The current shortage of forage is causing many producers to ask what their alternatives to feeding may be and are they safe.  According to MU Extension Livestock Specialist Jim Humphrey there are several options available.

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Silage is a great option but there is one major concern that could be fatal to livestock.

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Local extension offices have the ability to let producers know if nitrates are present in their expected feed.

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Nitrates can also be a concern for grazing cattle.

 

 

Nature and History of the Nitrate Problem

G. B. Garner
Department of Biochemistry

W. H. Pfander
Department of Animal Sciences

G. E. Smith
Department of Agronomy

A. A. Case
College of Veterinary Medicine

Nitrate is a desirable part of our environment. When nitrate concentrations are excessive and/or out of place with respect to nature’s systems, certain complex interactions occur.

The three principle sources of nitrate for humans and their animals in plants, water and air are interrelated. Thus, when people take nitrogen from the
cycle, they must return that nitrogen so that nature can re-use it, or they must add chemical fertilizer nitrogen to maintain production.

Agricultural practices have increased plant production by increasing the amount of nitrogen and other plant nutrients available to crops. This increases the chance of getting the nitrogen cycle out of balance. Even when growers have made proper fertility and crop selection decisions, they have not been able to
control the environment (rainfall, temperature, sunlight, shifting seasons, etc.), which can alter the nitrate concentration in crops and in the water
supply. Nitrate concentration may be great enough in either plants or water consumed by humans and animals to result in losses of productivity, reproduction
and even loss of life.

Classical acute nitrate/nitrite poisoning

Acute nitrate/nitrite poisoning is caused by the presence of nitrite in the blood at a level sufficient to cause anoxia (internal suffocation). Nitrate (NO3-) can be reduced to nitrite (NO2-) by the microorganism in the gastrointestinal tract at a rate that overwhelms the body’s defense system. Nitrite combines with the hemoglobin of the red blood cells to form methemoglobin. Methemoglobin cannot transport oxygen to the body tissues. Thus the transport of oxygen varies
directly with the amount of nitrite ingested or produced in the gut per unit of  body weight in a given time.

The chief symptom, anoxia or oxygen deprivation, causes a bluish color of the mucous membranes of stricken animals. The blood is chocolate-brown in color due to methemoglobin formation. These characteristics are very indicative of acute nitrate/nitrite poisoning. Abortion of fetuses may result.

One type of the “Blue-baby” syndrome (methemoglobinemia) is caused by the infant’s receiving formula made with water from, or drinking water
from, wells or cisterns with higher than permissible levels of nitrate.

Historically, acute nitrate/nitrite poisoning was first reported in this country a century ago in connection with deliberate attempts to poison sheep on disputed western ranges. Oat hay poisoning was known for years before being recognized by Colorado and Wyoming workers in 1939 as a nitrate/nitrite acute intoxication.

In Kansas, Missouri and other Cornbelt areas, Cornstalk poisoning had been observed well before 1900, but the true nature of this nitrite intoxication was recognized as recently as 1954. This condition has been associated with corn growing under drought conditions on a wide range of soil types with adequate to high levels of available nitrogen for plant growth.

Farm animals today show the same symptoms (anoxia, cyanosis, staggers) before death when allowed access to inorganic salts of nitrate or nitrite. Careless use or storage in non-animal proof facilities of fertilizers and inorganic herbicides leads to many accidental nitrate/nitrite poisonings. The chemicals are sometimes mistakenly used in place of common salt (NaCl) in ration formulation with disastrous losses. Swine have been poisoned by nitrite added to fish meal as a preservative and from nitrate in byproducts of cheese manufacture where nitrate was added in the process.

Water supplies may contain enough nitrate to produce acute poisoning. Dried forage (hay and fodder) that has been grown on highly fertilized or manured soil
may also contain sufficient nitrate to cause acute nitrate/nitrite poisoning. This is especially true when adverse weather (cold, cloudy or droughty) conditions exist just before harvest. Green chopped forage crops with high levels of nitrate are less likely to cause the acute type of poisoning, but may do so when fed to hungry unacclimated cattle.

Animal sensitivity to nitrite

Young animals are highly sensitive to nitrite as compared to mature animals of the same species, because fetal hemoglobin is more sensitive to nitrite than
adult hemoglobin. Pregnant animals often lose their fetuses because of anoxia (methoglobinemia) without any apparent long-range damage to themselves in
nitrate/nitrite poisoning.

Hungry, half-starved and depleted animals are less tolerant to nitrate/nitrite intake than are well-fed animals on adequate rations.

Aged animals, especially those in poor nutritional state, are more sensitive than are younger mature animals to excessive nitrite, or the parent substance
nitrate.

Levels of acute nitrite and nitrate poisoning, on a dose basis, have been determined for a number of species. On a milligram nitrite-nitrogen per kilogram
body weight (NO2-N/KgBW) the values are: pig, 10, and for cattle and sheep, 15. For nitrate -N/KgBW, the value is 100 for sheep and 50 for cattle.

Experimental results with forages have indicated 0.25 percent nitrate-nitrogen or 0.08 percent nitrate-N of the total ration can be fed with without danger to livestock. When the water supply contains nitrate and/or nitrite, less nitrate/nitrite can be allowed in the feed. If animals are gradually acclimated to nitrate and no other stress is applied, the 0.25 percent level of nitrate-N may be tolerated.

