⇦ Back to Livestock and Feedstuff Management Home
📄 View PDF
Nitrate toxicity (methemoglobinemia) is a serious threat to livestock fed certain types of forages and roughages, especially if those forages have been stressed by drought, hail, or other poor growing conditions. Stress conditions may cause excessive nitrate levels in these forages. Animals consuming these forages are at risk. Nitrate toxicity occurs most often in cattle and less often in other ruminants, like sheep and goats. It rarely occurs in other animals, like horses, dogs, or swine.
“Nitrate toxicity” actually not due to nitrate
Nitrate is relatively nontoxic.
Exact symptoms of nitrate toxicity will vary
Depends on forage and animal characteristics.
Symptoms may be "acute" (lethal) or "chronic" (sublethal).
Toxicity caused by nitrite.
Is intermediate product.
Is ten times more toxic than nitrate.
Ruminants consume nitrate in their feed or water
Nitrate (NO3) rapidly converted to nitrite (NO2) by rumen microorganisms
Nitrite converted to ammonia (NH3).
Ammonia further converted by rumen microorganisms into amino acids and microbial protein for subsequent digestion.
Excess ammonia absorbed into the blood.
Excreted as urea in the urine.
If ruminant consumes feed with higher-than-normal nitrate.
Nitrate converts to nitrite faster than nitrite converts to ammonia.
Microorganisms cannot convert all of the nitrate to nitrite or all of the nitrite to ammonia quickly enough.
Nitrate and nitrite accumulate in rumen.
More nitrate and nitrite accumulate in the rumen as the animal consumes more feed.
Accumulated nitrate and nitrite can exceed microorganism capacity to convert nitrite to ammonia.
Excess, accumulated nitrite passes through rumen wall directly into bloodstream.
Nitrate in bloodstream can be recycled back into rumen through saliva or intestinal secretions
Nitrate alone does not create a problem.
Recycled nitrate can be converted to nitrite in rumen, which adds to nitrite accumulation.
Single-stomached (monogastrics), nonruminant animals
e.g., horses and swine
Nitrate-to-nitrite conversion occurs in the intestine.
Is closer to end of the digestive tract.
Figure 1. Comparison of blood color from an animal with nitrate poisoning (left) and a healthy animal (right).
Hemoglobin: red-colored blood pigment that carries oxygen from lungs to other body tissues.
Nitrite absorbed into bloodstream oxidizes ferrous iron in hemoglobin molecule
This converts ferrous iron to ferric iron.
Forms “methemoglobin”
Methemoglobin: dark-colored compound which cannot carry oxygen.
Toxicity due to increasing methemoglobin levels
Can lower blood oxygen-carrying capacity below critical level.
Causes oxygen starvation of body tissue,
Results in gradual asphyxiation,
Can be fatal
Methemoglobin as percentage of total hemoglobin is important
More than 10% methemoglobin
Blood takes on a chocolate-brown or purplish-brown color
About 30% methemoglobin
Slight toxicity symptoms may occur
Methemoglobin levels of 50% to 60%
Animals may possibly survive
More than 70% methemoglobin
Toxicity is usually fatal
Toxic nitrate level is hard to pinpoint.
All roughages contain some nitrate; animals can normally consume small amounts without toxic effects.
Toxicity potential depends on several conditions.
Forage nitrate level
Amount and rate of feed consumption.
Nitrate-to-ammonia conversion rate in rumen.
Feed digestion rate and passage rate
Animal size, maturity, and conditon
Animal condition
Animals in poor health, malnourished, or under stress.
More susceptible to nitrate toxicity.
May show toxicity symptoms after consuming less nitrate than unstressed animals in good condition
¶ D. Livestock species and toxicity potential
Cattle (bovine species) may be most susceptible.
Sheep (ovine species) are generally less affected.
Can apparently convert nitrate more rapidly than cattle.
Comparatively rare in horses (equine species)
Can generally tolerate comparatively high nitrate concentrations.
