Nitrite Poisoning of Livestock

Nitrite Poisoning of Livestock

(Cornstalk disease)

Introduction

Nitrates in Plants

            Plants absorb nitrogen from the soil in the form of nitrates, regardless of the form of nitrogen fertilizer (including manure) applied, which are then converted into proteins and other nitrogen-containing substances. Apart from high natural availability of soil nitrogen, various other factors promote high concentrations of nitrate in plants. These include moisture stress, decreased light (cloudiness, short day length), and low temperatures. The use of nitrogenous fertilisers, and spraying plants with hormone-type herbicides (such as 2,4-D) can also cause a build-up of nitrate levels in plants. Normally plants contain relatively small amounts of nitrate as such, because the conversions take place fairly rapidly inside the leaf. However, under certain conditions, the amount of nitrate in the soil can increase greatly because of lack of leaching, reduced uptake by plants, and decomposition of organic matter. After the drought breaks nitrate uptake by plants may be high. While high concentrations of nitrate are not toxic to plants, animals grazing on such plants may suffer from poisoning.

            Many weeds, crop and pasture plants have been reported as capable of causing nitrate and/or nitrite poisoning. Capeweed, variegated thistle, lamb's-quarter, Jimson weed, fireweed (Kochia), smartweed, dock, and Johnson grass are well-known accumulators of nitrate. Many of the major crop plants have been implicated, including maize, rape, soybean, linseed, sorghum, millet, wheat, oats, sunflower, sudangrass and barley. Lucerne, subterranean clover, and Tama ryegrass have also been reported to be capable of accumulating large amounts of nitrate in their leaves and stems. Vegetables capable of accumulating large amounts of nitrate that are most frequently grazed include sugar beets, lettuce, cabbage, potatoes and carrots.

            Nitrate, which does not selectively accumulate in fruits or grain, is found chiefly in the lower stalk with lesser amounts in the upper stalk and leaves. Nitrate in plants can be converted to nitrite under the proper conditions of moisture, heat, and microbial activity after harvesting.

Factors that facilitate uptake of nitrate by plants include:

• use of nitrogen-containing fertilisers;

• low soil sulfur and molybdenum;

• areas where stock have congregated and urinated/defaecated (e.g. yards).

Factors which cause nitrate to accumulate in the plant include:

  • drought;

            • cloudy or cold weather;

            • herbicide application – especially phenoxy herbicides such as 2,4-D;

            • wilting.                           

The amount of nitrate in plant tissues also depends on:

            • plant species;

            • stage of maturity;

            • part of the plant.

            Nitrate concentrations are usually higher in young plants and decrease as plants mature. Most of the plant nitrate is also located in the bottom third of the stalk, hence the leaves contain less nitrate and the flowers or grain contain little to no nitrate.

            Well-aerated soil with a low pH, and low or deficient amounts of molybdenum, sulfur, or phosphorus in soil tend to enhance nitrate uptake, whereas soil deficiencies of copper, cobalt, or manganese tend to have opposing effects.

            Anything that stunts growth increases nitrate accumulation in the lower part of the plant.

            Phenoxy acid derivative herbicides (eg, 2,4-D and 2,4,5-T), applied to nitrate-accumulating plants during early stages, cause increased growth and a high nitrate residual (10%–30%) in surviving plants, which are lush and eaten with apparent relish even though previously avoided.

            Nitrate, which does not selectively accumulate in fruits or grain, is found chiefly in the lower stalk with lesser amounts in the upper stalk and leaves.

            Anhydrous ammonia and nitrate fertilizers and soils naturally high in nitrogen tend to increase nitrate content in forage.

Hay and silage

            Hays made from cereal crops, especially those grown under drought conditions and cut while ‘sappy’, can develop toxic nitrite levels when they heat up. Oaten hay is particularly risky and becomes poisonous if previously dry hay is dampened by rain or snow some time before feeding out.

            Hays made from nitrate-rich materials contain almost as much nitrate as when first made, unless some is converted to nitrite by heating or mould.

