(Update: July 19, 1995; Web Version August 25, 1999)

UREA POISONING

Urea poisoning is reviewed in detail by Clarke & Clarke (1975), Blood et al (1979) and Bartik & Piskac (1981). Urea (NH₂-CO-NH₂, 46.7% N) is a useful cheap source of non-protein nitrogen for ruminants, in which 100 g urea is equivalent to 220 g digestible crude protein. Fed in 2 or more feeds daily, urea-N can usefully replace up to 16% of total dietary-N for dairy cows (Anon 1977) but much higher levels can be fed safely if other animal- and dietary- factors are optimal.

Sources of urea: Plants usually contain little or no urea. The most common source of poisoning of cattle and sheep is via ingestion of toxic levels in concentrate feed, due to an error in urea addition or due to uneven mixing. A less common source of poisoning is via direct ingestion from liquid preparations of urea, from bags of urea, or of urea granules concentrated on pasture due to spillage or uneven spread of fertiliser.

Urea is also used as a means of ammoniation of hay, straw or whole-crop cereals. Excessive addition of urea or failure to convert to ammonia (NH₃) in the treated feed can lead to urea poisoning in animals.

Toxicity of urea: Rumen microbes convert urea to microbial protein and NH₃. The microbial protein flows past the rumen, for digestion and absorption mainly in the small intestine. The NH₃ is absorbed in the rumen, reticulum and omasum. It is carried in the portal vein to the liver, where it is detoxified to urea, amino-acids, etc. Some NH₃ escapes from the liver into the general circulation.

Oral urea poisoning is basically poisoning due to excessive NH₃ production in the rumen. Normal levels of NH₃-N are 60-680 mg/L in rumen fluid and 0.8-2.5 mg/L in blood. When NH₃ levels in rumen fluid exceed 500-800 mg/L, NH₃ levels increase in the peripheral blood. Thus, after ingestion of urea, levels of NH₃ in rumen fluid and NH₃ and urea in blood increase markedly and rapidly. When NH₃-N levels exceed 6 mg/L in peripheral blood, signs of poisoning may occur in cattle. Clinical signs correlate roughly with blood NH₃-N level: ataxia occurs at levels >20 mg/L and death occurs later at levels >49 mg/L. In sheep, deaths occur at blood NH₃-N levels >32 mg/L. In both species, the pH of rumen fluid (post-mortem) is alkaline (7.1-7.9) and has high NH₃ levels. (The pH is much lower (6.4-7.1) in healthy sheep and cattle).

Tolerable and toxic doses of urea: It is difficult to define a toxic level of dietary urea for ruminants, as their ability to metabolise large amounts of dietary urea safely depends on many factors. These include: adaptation of the ruminal microbes; specific dietary factors and other factors. If the amount of urea entering the rumen is excessive over a short period of time, or if the ruminal environment favours very rapid conversion of urea to NH₃, levels of NH₃ in rumen fluid and NH₃ and urea in blood may reach toxic levels.

Thus, the toxic dose of urea varies. A single oral dose of 330 mg urea/kg live weight (LW) causes increased NH₃ levels in blood of starved naive cattle. Assuming a dietary total dry matter (DM) intake (TDMI) of 3% LW/d, this is equivalent to about 1.1% urea in DM if the TDMI is eaten in a few hours. An oral dose of 200-500 mg/kg LW (about 0.67-1.67% urea in DM, if eaten quickly) can cause signs of poisoning in naive cattle. Single doses of 1000-1500 mg/kg LW are lethal (about 3.3-5.0% urea in DM, if eaten quickly).

