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Poisoning
Nitrate and Nitrite Poisoning
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  • Introduction to Poisoning
  • Metabolism of Poisons
  • Factors Affecting the Activity of Poisons
  • Diagnosis of Poisoning
  • General Treatment of Poisoning
  • Algal Poisoning
  • Arsenic Poisoning
  • Bracken Fern Poisoning
  • Cantharidin Poisoning (Blister Beetle Poisoning)
  • Coal-tar Poisoning
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  • Ethylene Glycol (Antifreeze) Poisoning
  • Fluoride Poisoning
  • Food Hazards
  • Fungal Poisoning
  • Gossypol Poisoning
  • Halogenated Aromatic Poisoning (PCB and Others)
  • Herbicide Poisoning
  • Household Hazards
  • Insecticide Poisoning
  • Lead Poisoning
  • Mercury Poisoning
  • Metaldehyde Poisoning
  • Nitrate and Nitrite Poisoning
  • Nonprotein Nitrogen Poisoning (Ammonia Poisoning)
  • Pentachlorophenol Poisoning (Penta Poisoning)
  • Petroleum Product Poisoning
  • Plants Poisonous to Animals
  • Poisoning from Human Over-the-Counter Drugs
  • Poisonings from Human Prescription Drugs
  • Poisonings from Illicit and Abused Drugs
  • Pyrrolizidine Alkaloidosis (Senecio Poisoning, Ragwort Poisoning)
  • Quercus Poisoning (Oak Bud Poisoning, Acorn Poisoning)
  • Rodenticide Poisoning
  • Ryegrass Poisoning
  • Salt Poisoning
  • Selenium Poisoning
  • Snakebite
  • Sorghum Poisoning (Sudan Grass Poisoning)
  • Spider Bites
  • Strychnine Poisoning
  • Sweet Clover Poisoning
  • Toad Poisoning
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Nitrate and Nitrite Poisoning

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Many species are susceptible to nitrate and nitrite poisoning, but cattle are affected most often. The effects of nitrite or nitrate toxicity are usually sudden but may be longterm.

Nitrates and nitrites are used in pickling and curing brines for preserving meats, certain machine oils and antirust tablets, gunpowder and explosives, and fertilizers. Poisonings occur most commonly from ingestion of plants that contain excess nitrate, especially by hungry animals that overeat and take in an enormous amount of nitrate. Nitrate poisoning can also result from accidental ingestion of fertilizer or other chemicals. Nitrate concentrations may be hazardous in ponds that receive extensive feedlot or fertilizer runoff; these types of nitrate sources may also contaminate shallow, poorly cased wells. Water transported in improperly cleaned liquid fertilizer tanks can also be extremely high in nitrate.

Crops that readily concentrate nitrate include cereal grasses (especially oats, millet, and rye), corn (maize), sunflower, and sorghums. Weeds that commonly have high nitrate concentrations are pigweed, lamb's quarter, thistle, Jimson weed, fireweed (Kochia), smartweed, dock, and Johnson grass. Anhydrous ammonia and nitrate fertilizers and soils naturally high in nitrogen tend to increase nitrate content in forage.

Signs of nitrite poisoning usually appear suddenly. Rapid, weak heartbeat with below normal body temperature and blood pressure, tremors, weakness, and lack of coordination are early signs of toxicosis. Brown and bluish mucous membranes develop quickly. Difficulty breathing, rapid breathing, anxiety, drooling, and frequent urination are common. The abdomen may be painful, and the animal may have vomiting and diarrhea. Affected animals can also die suddenly without showing signs or have seizures. Under certain conditions, signs may not be apparent until animals have been eating nitrate-containing forages for days to weeks. Some animals develop emphysema and breathing distress, but most of these recover fully within 10 to 14 days. In longterm poisoning, signs include retarded growth, lowered milk production, vitamin A deficiency, reproductive problems, and increased susceptibility to infection.

Diagnosis relies on signs and blood tests to measure nitrate and nitrite levels in animals. Field tests for nitrate can also be performed.

Treatment includes slow intravenous injection of 1% methylene blue in various fluids. Trace mineral supplements and a balanced diet can help prevent nutritional or metabolic disorders associated with longterm excess dietary nitrate consumption. Feeding grain with high-nitrate forages may reduce nitrite production.

Last full review/revision July 2011 by Barry R. Blakley, DVM, PhD; Cheryl L. Waldner, DVM, PhD; Rob Bildfell, DVM, MSc, DACVP; William D. Black, MSc, DVM, PhD; Herman J. Boermans, DVM, MSc, PhD; Cecil F. Brownie, DVM, PhD, DABVT, DABT, DABFE, DABFM, FACFEI; Raymond Cahill-Morasco, MS, DVM; Keith A. Clark, DVM, PhD; Gregory F. Grauer, DVM, MS, DACVIM; Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT; Larry G. Hansen, PhD; Safdar A. Khan, DVM, MS, PhD, DABVT; Garrick C. M. Latch, MASc, PhD; Gavin L. Meerdink, DVM, DABVT; Lisa A. Murphy, VMD; Frederick W. Oehme, DVM, PhD; Gary D. Osweiler, DVM, MS, PhD, DABVT; Mary M. Schell, DVM; David G. Schmitz, DVM, MS, DACVIM; Norman R. Schneider, DVM, MSc, DABVT

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