Do not have a rumen.
Conversion of nitrate to nitrite to ammonia reaction takes place in the cecum (hindgut).
Only about 25% of nitrate consumed is converted to nitrite in the cecum
Remaining nitrate can be excreted.
Comparatively rare in swine, poultry, and dogs.
Typically do not consume forage
Animal is in critical condition.
Poisoning symptoms of acute nitrate toxicity occur rapidly
Often within 30 minutes to a few hours after feeding.
First evidence of toxicity is often a dead animal.
Animals are often found lying down after short struggle.
Acute symptoms of clinical nitrate poisoning include:
“Cyanosis”
Darkening or bluing of mucous membranes in eyes, nose, and mouth
Hemoglobin conversion to methemoglobin is not permanent.
Methemoglobin reductase: blood enzyme.
Converts methemoglobin rapidly back to hemoglobin.
Animals that recover from nitrate toxicity are likely not to show aftereffects
Below-normal temperature
Frequent urination and/or diarrhea
Labored breathing
Rapid, weak pulse
Staggering and lack of coordination
Convulsions and muscle tremors
Weakness and collapsing
¶ F. Standard treatment for acute toxicity
Intravenous injection of a methylene blue and dextrose solution
Toxicity symptoms often occur so suddenly that treatment is not possible or applied too late to be effective
. If nitrate toxicity symptoms are recognized and animals are treated immediately, some may be saved
Effects of sublethal doses of nitrate are unclear.
Are not easily observed and may not be economic.
Chronic toxicity may occur where clinical symptoms are not noted
Should not automatically assume that nitrates are to blame for poor health or performance.
Chronic symptoms may include:
Depressed appetite, weight loss
Slow growth, slow weight gain
Lower milk production
Abortion
Vitamin A deficiency
Nitrate may interfere with conversion of carotene to Vitamin A.
Is only concern only if the carotene in green roughages is sole source of Vitamin A.
Animals receiving Vitamin A supplement or injection should not be affected.
Fetal abortion
Common after-effect of pregnant animals recovering from acute nitrate poisoning
Chronic nitrate poisoning can cause abortions to occur within first 100 days of pregnancy
Are ejecting fetal animal that has died of oxygen starvation
Nitrates interfere with egg implantation in the uterus.
If the egg is not implanted, fetus dies and reabsorbed
No obvious signs of abortion during first trimester
Reproductive problems may also occur due to nitrate or nitrite induced hormone imbalance.
Are often not recognized as caused by chronic toxicity
Calves affected by nitrate poisoning during the last three months of gestation are usually born one to four weeks premature
Most appear normal, but die within 18 to 24 hours of birth
Surviving newborn calves that survive may have convulsions and seizures
Schroder, J. 2008. Drought and feed poisoning in dairy cattle. DS-16-97. North Dakota State Univ. Ext. Serv., Fargo ND. (accessed 08/30/2010) http://www.ag.ndsu.edu/disaster/drought/droughtfeedpoisoning.html
Poore, M., et. al. 1999. Nitrate management in beef cattle production systems. West Virginia Univ. Ext. Svc., Morgantown, WV (accessed 08/31/2010) http://www.wvu.edu/~agexten/forglvst/Nitrdrot.htm
Yaremcio, B. 1991. Nitrate poisoning and feeding nitrate feeds to livestock. Alberta Agric. and Rural Dev., Edmonton, AB (accessed 08/31/2010) http://www1.agric.gov.ab.ca/$department/deptdocs.nsf/all/agdex851
Waldridge, B. Nitrate and Nitrite Toxicity in Horses. Kentucky Equine Research. http://www.ker.com/library/health/2010/07/nitrate-and-nitrite-toxicity-inhorses.html
Anderson, B. 2016. Nitrate Awareness: Is Your Herd Safe? https://onpasture.com/2016/11/28/nitrate-awareness-is-your-herd-safe/ accessed 22Sep2018
📄 View PDF