Nitrate and cyanide poisoning in animals
Dr. Parvinder Kaur Lubana
Veterinary officer ,NRDDL
Jalandhar Punjab
9814652576
Cyanide poisoning: cyanides are found in plants, fumigants, soil fertilizers and rodenticides ( eg calcium cyanomide ) . Toxicity can result from improper or malicious use ,but in the case of livestock,the most frequent cause is ingestion of plants that contain cyanogenic glycosides .These include Triglochin maritime( arrow grass ),sorghum spp (Sudan grass, common sorghum ),Prunus spp ( apricot,peach),apple ( Pyrus malus ) Zea mays ( corn) ,and Linum spp (flax) .The seeds of several plants such as the peach have been the source of cyanogenic glycosides in many cases .Eucalyptus spp, kept as ornamental house plants , have been implicated in death of small animals .The cyanogenic glycosides in plants yield free hydrocyanic acid (HCN) , otherwise known as prussic acid, when hydrolyzed by β- glycosidase or when other plant cell structure is disrupted or damaged ,eg, by freezing ,chopping, or chewing. Microbial action in the rumen can further release free cyanide.
In sorghum spp forage grasses, leaves usually produce 2-25 times more hcn than do stems; seeds contain none. New shoots from young, rapidly growing plants often contain high concentrations of prussic acid glycosides. The cyanogenic glycosides potential of plants can be increased by heavy nitrate fertilization, especially in phosphorus- deficient soils. Spraying of cyanogenic forage plants with foliar herbicides such as 2,4-D can increase their prussic acid concentrations for several weeks after application .
The cyanogenic glycoside potential is low to decrease in drought –stricken plants containing mostly leaves. Grazing stunted plants during drought is the most common cause of poisoning of livestock by plants that produce prussic acid.
Ruminants are more susceptible than monogastric animals and cattle slightly more than sheep and goat.
Arrow grass Sudan grass Zea mays (corn )
Clinical Findings : -Signs can occur within 15-20 min to a few hours after animals consume toxic forage . Excitement can be displayed initially, accompanied by rapid respiration rate . Dyspnoea follows shortly, with tachycardia. Salivation, excess lacrimation and voiding of urine and faeces may occur .Vomiting may occur, especially in pigs. Muscle fasciculation is common and progress to generalised spasms before death. Animals stagger and struggle before collapse .mucous membranes are bright red but many become cyanotic terminally. Death occur during severe asphyxial convulsions .the heart may continue to beat for several minutes after struggling and breathing stops .the whole syndrome usually does not exceed 30-45 min.most animals that live > 2 hr after onset of clinical signs recover ,unless continuous absorption of cyanide from the GI tract occurs .
Lesions:– In acute and per acute cyanide toxicoses ,blood may be bright cherry red initially but can be dark red if necropsy is delayed ; it may clot slowly or not at all. Mucous membranes may also be pink initially , then become cyanotic after respiration ceases . the rumen may be distended with gas,and the odour of “ bitter almonds” may be detected after opening .heart ,liver ,serosal surface , tracheal mucosa and lungs may be congested or hemorrhagic ; some froth may be seen in respiratory passages .
Multiple foci of degeneration or necrosis may be seen in the CNS of dogs chronically exposed to sub lethal amounts of cyanide. These lesions have not been reported in livestock.
Diagnosis: appropriate history, clinical signs, post-mortem findings and demonstration of HCN in rumen (stomach) contents or other diagnostic specimens support a diagnosis of cyanide poisoning.
Specimens recommended for cyanide analysis ; The suspected source (plant or otherwise), Rumen or stomach contents, Blood in heparinised vial & liver.
Test procedure: take : The grinded mixture of the sample in a test tube and add 0.5 ml of chloroform and 1.0 ml of conc. Sulphuric acid .Put the picrate paper ( prepare picrate paper by dissolving 5.0gm sodium bicarb and 0.5 gm of picric acid in 100 ml of distilled water .dip the filter paper strips and air dry ) on the mouth of the tube heat the tube . If the picrate paper turns brownish to brick red then it is suggestive of presence of hydrocyanic acid
Picric acid and Sod.Bicarb Picric acid strip turns brown after heating
Hay, green chop, silage, or growing plants containing > 220 ppm cyanide as HCN on a wet basis are very dangerous as animal feed. Forage containing < 100 ppm HCN, wet weight is usually safe to pasture.
