SEMINA

R
ON

Cyanide and nitrate poisoning in

cattle

Presented by:
Umesh Sontakke
CYANIDE POISIONING
 Cyanogenic glycosides:

 Cyanide poisoning occur in animal due to cyanogenic glycoside present in

certain plant

 Cyanogens are glycosides of sugare & a cyanide containing aglycone.

 21 cyanogenic glycosides are known

 Distributed in 250 plant Genera & 1000 plant species

 CYANIDE CONTENT IN CYANOGENIC PLANT

Cyanogenic plant mg CN / 100 gm plant tissue

Sorghum 250

wild cheeries 140 -370

Arrow grass 77

Lima beans 10 - 300

Bamboo tips 800

Linseed meal 53

(Montogomery 1980; Kingsbury 1964)

 cyanogens of importance in animal nutrition
AMYGADALINE
This glycoside found in Rosaceae such as-
1 chokecherries.
2 wild cheries
3 Mountain mohagany
4 Kernels of apricorts, almonds,peaches,apples etc..

DHURRIN
Occure in sorghum species
1 sorghum grain & its forage
2 sudan grass,johanson grass

LINAMARIN
Found in white clover, flax (linseed),cassava, lima beans.

Sorghum varieties have cyanide potential between 400 and 900 ppm on a dry
weight basis. (John et al. )
 Metabolism

HCN is formed when these glycosides are hydrolyzed by plant enzymes in

following steps

B-
1 cyanogenic glycosides glycosidase Sugar + aglycone
Hydozynitrile lyase
2 Aglycone HCN +aldehyde or ketone

Glycosides occur in vacuoles in plant

Beta glycosidase enzyme are found in cytosol
Damage to plant from trampling, mastication,frost,drought
Result in enzymes & glycosides coming together
 HCN is formed
 Specific reactions for each types of cyanogens
CN CN
| |
H-C-glucose-glucose H-C-OH
| |
B-glucosidase
2 glucose +

AMYGADALIN MANDELONITRILE
CN
| H-C=O
H-C-OH
| |
B-glucosidase
HCN +
MANDELONITRILE BENZALDEHYDE

(Peter, 1985)
 CN CN
| |
H-C-glucose-glucose H-C-OH
| |
B-glucosidase
2 Glucose +
| |
OH OH

DHURRIN P-HYDROXYMANDELONITRILE

CN
| H-C=O
H-C-OH |
|
B-glucosidase
HCN +
|
| OH
OH
P-HYDROXYMANDELONITRILE P-HYDROXYBENZYALDEHYDE
 LINAMARIN

CH3
CH3
|
| B-glycosidase C=O
Glucose-C-CN HCN+ Glucose +
|
| CH3
CH3

ACETONE
LINAMARIN

(Peter R .Cheekk 1985;)

 HCN

ENTERS INDIVISUAL TISSUE

INHIBIT CYTOCHROME OXIDASE

ATP FORMATION CEASES

ENERGY DEPRIVATION

DEATH
 SIGNS OF CYANIDE POISIONG

 DYSPNEA
 EXCITEMENT
 GASPING
 STAGGERING
 PARALYSIS
 CONVULSION
 COMA
 DEATH
 DETOXIFICATION

 Cyanide readily detoxify by Liver, kidney, thyroid tissue as they have

“RHODANASE” (Thiosulfate sulfurtransferase) enzyme
RHODANASE
 S2o32- + CN - SO2-3 + SCN
thiocyanate
 Thiocyanate is excreted in urine.

 Lethal dose of cyanide =0.5 to 3mg/kg body weight

 TERATOGENIC EFFECT OF CYANIDE

 Outbreak of swine malformation in Missouri associated with

maternal consumption of “wild black cherries” during
pregnancy
(Selby et al. 1971)
Fetal deformality in foals from mares grazing on “Sudan grass”
(Pritchard et al.1967)

 Limb deformality in calves from heifers grazing on Sudan

grass
(Seaman et al. 1981)
 TREATMENT

 Injection (i/v ) of sodium thiosulfate & sodium

nitrate
 Dose: cattle- 3 gm sodium nitrate
15 gm sodium thiosulfate
200 ml water

 Nitrate methaemoglobin

 Methaemoglobin combines with cyanide because of

more affinity than cytochome oxidase
 The golden rules for using sorghum crops for fodder are:

 Avoid grazing stressed (droughted) plants and in particular, avoid regrowth such as crops
ratooning as a result of storm rain.

