Nitrate poisoning occurs when animals eat forage material with a high nitrate content (in excess of 0.35% to 0.45% nitrate in the diet). Under these circumstances, the nitrate is converted to nitrite in the rumen. The nitrite is absorbed into the blood, converting hemoglobin into methemoglobin, a substance which is incapable of transporting oxygen. When it is not fatal, nitrate poisoning produces subclinical conditions, which result in poor animal performance and a general lack of condition. The animal's response to nitrate poisoning is influenced by other components of the ration, particularly the availability of carbohydrates.

The plant produces or accumulates nitrates because the first step of protein synthesis involves the use of these substances. Consequently, anything which influences the sink-source relationship between protein production and nitrate accumulation will influence the nitrate content of the plant's tissue. The most common causes of high nitrate content in forage tissue are the following:

  1. High applications of nitrogen fertilizers or high soil fertility.
  2. Drought conditions.
  3. Damage to plant tissue (such as defoliation as a result of grazing or hail damage), which will stop or reduce photosynthetic activity.
  4. Low light intensity.
  5. Plant species (some plants convert amino acids to proteins rather slowly).
  6. Management (if animals are made to graze closely, they will eat more of the lower stem tissue).

The frequent use of nitrogen fertilizers in recent years has resulted in an increased incidence of nitrate poisoning. The belief that nitrate poisoning occurs only when annual forages are fed is quite untrue. Perennial forages are just as likely to accumulate nitrates where high fertilizer dressings are used.

Understanding Nitrate Toxicity

Nitrates normally occur in plants and are a necessary soil nutrient for crop growth. Nitrate that is ingested by cattle is converted to nitrite (nitrion is about 10 times more toxic to the animal than the nitration) and then to ammonia by ruminal bacteria (Cowley and Collings 1977; Emerick 1974). Ammonia is a protein-building chemical. If excess nitrates are ingested, excess nitries accumulate in the rumen because the bacteria are unable to convert all the nitrite into ammonia. Nitrite is absorbed into the oxygen transporting chemical hemoglobin. The blood can no longer transport oxygen to the body tissue and the animal's heart rate increases, the normal pink tissue color changes to blue, muscle tremors develop, the animal staggers, falls to the ground and dies (Cowley and Collings 1977; Emerick 1974; Hibbs et al. 1978).

Many publications report that consumption of nitrates at levels above normal, but below toxic stage, can cause lower milk production, reduced weight gains, and vitamin a deficiency. It also can increase the incidence of stillborn calves, abortions, retained placenta, and cystic ovaries (Hibbs it al. 1978; Johnson et al. 1983; Osweiler et al, 1985). In one New Mexico case where nitrate toxicosis was reported, 226 head of cattle were lost from a heard, of 390 head, and 42 cows aborted. Abortions started 48 hours after the exposure and continued for 3 weeks. In another cast, 22 out of 242 cows were lost. Nine abortions occurred from 96 hours to 7 days after esposure. These symptoms may be subtle and have been difficult to reproduce experimentally.

Cattle can tolerate a wide range of nitrates (Cowley and Collings 1977; National Academy of Sciences 1972; Osweiler et al. 1985). The potential for a toxic reaction is increased if the general health of the cattle is poor, or if a sudden dietary change introduces the suspect forage. Anemic catle, commonly due to lice or stomach worm infestations, are more likely to be affected by nitrate poisoning.

Diagnosis of nitrate poisoning is difficult. Producers should be suspicious of nitrate poisoning if the diet includes crops prone to nitrate accumulation. Grazing of fields withsuch crops or fields infested with nitrate-accumulating weeds should be avoided. Animals dying from nitrate poisoning will undergo rapid post-postmortem changes suggestive of ruminal bloat. A poast-postmortem examination by a veterinarian is necessarry to determin the cause of death. testing forage and drinking water before there is trouble is advised. Cattle should not have access to farm chemicals.

Management Practices to Minimize Nitrate Poisoning

Do not feed known nitrate accumulating forages (i.e., sudan, sorghum or oat hay) without a chemical analysis. Follow proper sampling procedures when collecting forage samples. Also, an analysis of water supplies is recommendd so that adjustments to the feeding program can take into accout the water nitrate contribution. Feeds being used to dilute nitrate hay should also be analyzed.

Consider making silage out of high-nitrate forages. The ensiling process will reduce nitrate levels by approximately 40 to 60 percent. However, forages cut for silage can be as high as 2 to 5 percent potassium nitrate (KNO3). Even if nitrate is reduced by half, toxicity may be a problem. It is suggested that silages be tested for nitrates before they are fed to livestock.