            Silage contains less nitrate than its parent crop due to the fermentation process that it undergoes. Forages high in nitrate can lose 40%–60% of their nitrate content during fermentation.

Nitrates in Water

            Nitrates and nitrites are water soluble.  They move with the water.  Any nitrate added to, or produced within, the soil may be leached or washed away by moving water either by surface run-off or ground water percolation.

            Nitrates are more concentrated below or near the area of waste accumulation or disposal such as manure piles, feedlots, septic tank disposal fields, cesspools, privies, etc.  Excess nitrates also are more apt to be found in ground water under low areas and waterways that collect or convey.

            Water samples from shallow, dug, bored and driven wells more frequently contain excess nitrates than water from deeper, drilled wells.  Nitrate levels generally are highest following wet periods and lowest, even down to zero nitrates, during dry periods which may cause a false sense of security.  Preferably, a well should be tested immediately following a wet period.

Water can contain toxic levels of nitrates. High-risk sources include:

            • water from deep wells fed by soil water from highly fertile soils;

            • condensed water from ventilating shafts in piggeries where there are high ammonia levels in the air;

            • fluids draining from silos containing materials rich in nitrates.

            Water contaminated by fertiliser, animal wastes or decaying organic matter may also be a source of toxic levels of nitrate. Marginally toxic levels of nitrate in water, combined with marginally toxic levels of nitrate in feed, can also lead to poisoning.

            Nitrate concentrations may be hazardous in ponds that receive extensive feedlot or fertilizer runoff; these types of nitrate sources may also contaminate shallow, poorly cased wells.      Water with both high nitrate content and significant coliform contamination has greater potential to adversely affect health and productivity than does either nitrate or bacteria alone. Livestock losses have occurred during cold weather due to the concentrating effect of freezing, which increases nitrate content of remaining water in stock tanks.

            Nitrates and nitrites are used in pickling and curing brines to preserve meats, and in certain machine oils and antirust tablets, gunpowder and explosives, and fertilizers. They may also serve as therapeutic agents for certain noninfectious diseases, e.g., cyanide poisoning. Nitrate toxicosis can also result from accidental ingestion of fertilizer or other chemicals.

Animal susceptibility

Species

ª      There is considerable variation between species in their susceptibility to nitrite poisoning. Pigs are the most susceptible, then, in order, cattle, sheep, and horses.

ª      Non-ruminants, such as horses and pigs, have no mechanism for converting nitrate to nitrite in their digestive tracts, so they are not susceptible to nitrite poisoning from excessive intake of nitrates. However, they are highly susceptible to poisoning from nitrite intake (for instance in mouldy hay) because they cannot convert the nitrite to ammonia.

ª      Sheep are more efficient at converting nitrite to ammonia, so this may be the reason why they are less susceptible to nitrite poisoning than cattle.

Hungry stock

            Hungry stock are at far greater risk than animals receiving regular and good fodder. This is because hungry stock consume more toxic feed, and, in the case of ruminants, their rumen microbes will not have had time to adapt to converting the nitrite to ammonia. For example, it takes about twice as much nitrate to kill a ruminant when the nitrate comes from forages that are eaten over a long period of time, compared to that which is consumed very quickly.

            Ruminant animals receiving carbohydrate-rich fodders tolerate high nitrate and nitrite levels better than those that are not. This is because energy from carbohydrates (grain) helps rumen microbes convert nitrite to ammonia.

            Animals that are stressed or in poor health or condition will also be more susceptible to nitrate/nitrite poisoning.

Adaptation or acquaintance

            Frequent intake of small amounts of high-nitrate feed increases the total amount of nitrate that can be consumed by ruminant animals without adverse effects. This is because rumen microbes are adapted to deal with the increased nitrate content of the feed.

            Toxicoses occur in unacclimated domestic animals, most commonly from ingestion of plants that contain excess nitrate, especially by hungry animals engorging themselves and taking in an enormous body burden of nitrate.

