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 The primary nutrient form of nitrogen in most soils is nitrate which is a normal compound found in many plants.  It can be found normally in various grazing and forage crops, soil, and water.  Under certain circumstances, nitrates can accumulate to abnormally high levels and become very toxic to ruminants.   Nitrate accumulation in plants varies widely between species and is influenced by several factors, especially those factors that tend to limit the growth of the plant while still allowing for the uptake of nitrate.  One of the most important factors affecting nitrate accumulation in plants is drought, although frost damage, treatment of crops with herbicides and shading can also result in higher than normal levels in some forages.  Water can also serve as a carrier for nitrate, gathering it from the soil, fertilizers, runoff from feedlots or sewer systems as well as from industrial sources.  Nitrate itself is not overly toxic to animals; however, when nitrate is reduced to nitrite by rumen microflora, it becomes very toxic.  The conversion of nitrate to nitrite occurs via microbial reduction in the rumen, in moist feeds prior to their consumption, or in water that is contaminated with organic matter.  Nitrate reduction and associated toxicity in ruminants will be the primary focus of this article.

Sources of nitrate

  There are several plant species that may accumulate nitrate, including the Brassica plants, green cereal grains (barley, wheat, rye and maize),  sorghum and Sudan grasses, corn, beets, rape, docks, sweet clover and nightshades.  Application of large amounts of fertilizer or drainage from fertilized fields and contaminated water sources can also serve as a source for nitrate.  Drought can also allow accumulation of nitrate in certain plants.

Species affected

  The toxic principle for all animals is nitrite.  Nitrate, prior to being reduced to nitrite, is not overtly toxic to non-ruminant species.  Nitrite is essentially equally toxic to both ruminant and non-ruminant species.  Toxicity in ruminants is primarily seen following the consumption of high amounts of nitrate, which is subsequently reduced to nitrite by rumen microbes.  Cattle, sheep and goats are the species that are most commonly affected by nitrate poisoning, with neonatal animals being at greater risk.

Mechanism of toxicity

  Plants absorb nitrate which is normally converted to nitrite by the nitrate reductase system and incorporated into amino acids and proteins.  Genetic or environmental factors that interfere with or inhibit the function of the nitrate reductase system allow for nitrate to accumulate in the plant.  For example, in response to stressful conditions, sorghum species have reduced reductase activity.  Drought and conditions of reduced sunlight will also decrease the activity of the nitrate reductase system.

  Despite the decreased activity, nitrate is continuously absorbed by the plant and accumulates to abnormally high levels.  Ruminants consuming these plants convert the nitrate to nitrite and then to ammonia.  Nitrate toxicity is a function of the amount and rate at which nitrate is consumed.  When the animal consumes a normal forage diet containing large amounts of nitrate, the conversion of nitrite to ammonia becomes the limiting factor allowing nitrite to accumulate to toxic levels.  Toxicity occurs following the absorption of nitrite into the blood which oxidizes iron in hemoglobin from the ferrous (+2) to ferric (+3) state.  The resultant methemoglobin has a very poor affinity for oxygen which greatly reduces the oxygen-carrying capacity of red blood cells.  Death from anoxia may occur if 70-80% of the hemoglobin is converted to methemoglobin.

Clinical signs, necropsy findings and diagnosis

  Nitrate toxicity is generally acute to subacute with signs seen within a few hours to a few days following consumption of large amounts of nitrate.  Common clinical signs seen include rapid but weak pulse, muscle tremors, tachypnea, blue-grey mucous membranes, ptylism, depression, weakness, staggering gait, disorientation, frequent urination and a subnormal body temperature.  If left untreated, the condition rapidly deteriorates to prostration, coma and death.  Death usually occurs within a few hours to days following onset of clinical signs. 

  High levels of methemoglobin can be noted at necropsy due to the presence of a chocolate-brown discoloration of the blood in about one half of the cases of nitrate poisoning.  When present, this unique discoloration is also evident throughout the mucosa, viscera, and sometimes the urine.  Presently, feed, serum and aqueous humor should be collected for chemical analysis.  Feed nitrate concentrations of approximately 1.0% or greater are cause for concern.  At postmortem, aqueous humor or an entire eyeball should be submitted.  Methemo-globinemia, caused by nitrate/nitrite toxicity, must be differentiated from that due to intoxication by chlorates and plants such as onions.

  Diagnosis is based on a history of ingestion of feed containing high levels of nitrates, clinical signs and, if present, chocolate-brown discoloration of the blood.  All suspect feed and water should be submitted for chemical analysis along with necropsy samples as previously stated.