Differential diagnosis include poisoning by nitrate or nitrite, urea, organophosphate, carbamate , chlorinated hydrocarbon pesticides , and toxic gasses ( carbon monoxide and hydrogen sulphide ) , as well as infectious or non-infectious diseases that cause sudden death.
Treatment:
Immediate treatment is necessary. Sodium nitrite ( 10gm/100 ml of distilled water or isotonic saline ) should be given IV @ 20 mg /kg body weight ,followed by Sodium Thiosulfate (20%) ,IV ,at 500 mg /kg ; the later may be repeated as needed with little hazard . sodium nitrite therapy may be carefully repeated at 10 mg /kg ,every 2-4 hr or as needed .
Sodium thiosulfate alone is also an effective antidotal therapy at > 500 mg /kg, IV, plus 30gm /cow, PO, to detoxify any remaining HCN in the rumen .oxygen may be helpful in supplementing nitrite or thiosulfate therapy, especially in small animals. Activated charcoal is not efficacious in absorbing cyanide and thus is not recommended PO for antidotal therapy.
Caution is indicated in treatment. Many clinical signs of nitrate and prussic acid poisoning are similar, and injecting nitrite induces methaemoglobinemia identical to that produced by nitrate poisoning .If in doubt of the diagnosis ,methylene blue ,IV ,at 4-22mg /kg ,may be used to induce methemoglobin. Because methylene blue can serve as both donor and acceptor of electrons, it can reduce methemoglobin in the presence of excess methemoglobin or induce methemoglobin when only haemoglobin is present (but sodium nitrate is the more effective treatment for cyanide poisoning if the diagnosis is certain. Control and Prevention
Grazing should be monitored closely during periods of environmental stress, eg drought or frost. Abundant re growth of sorghum can be dangerous; shoots should be frozen and wilted before grazing.
Green chop forces livestock to eat both stems and leaves, thereby reducing problems caused by selective grazing.
Sorghum hay and silage usually lose >50% of prussic acid content during curing and ensiling processes. Free cyanide is released by enzyme activity and escapes as a gas. Hay has been dried at oven temperature for up to 4 days with no significant loss of cyanide potential. These feeds should be analysed before use whenever high prussic acid concentrations are suspected.
Nitrate and Nitrite Poisoning
Many species are susceptible to nitrate and nitrite poisoning , but cattle are affected most frequently .ruminants are especially venerable because the ruminal flora reduces nitrate to ammonia ,with nitrite ( ~ 10 times more toxic than nitrate ) as an intermediate product , nitrate reduction ( and nitrite production ) occurs in the cecum of equids but not to the same extent as in ruminants . Young pigs also have GI microflora capable of reducing nitrate to nitrite, but mature monogastric animals (except equids ) are more resistant to nitrate toxicosis because this pathway is age limited .
Acute intoxication is manifested primarily by methemoglobin formation (nitrite ion in contact with RBC oxidises ferrous iron in Hgb to the ferric state, forming stable methemoglobin incapable of oxygen transport) and result in anoxia. Secondary effects due to vasodilatory action of the nitrite ion on vascular smooth muscle may occur .the nitrite ion may also alter metabolic protein enzymes; ingested nitrates may directly irritate the GI mucosa and produce abdominal pain and diarrhoea.
Toxicoses occur in unacclimated domestic animals most commonly from ingestion of plants that contain excess nitrate, especially by hungry animals engorging themselves and taking in an enormous body burden of nitrate. Nitrate toxicosis can also result from accidental ingestion of fertilizer or other chemicals.
Water with both high nitrate content and significant coliform contamination has greater potential to affect health adversely and lower productivity than do either nitrate or bacteria alone. Livestock losses have occurred during cold weather due to the concentrating effect of freezing, which increases nitrate content of remaining water in stock tanks.
Crops that readily concentrate nitrate include cereal grasses (oats, millet, and rye), corn (maize), sunflower and sorghum. Many weeds commonly have high nitrate conc. anhydrous ammonia and nitrate fertilizers and soils naturally high in nitrogen tend to increase nitrate content in forage.