            Confounding interactions with nonprotein nitrogen, monensin, and other feed components may exacerbate effects of excessive nitrate content in livestock diets, especially when coupled with management errors.

Toxicity Variation

            Ruminant livestock can tolerate a wide range of nitrate, depending on several factors.  Ruminants are especially vulnerable because the ruminal flora reduces nitrate to ammonia, with nitrite (~10 times more toxic than nitrate) as an intermediate product. Nitrate reduction (and nitrite production) occurs in the cecum of equids but not to the same extent as in ruminants. Young pigs also have GI microflora capable of reducing nitrate to nitrite, but mature monogastric animals (except equids) are more resistant to nitrate toxicosis because this pathway is age-limited.

Factors making nitrate less toxic include:

            The animal can become conditioned to eat larger amounts of feed with high nitrate content if the increase is gradual.

            Healthy animals are less likely to be adversely affected than animals in poor health.

            Adequate amounts of available carbohydrates (grain) allow the animal to consume more nitrate because carbohydrates enhance the conversion process from nitrate to microbial protein.

Factors making nitrate more toxic include:

¨      Rapid diet changes can trigger nitrate poisoning.

¨      Parasitism or other conditions causing anemia will increase susceptibility.

¨      Nitrate in more than one diet component (e.g. water and forage).

MECHANISM OF POISONING

            Nitrate accumulation in plants is a potential danger to grazing animals. It can cause two different disorders - nitrate poisoning and nitrite poisoning.

                Nitrates and nitrites are closely linked as causes of poisoning.

            Nitrate is not always toxic to animals.

            When feed containing nitrate is eaten by ruminant animals, nitrate is converted to nitrite, and then to ammonia and microbial protein, by rumen microbes. Non-ruminant animals are unable to do this. Although poisoning from the various forms of ni­trate is referred to as “nitrate poisoning,” the nitrate ion itself is relatively nontoxic. The reduction of nitrate to nitrite occurs much more rapidly in the rumen than the reduction of nitrite to ammonia. Consequently, when ruminants consume plants high in nitrate, some nitrite formed in the rumen enters the bloodstream where it converts blood hemoglobin to methemoglobin (nitrite ion in contact with RBCs oxidizes ferrous iron in Hgb to the ferric state, forming stable methemoglobin incapable of oxygen transport). This greatly reduc­es the oxygen-carrying capacity of blood, and the animal suffers from oxygen starvation of the tissues. Prussic acid also produces death by tissue asphyxia­tion, but by an entirely different process.

            The methemoglobin content of the blood of cattle succumbing to nitrate poisoning may be as high as 80 percent. Conversion of one-third of the hemoglobin to methemoglobin produces only slight symptoms; life is still possible when 60 per­cent of the hemoglobin has been converted, but death is a certainty when hemoglobin has fallen to one-third normal levels.          

            Secondary effects due to vasodilatory action of the nitrite ion on vascular smooth muscle may occur. The nitrite ion may also alter metabolic protein enzymes.

            Nitrates have a direct, caustic effect on the lining of the gut if consumed in large quantities. Signs of poisoning include diarrhoea, salivation and abdominal pain.

            Nitrites are much more toxic. These are formed from nitrates during ruminant digestion and may also occur if stored plant materials heat up or are attacked by bacteria or fungi.When high levels of nitrites accumulate in the gastrointestinal tract, they are absorbed into the bloodstream. Nitrite in the bloodstream changes haemoglobin (the oxygen- carrying part of blood) to methaemoglobin (which cannot carry oxygen). If enough methaemoglobin is produced, the animal will die. Some animals can tolerate up to 50% conversion of their haemoglobin without ill-effects; however, when more than 80% haemoglobin is converted, death occurs.

            Although usually acute, the effects of nitrite or nitrate toxicity may be subacute or chronic and are reported to include retarded growth, lowered milk production, vitamin A deficiency, minor transitory goitrogenic effects, abortions and fetotoxicity, and increased susceptibility to infection. Chronic nitrate toxicosis remains a controversial issue and is not as yet well characterized, but most current evidence does not support assertions of lowered milk production in dairy cows due to excessive dietary nitrate exposure alone.

