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Syndrome in
Veal Calves


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Nitrate poisoning occurs most often in cattle and less often in other ruminants, but it can occur in horses, dogs and cats.  It is seldom reported in swine.  Clinical diagno­sis, treatment, confirmation and pre­vention of nitrate poisoning is pre­sented with cattle as the principle species; other species will be men­tioned where applicable.


Diagnosis requires identification of the clinical syndromes associated with acute and chronic nitrate poi­soning.  Acute toxicity can be de­scribed in three clinical phases:

gastrointestinal, cardiovascular and central nervous.  Chronic toxicity is discussed separately.  Clinical signs are usually apparent within 0.5-4.0 hr(s) of ingest ion of toxic concen­trations of nitrate.  Abdominal pain evidenced by a tucked abdomen, fre­quent urination, diarrhea and other signs of colic in the gastrointesti­nal phase may rapidly merge with those of cardiovascular insufficiency caused by vasodilation and methemo-globinemia.  Dyspnea, tachycardia, and brown or chocolate discoloration of mucous membranes are reported most often, but apparent cyanosis is seen in some individuals.  Cytotoxic anox­ia causes tremors, ataxia, and bel-ligerence which can progress to col­lapse, coma and occasionally convul­sions.

Vasodilation causes peripheral and splanchnic congestion with brown discoloration, petechiation, and ecchymoses on mucosal and serosal surfaces.

Other diagnostic considerations to be ruled out include causes of sudden death (cyanide, Japanese yew), hypo-tensives in companion animals (amyi nitrate), and other methemoglobin producers (Table 1).

Chronic nitrate poisoning is correlated with abortions,

Still births and stunted calves. Abortion is attributed to ma­ternal and fetalmethemoglobinemia resulting in fetal anoxia (particularly in the last tri­mester of pregnancy). More re­cently, unpublished data indi­cates serum progesterone is reduced in chronic nitrate tox­icosis in cattle and, possibly, horses.  Chronic nitrate toxicosis causes loss of condition, loss of weight, reduced milk production and weakness.  Hypo-vitaminosis A, hypovitaminosis E, and hypothyroidism are re­ported in cattle and swine.


Treatment of acute nitrate poison­ing is directed at reduction of methemoglobin to oxyhemoglobin by methylene blue.  A 1% solution (W/V) of methylene blue in isotonic saline is administered slowly intravenously at 8.8 mg/kg body weight in rumi­nants, and at 4.4 mg/kg body weight in ruminants in refractory cases. Some caution should be used in using methylene blue in the dog as at high­er doses it causes Heinz body forma­tion.  It should not be used in cats. Treatment can be repeated in 15-30 min.  Additional treatment includes oxygen therapy and inhibition of gas­trointestinal bacteria that convert nitrate to nitrite.  Sodium citrate has been suggested as a possible treatment for methemoglobinemia in the cat.  In chronic toxicity supple­mentation with vitamin A, vitamin E, vitamin D, and minerals may be bene­ficial.  Repositol progesterone may reduce abortions in cattle.


Confirmation of nitrate toxicosis requires analyzing the suspect source of poisoning, seru, ocular fluid, or frozen rumen contents for nitrate/ni­trite or measuring methemoglobin in

whole blood.  Concentrations of ni­trate/nitrite associated with toxico­sis are listed in Table 2.  Methemo-glob in concentrations of 65-80% are associated with death (lower concen­trations in active animals).  Clini­cal signs are usually seen when methemoglobin reaches 30-W%.  Blood samples for methemoglobin analysis should be rapidly frozen within 2 hrs. after death.

Other sources of nitrates in­clude standing water (farm ponds, field creeks, pig swills), contaminated ground water, slurry pits, limestone pits, fertilizer wagons, whey and silage.

John M. Sullivan, DVM

Graduate Student



Prevention of nitrate poisoning requires removal of inciting causes. The most cannon source of poisoning in the herbivore is ingestion of tox­ic forage. Plants accumulate nitrate in acid soils with low molybdenum, low sulfur,low phosphorus, low man­ganese, low magnesium and high ni­trate; particularly in aerated soils at lower temperatures or during drought conditions. Cloudy weather decreases reduction of nitrate to an mom a in the plant and causes ni­trate accumulation. Any additional stress to the plant can modify me-thobolism allowing nitrate accumula­tion. Phenoxyherbicides(2,4-D;2,4,5-T) are corrmonly associated with increasing the palatability of nitrate accumulating plants.

Hay can be a particular problem, especially in improperly cured or stored bales. Bacterial action can convert available nitrate to ni­trite which is 7 to 10 times more toxic than nitrate. Levels of ni­trate are not significantly reduced in curing and will actually increase on a wet weight basis. Adequate testing of stands, or bales of sus­pect forage, can be done quickly with the  diphenylamine test kit.  The test provides reproducible results in identifying forage with >1.0% nitrate

Suspect forage should be har­vested late on sunny days at least 1 week following signifi­cant periods of rainfall or cloudy weather, particularly when ending a drought.  Lists of plants commonly known to be nitrate accumulators are widely available.


fertilizer chlorates nitrobenzene
 acetaniline acetaminophen  iodate
 bromate  hydroquinone  organic nitrates
 anyl nitrate trinitrotoluene  sulfonamides
phenylhydrazine  cuprous copper  Acer rubrum
other causes of Heinz body anemia












humans, adult









MLDs are given in mg/kg




 40 ppm-U.S. Public Health Service Drinking WaterSafety Standard

400 ppm-considered safe for domestic animals

2000 ppm-no signs of toxicity within 35 days

3000 ppm-acute toxicity in cattle after 3 days



Ocular fluid/serum

20 ppb-highly suggestive of toxicity

> 30 ppb-diagnostic of toxicosis


0.12-0.15%-possible link to abortions (lowered serumprogesterone)

0.21%-hypovitaminosis A in ruminants

0.44%-generally considered safe

0.50-1.00%-use with caution

>1.0-1.5%- toxic



The following tips may be helpful to those of you submitting aquacul-ture samples to the ADDL for diagnos­tic purposes.


submit live fish for diagnostic eval­uation.  Live fish acutely affected with a disease that has not been treated is the best submission.  Live fish should be placed in a strong plastic bag with enough water to cov­er the fish and the bag can then be filled with compressed air or oxygen. During the sunrmer months, crushed ice should be packed around the bag for overnight shipment or personal deliv­ery.


submit fish found dead in the water. It would be of very limited value for microscopic examination, since fish autolyze rapidly.  Similarly, tissue from autolytic fish are of little value for bacterio1ogic evaluation since there is marked post mortem contamination of fish.


submit water samples for toxicologic evaluation where toxicity is suspect­ed.  Examples of toxins which can be detected fror; tank or pond water sam­ples include copper, nitrates, pesti­cides, and insecticides.


submit water samples for oxygen con­tent determination.  The oxygen con­centration of water samples submitted will change subject to the diffusion of gases into and out of the sample. Encourage producers to purchase "test kits" for oxygen concentration deter­minations since it must be performed on-site for accurate results.

If you have questions concerning fish diseases or other aspects of aquaculture please call Dr. Randy White, ACC.L (317-494-7440) or Mr. La-Don Swann, Aquaculture Extension Spe­cialist at (317-494-6264).

Dr. M.Randall White Veterinary Pathologist


ADDL-West Lafayette:
406 S. University
West Lafayette, IN 47907
Phone: 765-494-7440
Fax: 765-494-9181

11367 E. Purdue Farm Road
Dubois, IN 47527
Phone: (812) 678-3401
Fax: (812) 678-3412

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