 Delay grazing until plants are over 45 cm high for shorter varieties or over 75 cm high for tall
varieties. This greatly reduces the risk of cyanide poisoning. Plants forming flowers or grain
are least likely to poison stock.

(John D. Bertram, )
 Watch your stock continuously for the first hour and then frequently for the first few
days.  Make a point of checking on them at least twice a day

 Keep a supply of sodium thiosulphate on hand for emergency treatment of cyanide

poisoning.

 Supplement stock on sorghum crops with sulphur (10% sulphur in a salt lick).
Sulphur is required for detoxifying cyanide in the rumen and liver and sorghums are
generally low in sulphur.

 For fodder conservation, don't make hay from sorghums that are considered unsafe to
graze. Ensile them. Get hay or silage samples tested for cyanide potential and nitrate
before feeding out.

(John D. Bertram, )
 Nitrate poisioning
• Nitrate in itself is not toxic to animals, but at elevated levels it
causes a condition called nitrate poisoning.

• Nitrates are normally found in forages are converted by the digestion

process to nitrite, and in turn the nitrite is converted to ammonia

• If cattle rapidly ingest large quantities of plants that contain high levels of
nitrate, nitrite will accumulate in the rumen.

• Nitrite is ten times (10 X) as toxic to cattle as nitrate.

MEAN NITRATE CONTENT IN SOME COMMON FEEDS
(Kapoor et al.)
FEEDS/ NITRATE FEEDS/ NITRATE
FODDERS CONTENT FODDERS CONTENT
(% KNO3) (% KNO3)
Maize grain 0.185 Doob grass 0.227
Barley 0.206 Berseem 0.038
Wheat bran 0.119 Lucerne 0.068
Rice bran 0.179 Maize green 0.100
Groundnut 0.237 Mustard Traces
cake green
Mustard cake 0.228 Oat green 0.098
Wheat straw 0.090 Bajara green 0.325
Paddy straw 0.22 Cow pea 0.033
Oat silage 0.057 Jowar green 0.044
FATE IN RUMEN
NITRATE & NITRITE IN PLANTS

PLANTS FEED TO ANIMALS

NITRATE S CONVERTS INTO NITRITES

NITRITES OXIDISES Hb Fe3+ to Fe 2+

METHAEMOGLOBINE
 The pathways of nitrate metabolism in the rumen

Overall reaction
• NO3-+2H+ H2O+NO2- --------------------1
• NO2-+6H+ H2O+ NH3 -------------------2

3HCO-2+NO2-+5H+ 3 CO2+NH+4+2H2O ---------- 3

• 3H2+NO2-+2H+ NH+4 +2H2O -----------4

• 3HS- + NO2- +5H+ 3S0 + NH+4 +2H2O

 Signs & symptom

 ANEMIC ANOXIA
 DYSPNOEA
 GASPING
 RAPID RESPIRATION
 A RAPID FEABLE & WEAK PULSE
 MUSULE TREMORE
 WEAKNESS
 STAGGERING GAIT
 TREATMENT

 METHYLENE BLUE:
 Converts back fe 2 + Hb to fe3+

 Pig & horses: 1-2 mg/kg body weight ., i/v

 Cattle & sheep : 20mg/kg body weight ., i/v

 Repetation of treatment is recommended as necessary at 6-8 hr

intervals
(Jones 1988)
 INCLUSION OF NITRATE IN DIET

 Toxicities from nitrite accumulation in and absorption from the rumen

appeared to be the major constraint to replacing urea with nitrate in low
protein diets

 Nitrite accumulation in the rumen only occurs where nitrate is introduced

abruptly and in excessive amounts.

 The rumen microorganism can readily adapt to nitrate as a source of

fermentable N (Megasphera elsedenii)
 Conti…

• Sheep on high energy diets supporting high growth rates were unaffected by
adding 3.4% nitrate to their diets.

• Dairy cows producing 16-19L milk/day were unaffected by inclusion of 2%

nitrate in feed (Farra and Satter, 1971)

• Sulphur balance was effected by nitrate inclusion in sheep fed concentrate

diets.

• Additional Mo in a diet boosted nitrite production from nitrate. Mo

suppresses sulphur reducing bacteria and production of hydrogen sulphide in
the rumen