Clinical Findings

            Signs of nitrite poisoning usually appear suddenly because of tissue hypoxia and low blood pressure as a consequence of vasodilation and symptoms may not be observed before animals are found dead. Animals being poisoned may stand apart from the herd, then collapse, or they may fall in their tracks if driven. Signs of poisoning, in the usual order of appearance, are weakness and unsteady gait, collapse, shallow and rapid breathing, rapid pulse, coma, and death - the latter accompanied by the usual terminal muscular reflex movements. Rapid, weak heartbeat with subnormal body temperature, muscular tremors, weakness, and ataxia are early signs of toxicosis when methaemoglobinemia reaches 30%–40%. Respiratory distress is not as obvious as when asso­ciated with choking or pneumonia. Brown, cyanotic mucous membranes develop rapidly as methaemoglobinemia exceeds 50%.  The unpigmented parts of the body, such as the white of the eye, the tongue, and lips, have a blue-brown discoloration from the onset, as a result of methaemoglobin circulat­ing in the superficial vessels. Dyspnea, tachypnea, anxiety, and frequent urination are common. Some monogastric animals, usually because of excess nitrate exposure from nonplant sources, exhibit salivation, vomiting, diarrhea, abdominal pain, and gastric hemorrhage. Affected animals may die suddenly without appearing ill, in terminal anoxic convulsions within 1 hr, or after a clinical course of 12–24 hr or longer. Acute lethal toxicoses almost always are due to development of ≥80% methaemoglobinemia.         

            Blood in which at least 10 percent of the he­moglobin has been converted to methaemoglobin is chocolate-brown in color. Fatal methaemoglobin levels range above 70 percent of the total hemoglo­bin, so the color of the blood of a dead animal may indicate poisoning. However, even though plant nitrate poisoning is suspected as a cause of death, be cautious in accepting the color of the blood of the dead animal as confirmatory evidence if some time has passed since death. A chemical analysis to determine the presence of methaemoglobin, nitrate, or nitrite in a blood sample is the most reliable method of determining nitrate poisoning.

            Under certain conditions, adverse effects may not be apparent until animals have been eating nitrate-containing forages for days to weeks. Some animals that develop marked dyspnea recover but then develop interstitial pulmonary emphysema and have continued respiratory distress; most of these recover fully within 10–14 days. Abortion and stillbirths may be seen in some cattle 5–14 days after excessive nitrate/nitrite exposure but likely only in cows that have survived a ≥50% methemoglobinemia for 6–12 hr or longer. Prolonged exposure to excess nitrate coupled with cold stress and inadequate nutrition may lead to the alert downer cow syndrome in pregnant beef cattle; sudden collapse and death can result.

            Following an abnormal exposure to nitrates or nitrites, a cow may abort a fetus that died because of oxygen starvation. The grazing of plants con­taining “borderline” levels of nitrate has also been associated with abortion, reduced milk flow, lower weight gains, and signs of vitamin A deficiency (Nitrate is thought to interfere with the conversion of plant carotene to vitamin A).

Signs of poisoning Signs of nitrate poisoning are: • diarrhoea and vomiting; • salivation; • abdominal pain. Signs of nitrite poisoning usually appear 6–24 hours after the toxic material is consumed. These include: • rapid, noisy and difficult breathing; • blue/chocolate-colouredmucous membranes; • rapid pulse; • salivation, bloat, tremors, staggering; • dark, chocolate-coloured blood; • abortions – pregnant females that survive nitrate/nitrite poisoning may abort due to a lack of oxygen to the foetus; abortions usually occur 10–14 days after exposure to nitrates; • weakness, coma, terminal convulsions, death.

Post-mortem findings

From nitrate poisoning:

            • severe reddening and stripping of the stomach and intestinal linings.

From nitrite poisoning:

            • dark red or coffee-brown blood that clots poorly;

            • pinpoint haemorrhages in internal organs and on internal surfaces;

            • accumulation of blood in the stomach wall.