Treatment and Prevention

  Methylene blue is a specific treatment for nitrate toxicity.  It causes a rapid conversion of methemoglobin to hemoglobin.  The dose of methylene blue is reported as 4-30 mg/kg IV of a 1% solution to be given as soon as clinical signs are identified.  However, methylene blue is not approved for use in food animals.  In addition, the stress associated with collecting, restraining and treating animals with severe methemaglobinemia must be considered.  Identification and removal of the source of nitrate is indicated as well.  The 9th edition of Veterinary Medicine by Radostits et al reports that less than 0.6% of nitrate in the total diet is recommended.  They also recommend that cows not be grazed on feed that contains more than 1% nitrate and slightly less when the cattle are not grazing the feed.  Identifying the nitrate source and reducing the exposure is the key to controlling nitrate toxicity.  When it occurs, however, rapid diagnosis and prompt treatment are necessary to prevent severe mortality loss.

-by Cody Wrathall, Class of 2001
-edited by Dr. Steve Hooser, ADDL Chief of Toxicology


1. Roder JD: 2001.  Veterinary Toxicology.  TexasTechUnivHealthSciCenter.  Butterworth-Heinemann

2.  Radostits M Otto et al: 2000.  Veterinary Med 9th ed. Harcourt

3.  Smith PB: 1996. Large Animal Internal Medicine 2nd ed. Mosby-Year Book Inc.

4. Rebhun, CW, Guard C and Richards C: 1995.  Diseases of Dairy Cattle. Williams & Wilkins

5. ChurchDC: 1993.  The Ruminant Animal: Digestive Physiology and Nutrition.  Waveland Press, Inc.

6.  Andrews AH et al: 1992.  Diseases and Husbandry of Cattle. Blackwell Scientific Publications

7. 1991. Nitrate Poisoning and Feeding Nitrate Feeds to Livestock.  Agdex 400/60-1


8. Stanton TL.  Nitrate Poisoning.  ColoradoStateUniversity Cooperative Extension.

http://www.ext.colostate.edu/pubs/livstk/ 01610.html

9. Smith J and Guthrie L. Nitrate Toxicity and Prussic Acid Poisoning in Dairy Cattle.  Univ of GeorgiaCollege of Agriculture and Environmental Sciences Cooperative Extension Service.  http://www.ces.uga.edu/pubcd/b1153-w.html

10. Kvasnicka B and Krysl LJ. Nitrate Poisoning in Livestock.  Cattle Producers Library CL 620.  http://forages.orst.edu/

From the ADDL Toxicology Section

Corn silage and sorghum/sudan grass hay can accumulate sufficient amounts of nitrates to poison livestock (particularly ruminants).  Nitrate accumulation in these forages occurs most often in heavily fertilized fields and under drought conditions.  A diet consisting of greater than 1% nitrate can potentially result in nitrate poisoning in ruminants.  Clinical signs of nitrate toxicosis occur when blood methemoglobin concentrations are between 30 and 40%.  The most common abnormal signs are dyspnea, weakness, ataxia and terminal convulsions.  Death occurs when blood methemoglobin concentrations exceed 80-90%.  Samples to submit when nitrate poisoning is suspected are feed, forage, hay, and water.  From animals, frozen samples of plasma, urine, and an eyeball (vitreous humor) should be collected and submitted for nitrate analysis.

Management suggestions for helping to prevent nitrate poisoning include:

1.  If possible, do not feed forages high in nitrates.

2.  If the forage is suspected of possibly being high in nitrates, submit a representative sample for testing.

3.  When harvesting suspect forages such as corn, raise the cutter bar approximately one foot since most of the nitrate accumulates in the lower portion of the stalk.

4.  Ensile the material and do not feed for at least 3 weeks until the ensiling is completed.  Ensiling will decrease the total nitrate content.  Be careful of potentially dangerous nitrogenous gases produced by the ensiling process.

5.  Drying does not appreciably decrease the amount of nitrate in the forage.  Therefore, even cured grass (sorghum X sudan hybrids particularly can accumulate large quantities of nitrates) with a high nitrate content will be hay with a high nitrate content.

6.  If feeding a suspect forage, also feed good quality carbohydrate feed (approximately 2 pounds of grain per 450 lb body weight.)

7.  Gradually introduce suspect feeds into the diet and feed several times per day in small amounts rather than all at once.

8.  Young, stressed and unhealthy animals are more susceptible to nitrate poisoning.

9.  Be sure that the nitrate concentration in the drinking water is below a toxic level.  Generally, water nitrate levels of 45 ppm or less are considered safe.

-by Jane Likens, BS, Toxicology Technician
   Christina Wilson, MS, Assistant Chemist
   Robert Everson, PhD, Analytical Chemist
   Stephen Hooser, DVM, PhD, Toxicologist


ADDL-West Lafayette:
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Phone: 765-494-7440
Fax: 765-494-9181

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Phone: (812) 678-3401
Fax: (812) 678-3412

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