Assuming that the diet of dairy cows has a total crude protein content of 16% DM (thus a total N content of 2.56% DM), urea-N can be fed safely up to 0.41% dietary DM, or 0.878% urea in dietary DM. This is equivalent to circa 132 g urea/cow/day in 15 kg dietary DM. Assuming that concentrates supply 41% of the total DMI (i.e. 7 kg concentrate (6.16 kg DM) in 15 kg TDMI) and that the urea is mixed in the concentrates (fed frequently during the day), the concentrates safely could contain up to 1.9% urea. If the urea intake is increased to 280 g/day (equivalent to 4% urea in 7 kg concentrate), milk yield may fall but other signs of toxicity may be absent (Anon 1977). Under optimal conditions, up to 600 mg urea/kg LW can be fed safely to fattening cattle (Anon 1977) but up to 1500 mg/kg LW can be eaten safely on well balanced diets, if eaten over the whole day. Assuming a TDMI by fattening cattle of 2.2% LW, urea levels of 600-1500 mg/kg LW are equivalent to 2.7-6.7% in TDMI. Given as a drench, a dose of 8-10 g urea can kill sheep, especially if they are malnourished or have liver damage.

Adaptation of rumen microbes: If the dietary content of urea is increased gradually, healthy cattle on a good diet can tolerate up to 5% urea in the TDMI.

Healthy sheep on a good diet can tolerate urea up to 6% in feed DM, provided it is well mixed with forage and is fed over the whole day. If, however, unadapted animals ingest a high level over a short period (see below), the result can be acute or subacute poisoning. Tolerance is lost rapidly; animals which receive no urea for 3 days again become susceptible to poisoning.

Specific dietary factors: A single dose of 25-45 g urea may kill sheep within 1 hour of ingestion. The presence of adequate amounts of fermentable carbohydrate in the rumen is essential for safe utilisation of urea. A urea-molasses mixture can be sprayed on roughage. Sheep given a mixture of urea-molasses can tolerate up to 18 g urea/day. A ad libitum intake of up to 10% urea in molasses in ball-lick feeders is safe for sheep or cattle. In other trials, sheep tolerated up to 100 g urea/day (up to 6.7% feed DM) without clinical signs of toxicity (Bartik & Piskac 1981). Feeding of lucerne increases tolerance to urea but fasting for 24 hours, starvation or a low-protein diet reduces tolerance. High-nitrate feeds (see nitrate poisoning, below) increase rumen NH₃ levels and increase the risk of urea toxicity.

Other factors: Soya meal contains urease. Urea mixed with soya meal is rapidly converted to NH₃ and can be dangerous.

Individual susceptibility: Intercurrent disease, malnutrition and liver damage can increase susceptibility to urea poisoning.

Clinical signs: The main signs of urea poisoning are due to the alkaline-corrosive effects of the high NH₃ levels in the digestive tract and other tissues and the neuro-toxic effect on the brain. Signs of poisoning arise within 10-30 minutes of ingestion of toxic doses. There are three main types of poisoning: acute (severe), subacute (moderate) and chronic (mild). Acute (severe) signs include salivation, severe abdominal colic, bloat, forced rapid breathing, muscle tremor, incoordination, bellowing, convulsions, violent struggling, weakness, recumbency, coma and death within 4 h of ingestion. Subacute (moderate) signs include abdominal colic and milder nervous and circulatory signs. Chronic (mild) signs include poor appetite, listlessness and lethargy.

Treatment: Once urea poisoning is suspected, the source should be withdrawn immediately and veterinary help should be sought.

Treatment aims to reduce or neutralise ruminal and blood NH₃ level and to treat the irritation in the digestive tract, liver, kidney and other tissues, caused by the alkaline-corrosive effect of NH₃. The only reliable treatment is to empty the rumen (by prompt rumenotomy or by large-bore stomach tube plus weak-acid lavage). Weak acids act as chemical antidotes to alkaline poisons. The dose is 3-5 l of table vinegar or 2% acetic acid by stomach tube to adult cattle; 0.5-1.0 l to sheep. Repeated doses may be needed, as signs may recur after 30 minutes. Demulcents, sedatives and stimulants may be used to control specific clinical signs. Treatment often fails.

Prevention: Urea should not be given to fasting or malnourished animals, or those with damaged livers. If urea is added to ruminant diets, it should be introduced gradually and increased to a safe level. Concentrate feeds with 3% urea or more in the DM should be regarded as high-urea feeds. Such feeds should be fed in restricted amounts, preferably spread over 12 hours or more of each day. Mixing urea with molasses, fodder/sugar beet or good quality silage reduces the risk of poisoning. Urea mixing in the feed should be thorough.