Lesions

            Blood that contains methemoglobin usually has a chocolate-brown color, although dark red hues may also be seen. There may be pinpoint or larger hemorrhages on serosal surfaces. Hydroperitoneum and ascites have been reported in stillborn calves, as well as edema and hemorrhage in the lungs and digestive system of perinatal calves with excessive maternal nitrate exposure. However, dark brown discoloration evident in moribund or recently dead animals is not pathognomonic, and other methemoglobin inducers must be considered. If necropsy is postponed too long, the brown discoloration may disappear with conversion of methemoglobin back to Hgb.

            Few tissue changes are evident at autopsy after ni­trate poisoning. Some inflammation of the respiratory and gastrointestinal tract may be noted, and there may be a few small hemorrhages, particularly on the heart.

Diagnosis

            Diagnosis is based on:

• observed clinical signs;

• possible exposure to toxic plants, feeds or water;

• post-mortem findings;

• laboratory tests.    

            Excess nitrate exposure can be assessed by laboratory analysis for nitrate in both pre- and postmortem specimens. High nitrate and nitrite values in postmortem specimens may be an incidental finding, indicative only of exposure and not toxicity. Plasma is the preferred premortem specimen, because some plasma protein–bound nitrite could be lost in the clot if serum was collected. Nitrite present in whole blood also continues to react with Hgb in vitro, so these specimens must be centrifuged immediately and plasma separated to prevent erroneous values of both. Additional postmortem specimens from either toxicoses or abortions include ocular fluids, fetal pleural or thoracic fluids, fetal stomach contents, and maternal uterine fluid. All specimens should be frozen in clean plastic or glass containers before submission, except when whole blood is collected for methemoglobin analysis. Because the amount of nitrate in rumen contents is not representative of concentrations in the diet, evaluation of rumen contents is not indicated.

Bacterial contamination of postmortem specimens, especially ocular fluid, is likely to cause conversion of nitrate to nitrite at room temperature or higher; such specimens may have abnormally high nitrite concentrations with reduced to absent nitrate concentrations. Endogenous biosynthesis of nitrate and nitrite by macrophages stimulated by lipopolysaccharide or other bacterial products may also complicate interpretation of analytical findings; this should be considered as a possible maternal or fetal response to an infection.

            Methemoglobin analysis alone is not a reliable indicator of excess nitrate or nitrite exposure except in acute toxicosis, because 50% of methemoglobin present will be converted back to Hgb in ~2 hr, and alternative forms of nonoxygenated Hgb that may be formed by reaction with nitrite are not detected by methemoglobin analysis. Nitrate and nitrite concentrations >20 mcg NO3/mL and >0.5 mcg NO2/mL, respectively, in maternal and perinatal serum, plasma, ocular fluid, and other similar biologic fluids are usually indicative of excessive nitrate or nitrite exposure in most domestic animal species; nitrate concentrations of up to 40 mcg NO3/mL have been present in the plasma of healthy calves at birth but are reduced rapidly as normal neonatal renal function eliminates nitrate in the urine. In acutely poisoned ruminant livestock, nitrate and nitrite concentrations as high as 300 mcg NO3/mL and 25–50 mcg NO2/mL, respectively, can be found in plasma or serum, with ~⅓ less in postmortem ocular fluid because of diffusion equilibrium delay. However, postmortem ocular fluid nitrate concentrations are relatively stable and remain diagnostically significant for up to 60 hr after death. Once collected, plasma, serum, and ocular fluid specimens have stable nitrate concentration for at least 1 mo at –20°C.

            Normally expected nitrate and nitrite concentrations in similar diagnostic specimens are usually <10 mcg NO3/mL and <0.2 mcg NO2/mL, respectively. Nitrate and nitrite concentrations >10 but <20 mcg NO3/mL and >0.2 but <0.5 mcg NO2/mL, respectively, are suspect and indicate nitrate or nitrite exposure of unknown duration, extent, or origin. The possible contribution of endogenous nitrate or nitrite synthesis by activated macrophages must also be considered. The biologic half-life of nitrate in beef cattle, sheep, and ponies was determined to be 7.7, 4.2, and 4.8 hr, respectively, so it will be at least five biologic half-lives (24–36 hr) before increased nitrate concentrations from excessive nitrate exposure diminish to normally expected values, allowing additional time for valid premortem specimen collection.

