sodium nitrite) i.v. immediately followed by sodium thiosulfate p.o. or intra ruminally plus artificial respiration with Oxygen.  Mechanism of treatment: NaNO2 + Hb(Fe2+) Methaemoglobin (Hb3+) Cytochrome Fe3+ oxidase-CN complex + Methaemoglobin Cyanomethaemoglobin + Cytochrome oxidase NaS2O3 + Cyanomethaemoglobin SCN (Thiocyanate)+ Hb+ Na2SO4