Fertilisers and feeds containing urea should be stored, used and disposed of properly. Spillage should be cleaned up or dispersed as it arises. Pasture should be rested for an adequate time before grazing or cutting after N-application.

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NITRATE AND NITRITE POISONING

Nitrate and nitrite poisoning are reviewed in detail by Clarke & Clarke (1975), Kemp et al (1978), Blood et al (1979), Bartik & Piskac (1981) and Guerink et al (1982).

Sources of nitrate (NO₃^-) and nitrite (NO₂^-): Exogenous sources of NO₂^- are much less common than those of NO₃^-. Plants usually contain little or no NO₂^-. NO₃^- in green cereal hays (especially oat hay or corn stalks) may be converted to NO₂^- if the hay is hot and wet and exposed to air, but long exposure converts NO₂^- to NH₃, some of which may evaporate. The most common source of NO₂^- for cattle and sheep is via ingestion of high levels of NO₃^- in plants. Reduction of NO₃^- to NO₂^- occurs in the rumen.

The main sources of NO₃^- include (a) NO₃^--accumulating plants; (b) grass (especially ryegrass), grass cubes, silage, cereal crops, hay.

Plant nitrates: NO₃^- absorbed from the soil by plant roots is converted to NH₃-N by the action of plant NO₃^- reductase enzymes. These enzymes are activated by light and are inhibited in darkness and in cloudy or foggy weather. Plants convert most of their NO₃^- to amino acids, via NH₃-N; plant proteins are formed from the amino acids.

Root uptake of excessive amounts of NO₃^-, or inhibition of the NO₃^- reductase system, allows high NO₃^- levels to accumulate in plants. High NO₃^- levels can accumulate in young plants after heavy N-fertilisation; during and after periods of drought; in cloudy or humid weather and after use of some herbicides (2-4-D). Young rapidly-growing plants usually contain higher levels than mature plants. Within the plant, root and stem usually have more NO₃^- than leaves and seeds and older leaves have more than younger leaves (Edwards & McCoy 1980).

NO₃^- accumulation in plants is said to be more likely when plant N exceeds 3% DM (Kemp et al 1978). If so, we should expect high NO₃^- levels in average Irish herbage, as its average N level exceeds 3%. This is uncommon, however.

(a) Nitrate-accumulating plants: Toxic levels of NO₃^- (0.9-12.0% DM) may occur in Brassicas and Cruciferae (cabbage, sprouts, rape, kale; freshly pulled turnips, swedes) and their tops; lettuce; other root crops (fodder- and sugar- beets, mangels, potatoes) and their tops. NO₃^- levels in root DM are usually higher than in the tops (stems and leaves). Dozens of weed species, including docks (Rumex), thistles (Carduus, Silybum), red-root (Amaranthus), capeweed (Arctotheca) and chickweed can concentrate NO₃^-. Beet tops and weeds may accumulate very high NO₃^- levels after use of the herbicide 2-4-D. Occasionally green soya, flax, alfalfa and millet can contain high levels.

(b) Grass (especially ryegrass), grass cubes, silage, cereal crops, hay: High NO₃^- in herbage can follow heavy application of human sewage sludge, animal slurry, commercial N-fertilisers, or combinations of these. At high levels of N-application (>400 kg N/ha/year), 20% of grass samples in Holland had >0.75% NO₃^- in DM. After heavy N-usage, herbage may accumulate up to 6% NO₃^- in the DM, especially in periods of rapid growth following drought. NO₃^- levels of 6.6-12.5% DM were reported in toxic ryegrass-clover herbage (which also contained some capeweed and red-root plants) in Australia. High NO₃^- levels are more likely to arise in new leys than in old permanent pasture.

Confirmed cases of poisoning in animals whose only NO₃^- source was grazed herbage are rare, but have occurred (Nicholls & Miles 1980). When grazed in situ, fresh grass usually is less dangerous than conserved grass (grass cubes, hay, silage or mown grass fed fresh or wilted indoors). Poisoning is more common after ingestion of heavily fertilised, fresh grass indoors (zero-grazing), or of dried hay, grass-cubes or silage harvested too soon after application of high levels of N-fertilisers. This is because DM intake/hour from conserved grass is more rapid than from fresh grass.