            A latent period may exist between excessive maternal dietary nitrate exposure and equilibrium in perinatal ocular fluids. Aqueous humor is actively secreted into the anterior chamber at a rate of ~0.1/mL/hr, and nitrate and nitrite are thought to enter the globe of the eye by this mechanism. Equilibrium between aqueous and vitreous humor is by passive diffusion rather than by active secretion, so nitrate or nitrite may be present in comparatively lesser concentrations in vitreous humor after acute exposure.

            Field tests for nitrate are presumptive and should be confirmed by standard analytical methods at a qualified laboratory. The diphenylamine blue test (1% in concentrated sulfuric acid) is more suitable to determine the presence or absence of nitrate in suspected forages. Nitrate test strips (dipsticks) are effective in determining nitrate values in water supplies and can be used to evaluate nitrate and nitrite content in serum, plasma, ocular fluid, and urine.

TESTING FOR NITRATES             The diphenylamine test for nitrates can be used in the field to detect dangerous nitrate levels in for­ages or rumen contents. The test reagent is made by dissolving 500 milligrams of diphenylamine in 20 milliliters of water and carefully adding enough sulfuric acid to make 100 milliliters. This stock so­lution should be stored in a brown bottle. The steps in conducting a quick nitrate test are:             1. Learn the environmental conditions conducive to high nitrate content in forages.             2. Obtain a forage sample that is representative of that eaten by the animal, or a sample of the rumen contents.             3. Finely crush the sample in a glass container, such as an ash tray.             4. Add 10 to 20 drops of distilled water and mix well, with crushing action.             5. Add a few drops of the diphenylamine-sulfuric acid solution.             6. Formation of a deep blue precipitate within 30 minutes indicates a high concentration of nitrate in the forage and the need for a more quantitative test.

Differential diagnoses include poisonings by cyanide, urea, pesticides, toxic gases (e.g., carbon monoxide, hydrogen sulfide), chlorates, aniline dyes, aminophenols, or drugs (e.g., sulfonamides, phenacetin, and acetaminophen), as well as infectious or noninfectious diseases (e.g., grain overload, hypocalcemia, hypomagnesemia, pulmonary adenomatosis, or emphysema) and any other cause of sudden unexplained deaths.

Treatment

            Urgent veterinary attention is required to confirm the tentative diagnosis and to treat affected animals. Death usually occurs so suddenly that treatment is not possible, and few treated animals recover.

            Stock should immediately be removed from suspect material, and be handled as little and as quietly as possible. Hay or some other low- nitrate herbage should be fed to dilute the nitrate and/or nitrite in the stomach.

            Handle poisoned animals quietly, and affected animals can be treated by intravenous injections of methylene blue, a powdered dye material. Methylene blue converts the methaemoglobin back to oxygen-carrying haemoglobin.

            Slow IV injection of 1% methylene blue in distilled water or isotonic saline should be given at 4–22 mg/kg or more, depending on severity of exposure. Lower dosages may be repeated in 20–30 min if the initial response is not satisfactory. Lower dosages of methylene blue can be used in all species, but only ruminants can safely tolerate higher dosages. If additional exposure or absorption occurs during therapy, retreating with methylene blue every 6–8 hr should be considered.

            Rumen lavage with cold water and antibiotics may stop the continuing microbial production of nitrite.

            Due to the vasodilation effect of nitrate, vasoconstrictor drugs such as adrenalin should be administered. In chronic poisoning, vitamin A should be given.

Management Practices

            Feeding rations high in carbohydrates will reduce and sometimes prevent losses from nitrate poisoning.