Crops that readily concentrate nitrate
Maize (corn) Rye grass Oats plant
Excess nitrate in plants is generally associated with damp weather conditions and cool temperatures, although high concentration is also likely to develop when growth is rapid during hot, humid weather. well aerated soil with a low pH, and low or deficient amounts of molybdenum ,sulphur ,or phosphorus in soil tend to enhance nitrate uptake ,whereas soil deficiencies of copper ,cobalt ,manganese tend to have opposing effect .anything that stunts growth increases nitrate accumulation in the lower part of plant . Nitrate, which does not selectively accumulate in fruits or grain, is found chiefly in the lower stalk with lesser amounts in the upper stalk and leaves. Nitrate in plants can be converted to nitrite under the proper conditions of moisture, heat and microbial activity after harvesting.
Clinical signs Signs of nitrate poisoning usually appear suddenly due to tissue hypoxia and low blood pressure as a consequence of vasodilatation. Rapid weak heart beat with subnormal body temperature, muscular tremors,weakness,and ataxia are early signs of toxicosis when methemoglobinemia reaches 30-40%.
Brown, cyanotic mucous membranes develop rapidly as methemoglobinemia exceeds 50%. Dyspnea, tachypnea, anxity, and frequent urination.
Some monogastric animals ,usually because of excess nitrate exposure from nonplant source exhibit salivation ,vomiting ,diarrhoea ,abdominal pain and gastric haemorrhage .affected animals may die suddenly with ought appearing ill , in terminal anoxic convulsions within 1 hr ,or after a clinical course of 12-24 hr or longer . Acute lethal toxicoses almost always are due to development of < 80% methemoglobinemia . Under certain conditions, adverse effects may not be apparent until animals have been eating nitrate –containing forages for days to weeks. abortion and stillbirths may be seen in some cattle 5-14 days after excessive nitrate /nitrite exposure , but likely only in cows that survived a > 50% methemoglobinemia for 6-12 hr or longer . Prolonged exposure to excess nitrate coupled with cold stress and inadequate nutrition may lead to the alert downer cow syndrome in pregnant cattle; sudden collapse and death can result.
Ruminal distension Hyper salivation
Lesions: Blood that contains methemoglobin usually has a chocolate brown colour. There may be pinpoint or larger haemorrhages on serosal surfaces. If necropsy is postponed too long, the brown discol- oration may disappear with conversion of methemoglobin back to haemoglobin.
Diagnosis; Excess nitrate exposure can be assessed by laboratory analysis for nitrate in both pre and post-mortem samples.
High nitrate and nitrite values in post-mortem samples may be an incidental finding, indicative only exposure and not toxicity. Post-mortem samples include ocular fluids, foetal thoracic fluids, foetal stomach content, and maternal uterine fluid. All specimens should be frozen in clean plastic or glass containers before submission. Because the amount of nitrate in rumen contents is not representative of concentrations in the diet, evaluation of rumen contents is not indicated.
Field test for nitrate: Take chopped green fodder from all corners of the field. As we all knew that nitrate is more accumulated in stem part of the fodder plant.
Diphenylamine blue test: `
How to prepare test reagent: Diphenylamine = 1 gm
Conc. Sulphuric acid = 80 ml
Distilled water = 20 ml
Sulphuric acid (concentrated) Diphenylamine
Take chopped fodder in Petri plate, put few drops very carefully in the chopped fodder, it will turn into dark blue colour.
chopped fodder Fodder turns blue
Differential diagnosis:–
Differential diagnosis includes poisoning by cyanide, urea pesticides toxic gasses (eg carbon monoxide, hydrogen sulphide) and drugs.
Treatment:Slow IV injection of 1% methylene blue in distilled water or isotonic saline should be given at 4-22 mg /kg body wt. or more ,depending on severity of exposure . Lower doses may be repeated in 20-30 min if the initial response is not satisfactory .Lower doses of methylene blue can be used in all species, but only ruminants can tolerate higher doses. Rumen lavage with cold water and antibiotics may stop the continuing microbial production of nitrite. Alkaline Ph of rumen can be corrected by giving vinegar intra -ruminally .Supportive treatment is always advisable.
Control: Animals may adapt to higher content in feeds, especially when grazing on sorghum –sudan hybrids. Multiple, small feedings help animals adapt. Trace mineral supplements and a balanced diet may help prevent nutritional or metabolic disorders associated with long-term excess dietary nitrate consumption. Feeding grains with high nitrate forages may reduce nitrite production.
Reference; Laboratory manual on cyanide & nitrate toxicity by Dr Vinay Mohan Wadhawan, MVSc, Animal Nutrition )MVM ,Retd. Joint Director NRDDL,Pb.
