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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
References
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
http://www.agric.gov.ab.ca/agdex/400/0006001.html
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
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