Subclinical nitrite poisoning

Subclinical nitrite poisoning may occur at levels that are high enough to cause reactivity of the vascular tissues of the brain and other organs such as lungs, heart, liver, kidneys and testes. Prolonged exposure to nitrate/nitrite may cause severe degeneration of these tissues. The affected animals may appear to be in normal health, but will abort their young, fail to settle to service, suffer a decline in lactation or lack ability to adjust to cold temperatures.

With more severe disturbance of normal health, the animals may show actual signs of chronic disease such as unthriftiness, harsh hair coats, inflammations
of the eye, or increased susceptibility to common environmental conditions; i.e., digestive disturbances of various kinds, especially rumenitis (founder in
cattle). The signs are related to the mild upsets of normal health best described as interference phenomena (or syndrome). Such interference syndromes
are not true poisoning, but are the result of a slow but persistent action of the strong oxidizer (nitrite) against vitamins in vital enzyme system or hormonal balance within the animal’s metabolic scheme.

Such interferences may be active for a period of months or even a year at low levels of intake such as five parts per million (nitrite) in a water supply. Nitrite poisoning of the acute type would require perhaps 25 to 50 times that amount. The chances for metabolic disturbances to occur increase directly as the
amount of nitrite increases and as the nitrate in the ration or water increases.

Thyroid function is impaired by nitrate causing a decrease in iodine uptake by the thyroid gland. Fortunately, iodized salt contains enough iodine to counteract levels of nitrate that would reduce uptake but not show any other signs of poisoning.

Diagnosis and safe-level recommendation

Acute nitrite poisoning is easily diagnosed by the anoxia, bluing of mucous membrane and chocolate-colored blood if the animal is seen at peak methemoglobin levels. For instance, a cow may have a methemoglobin level of 70 percent and survive. Later she aborts and normal methemoglobin levels are found. It might be concluded that “sub-lethal nitrate” or reproductive disease was responsible, but a better diagnosis would be that the 70 percent level was lethal to the fetus which was aborted later.

Subclinical nitrate/nitrite poisoning is difficult to diagnose because other conditions for which nitrite is responsible, in whole or part, are similar to symptoms produced by a large number of infectious and noninfectious diseases. Clinical and analytical laboratories can be used to determine what condition exists. The first step should be to test for nitrate/nitrite all ration component s, water supplies and weeds to which animals have access. Then proceed to other possibilities in a logical order of elimination.

A safe level of nitrate/nitrite is virtually impossible to set because of all the variables, i.e. extremely wide ranges of individual animal tolerance, great variability of conversion of nitrate to nitrite in animals’ intestines, dietary history, disease level and environmental conditions. When possible, nitrate-nitrogen in drinking water should be below 10 parts per million (ppm) and be free of nitrites. Total rations should contain less than 0.07 percent nitrate-nitrogen and be free of nitrite.

Fuming silos, a source of toxic gases from nitrate

The heavy, lethal gas is a mixture of the oxides of nitrogen, some of which are lethal to all living forms. The gases form in silos during filling and for a week or so afterwards. It comes from forage nitrate. The amount of forage nitrate need not be high for the reaction to occur. However, these appear to be an increased incidence with droughty conditions. The gases range from colorless to yellowish-red to reddish-brown and have a pungent, very irritating odor similar to a strong bleaching agent. These gases are toxic at amounts greater than 10 to 20 ppm; a silo may generate enough gas to raise the level in surrounding air to many hundreds of parts per million. The gases are heavier than air and settle in the silo chute and/or buildings at the base of the silo.

The silage, after 21 days of ensiling, should be stabilized and the level of nitrate reduced to a safe level for feeding. However, a test for nitrate should be made to determine the nitrate status.

Drainage from all silos including fuming silos may be toxic to animals allowed access to them. Take care to prevent transferring nitrate/nitrite and other substances from silos to wells, ponds or streams via the liquid from silos.

Summary

Excessive nitrate in feedstuffs and water is an important consideration in animal health. Forage plants, oats, sorghums, corn and certain weeds have long
been known to accumulate nitrate to levels that kill cattle, sheep and horses. Drought, unusually cold and cloudy weather, and excessive nitrogen fertility
beyond the crop’s ability to assimilate the nitrogen, cause plants to have potentially toxic levels of nitrate.

Water supplies may contain toxic levels of nitrate from surface water contamination, close proximity to old feedlots or farm buildings used to house llivestock, and in some areas from leaching of the fertilizer nitrogen into groundwater supplies. Acute poisoning of human infants and livestock, especially young pigs and cattle, continues to occur from water supplies containing excessive nitrate/nitrite.

The interference syndrome or subclinical level of nitrate/nitrite intoxication is difficult to recognize because infectious diseases, i.e. brucellosis and leptospirosis, cause similar symptoms.

Veterinarians, state diagnostic services, area extension specialists and state extension agricultural specialists can be called on to help in suspected cases of nitrate/nitrite intoxication.

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1993 to 2011 University of Missouri. Published by MU Extension, all rights reserved.