Feeding dried grass cubes containing 2.5-3.1% NO₃^- in DM produced clinical signs of poisoning and death in cattle in Northern Ireland within days (Purcell et al 1971). Grass cubes with 0.70 % NO₃^- in the DM produced no clinical signs but other authors suggest that levels >0.7% DM in grass cubes can be toxic.

Ensiling of grass may reduce the NO₃^- level in silage DM by 40-60%: some NO₃^- escapes in the effluent and some is destroyed normal fermentation. The intake of silage DM is usually spread over many hours each day and seldom exceeds 1.5-2.0% LW/day. Thus, most grass silage is safe. However, if levels of NO₃^- are very high in ensiled grass, silage effluent may be toxic and NO₃^- levels in the silage DM occasionally may be >2% DM and may be toxic.

Cereal crops, cereal stalks and green cereal hays (barley, rye, wheat, oats, maize, sorghum, Sudan grass) and grass hay may contain high NO₃^- levels and have been toxic to cattle and sheep. NO₃^- levels up to 10% DM may arise in toxic hay.

NO₃^- levels in plant samples vary widely (up to 10-fold or more) within and between fields. Uneven N-application (concentrating N application in some areas) and plant regrowth in dung-pad and urine-contaminated patches, explain some of the variation. Harvesting of herbage as large bales of hay or silage can lead to toxic NO₃^- levels in individual bales, while others can be safe. Thus, the mean NO₃^- level in a few samples of forage can be misleading. When investigating a suspected outbreak of NO₃^- poisoning from forage, many samples (representing individual bales or parts of the field) should be analysed individually.

In samples of herbage from Irish grazing pastures, NO₃^- levels are usually <0.2% DM. They seldom exceed 0.3% DM, unless very high levels of fertiliser-N (>600 kg N/ha/year) are used. Levels >2% DM are very rare. One sample (Grange 1980) had 2.4% NO₃^- in the DM but no obvious problems occurred in cattle on that field. In Irish grass silage, most NO₃^- levels are also <0.2% DM but a few samples analysed in connection with suspected NO₃^- toxicity had levels in the range 2-4% DM.

Less common sources of NO₃^-/NO₂^- poisoning include:

(c) fertilisers containing ammonium salts, urea, NO₃^- or NO₂^-

(d) Cattle, sheep and pigs may be poisoned by contaminated deep bore well-water; open water-storage tanks; tanks containing run-off water from roofs or gutters containing rotting organic matter or condensation water. Such water may contain 122-10000 mg NO₃^-/l. High NO₃^- levels in swill, brines or preserved whey can be converted to NO₂^- by gentle cooking, as in preparation of swill for pigs.

(e) Monensin, at recommended levels, may precipitate NO₂^- poisoning in cattle fed rations high in NO₃^- (Malone 1978). This may be due to a rapid shift in rumen microbial population, favouring NO₂^--producing bacteria

(f) high NO₃^- levels in certain oils

(g) discarded dynamite (containing ammonium nitrate)

Toxicity of nitrates and nitrites: NO₃^- and NO₂^- are linked closely as causes of poisoning. Weight for weight, NO₂^- are about 5-6 times more toxic than NO₃^- to ruminants. Ruminal microbes can reduce NO₃^- to NO₂^-, an intermediate step in the conversion of NO₃^- to NH₃. Toxicity is less likely if rumen NO₃^- is not reduced to NO₂^-, or if complete reduction to NH₃ is rapid. Sheep are less prone to poisoning than cattle. Restriction of water intake increases the risk of toxicity: the greater the water intake, the faster the elimination of NO₃^-/NO₂^- in urine.

High NO₃^- intake is associated with high levels of NH₃ in rumen fluid and blood. NO₃^- may cause gastroenteritis but their main effect is to act as a source of NO₂^-, which may be formed before or after ingestion of NO₃^-.