• Control weeds that accumulate nitrates. Freshly sprayed plants may become more palatable, so defer grazing of sprayed areas.

• During periods of cool or cloudy weather, avoid grazing a suspect area if possible. During periods of sunlight, allow animals to eat large quantities of dry forage and then graze the area.

• Test the nitrate content of forage when in doubt.

• Distinguish nitrate poisoning from prussic acid poisoning or grass tetany, so the appropriate treatment may be administered.

Control

            Animals may adapt to higher nitrate content in feeds, especially when grazing summer annuals such as sorghum-Sudan hybrids.

            Multiple, small feedings help animals adapt.

            Trace mineral supplements and a balanced diet may help prevent nutritional or metabolic disorders associated with longterm excess dietary nitrate consumption.

            Feeding grain with high-nitrate forages may reduce nitrite production. However, caution is advised when combining other feed additives/components, including nonprotein nitrogen, ionophores (such as monensin) and other growth and performance enhancers, with high-nitrate diets in ruminants.

            Proper management, especially regarding acclimation, is critical. Forage nitrate concentrations >1% nitrate dry-weight basis (10,000 ppm NO3) may cause acute toxicoses in unacclimated animals, and forage nitrate concentrations ≤5,000 ppm NO3 (dry-weight basis) are recommended for pregnant beef cows. However, even forage concentrations of 1,000 ppm NO3 dry-weight basis have been lethal to hungry cows engorging themselves in a single feeding within an hour, so the total dose of nitrate ingested is a deciding factor.

            High-nitrate forages may also be harvested and stored as ensilage rather than dried hay or green chop; this may reduce the nitrate content in forages by up to 50%. Raising cutter heads of machinery during harvesting operations selectively leaves the more hazardous stalk bases in the field.

            Hay appears to be more hazardous than fresh green chop or pasture with similar nitrate content. Heating may assist bacterial conversion of nitrate to nitrite; feeding high-nitrate hay, straw, or fodder that has been damp or wet for several days, or stockpiled, green-chopped forage should be avoided. Large round bales with excess nitrate are especially dangerous if stored uncovered outside; rain or snow can leach and subsequently concentrate most of the total nitrate present into the lower third of these bales.

            Water transported in improperly cleaned liquid fertilizer tanks may be extremely high in nitrate. Young, unweaned livestock, especially neonatal pigs, can be more sensitive to nitrate in water.

            The risk of poisoning can be reduced by:

• having feeds and forages analysed for nitrate when in doubt, such as drought-stressed, small- grain forages;

• not grazing stock on forages that are potentially dangerous;

• observing stock frequently when put on potentially risky feed;

• feeding hungry stock on dry hay or mature grass before allowing free access to immature cereal crops or root-crop tops;

• feeding only well-dried cereal hays;

• preventing hungry stock from gorging recently sprayed weeds;

• preventing hungry stock from gorging highly fertilised crops;

• not overstocking risky pastures / grazing crops – overstocking can result in more stalk material being consumed (the stalk contains the most nitrate in the plant). Avoid strip grazing for the same reason;

• not grazing high-nitrate pastures or crops for 7 days after periods of rainfall, cloudy days, frosts, or high temperatures that cause wilting;

• grazing stock on high-nitrate pastures or crops during sunny afternoons (when the temperature is above 15°C) and removing them at night. This reduces the amount of high-nitrate forage consumed and helps rumen microbes to adapt; preventing access to high-risk weeds around yards/sheds;

• feeding risky material in small amounts diluted with safe feed, preferably high-carbohydrate feed such as grain (if accustomed to grain feeding), and gradually increasing the amount fed – this applies only to ruminants;

• ensuring that water does not contain high levels of nitrates;

• not feeding green chop that has heated after cutting;

• never feeding mouldy hay.

            Another option for reducing the risk of nitrate/nitrite poisoning is to harvest and feed high-nitrate forages as silage. This is because nitrate levels are reduced by the fermentation process when feed is ensiled. Harvest these feed crops at least 7 days after rain or cloudy weather, preferably later in the day.