Change rations gradually, over a 7- to 10-day period, especially when new feed is known or suspected to contain nitrates. Runinants have the ability to adapt to gradually increasing nitrate levels, up to apoint. Too rapid change inthe diet can trigger nitrate poisoning.

Dilute high-nitrate feeds with feeds lower in nitrate. A balanced, high energy ration will help ruminats. Grain feeding seems to be helpful in addition to its effect in diluting the nitrate content of the feed. Energy from the grain apparently helps to complete the conversion of nitrate to ammonia, which is then used by the ruminal bacteria.

If grazing pasture with suspected elevated nitrate levels, graze only a couple of animals the first week. If problems do not arise, put the rest of livestock on pasture. Nitrates are less of a problem if pasture forages are not actively growing.

Frequent intake of small amounts of a high-nitrate feen increases the total amount of nitrate that can be consumed daily without toxic effects. More of a high-nitrate forage can be fed witout harmful effects by feeding it in limited amounts several times daily rather thatn feeding large amounts once or twice daily. When nitrate is fed continuously, animals become adapted to higher nitrate concentrations and may be able to use a portion of dietary nitrate as nonprotein nitrogen.

Do not use damp feed for livestock. Dampness tends to heighten toxicity. The probable explanation is that some of the nitrate is converted by bacterial denitrification to nitrite before animal consumption.

Herd health is an important consideration. Healthy animals are less affected than animals in poor health. Parasitism or other conditions causing anemia will increase susceptibility.

Nitrate toxicity does not appear to be altered and is not enhanced by simultaneous feeding or urea.

Table 1. Level of potassium nitrate (KNO3) in feed and animal response.
% KNO3 in feed Comment or animal response
.0 to .44 Safe to feed. Use caution with pregnant or young animals at the upper level.
45 to .88 Generally safe when fed with balanced ration. For pregnant animals limit nitrate feed to 1/2 of daily dry matter intake.
.89 to 1.50 Limit to 1/4 of the total daily ration Ration should be well fortified with energy, minerals, and vitamins.
over 1.5 Toxic. Extreme caution should be used. A well-mixed feed, below a 1 inch chop, or pelleting the feed will reduce sorting by animals. Amount of dilution with other feeds depends on nitrate level.

Table 2. Water potassium nitrate (KNO3) level in relation to nitrate toxicity.
KNO3 in water (ppm) Comment
0 to 69 Safe
70 to 209 Doubtful
210 to 349 Risky, subclinical toxicity
350 to 699 do not use, subclinical toxicity
700 to 1.050 do not use, sublethal but toxic
over 1,050 do not use, acute toxicity and lethal
1ppm = parts per million

Formulas for Converting Methods of Reporting

  • potassium nitrate = nitrate x 1.6
  • potassium mitrate = nitrate nitrogen x 7.0
  • nitrate = potassium nitrate x 0.6
  • nitrate = nitrate nitrogen x 4.4
  • nitrate nitrogen = potassium nitrate x 0.14
  • nitrate nitrogen = nitrate x 0.23
  • parts per million = o/o x 10,000
  • 0/0 = perst per million / 10,000

For Further Reading

  • Cowley, G. D., and D. F. Collings. 1977. Nitrate poisoning. Veterinary Record 101:305-306
  • Emerick, R. J. 1974. consequences of high nitrate levels in feed and water supplies. Fed. Proc. 33:1,183.
  • Hibbs, C. M., E. L. Stencel, and R. M. Hill. 1978. Nitrate toxicosis in cattle. Beterinary and Human Toxicology. 20:1-2.
  • Hibbs, C. M. 1979. Cyanide and nitrate toxicosis of cattle. Veterinary and Human Toxicology. 21:401-403.
  • Johnson, J. L., N. R. Schneider, C. L. Kelling, and A. R. Koster. 1983. Nitrate exposure in perenatal beef calves. Aver. Assn. Veterinary Laboratory Diagnosticians 26th Annual Proceedings.
  • National Academy of Sciences. 1972. Accumulation of nitrate. Printing and Publiching Office, Washington, D.C.
  • Osweiler, G. D., T. L. Carson, W. B. Buck, and G. A. VanGelder. 1985. Clinical and Diagnostic Veterinary Toxicology. Kendall/Hunt Publ. Co. Dubuqua, Iowa.

Source

Kvasnicka, B. and L. J. Krysl. Cattle Producer's Library CL 620. Nitrate Poisoning in Livestock. University of Nevada