When NO₂^- is absorbed from the digestive tract into the blood, it converts the red pigment haemoglobin (Hb) to a dark pigment (met-Hb). Met-Hb can not carry oxygen to the tissues and a syndrome of respiratory distress, due to anaemic anoxia, follows. At a conversion rate of Hb to met-Hb of 20%, the colour of blood may be a light or grey-brown; at 50% it may be brown-black; at 80% it is usually dark brown to black.

At 10-20% conversion to met-Hb, the animals may show no visible signs of poisoning or only mild or chronic signs. Severe signs may occur when met-Hb exceeds 50%. Death due to oxygen-starvation of the brain and other vital tissues can occur when conversion exceeds 80%.

The degree of conversion of Hb to met-Hb is correlated with the level of NO₂^- in blood. As blood NO₂^- increases from 50 to 150 mg/L, met-Hb conversion increases from 24 to 70 %; at 250 mg NO₂^-/l blood, met-Hb conversion is near 100%. Peak met-Hb in blood occurs quickly (1-2 hours) after intake of feed with NO₃^- levels <1% DM but is delayed for up to 4-6 hours as feed NO₃^- increases to near 6% DM (Guerink et al 1982).

High levels of NO₂^- in blood also cause vasodilation, drop in blood pressure and circulatory shock.

Tolerable and toxic doses of nitrite and nitrate: These are difficult to define, as there is wide variation in the amount of met-Hb produced by the same dose of NO₃^-. This variation depends on whether the NO₃^- dose is ingested in a short time (0-4 hours) or over a long time (12-24 hours); on the degree of adaptation of the rumen microbes (the rate at which they reduce NO₃^- to NO₂^- or to NH₃) and other factors. High-energy diets (containing rapidly fermentable carbohydrate) decrease rumen reduction of NO₃^- to NO₂^-. Cattle on a high-energy diet may be able to tolerate up to 50% conversion of Hb to met-Hb with no ill effect.

Intercurrent disease, poor liver function, cold stress (by increasing the energy requirement), fasting or a low-energy diet, etc increases susceptibility to NO₃^- and NO₂^- poisoning, so that at 20-50% conversion of Hb to met-Hb, signs of respiratory and circulatory stress may arise.

The minimum lethal dose of NO₂^- (in one dose) for cattle and sheep was 67-110 mg/kg LW (Bartik & Piskac 1981). This translates to 40-66 g NO₂^- in a single dose for a 600 kg cow.

If the NO₃^- is eaten in small amounts over a 12-24 hour period, healthy animals adapted to NO₃^- and on a high-energy diet can ingest large quantities with minimal or no adverse effects. Similar or smaller daily doses, if eaten in a short period, can kill.

Sheep tolerated 224 mg NO₃^-/kg LW over 24 hours but that amount was lethal as a single dose (Sinclair & Jones 1967). A single dose of 345 mg NO₃^-/kg LW was lethal in sheep and chronic dosing of 260 mg NO₃^-/kg LW, given in the feed daily, had no immediate effect on sheep but deaths occurred 2-3 months later (Setchell & Williams 1968). Bartik & Piskac (1981) quote lethal doses of NO₃^- for sheep as 271-547 mg/kg LW. These data suggest a toxic dose for sheep in the range 224-547 mg NO₃^-/kg LW. Assuming a feed DM intake of 2.5% LW, feed NO₃^- in the range 0.9-2.2% DM (or more) could be toxic for sheep if eaten rapidly. However, up to 0.9% NO₃^- in feed DM was safe for sheep if eaten slowly but above 1.2% caused death in 6-10 weeks, with little signs of met-Hb in blood.

Bartik & Piskac (1981) quote lethal doses of NO₃^- for cattle as 122-547 mg/kg LW. As a single dose, the minimum lethal dose (MLD) of NO₃^- for cattle was 370-550 mg/kg LW. This translates to a single dose of 222-330 g NO₃^- for a cow of 600 kg. If eaten over 4 hours, 320 mg NO₃^-/kg LW may poison calves but more than 3 times that amount may be tolerated if fed over 24 hours. NO₃^- at 610-900 mg/kg LW was lethal in cattle, sheep and also. These data suggest that 122-900 mg NO₃^-/kg LW may be lethal for cattle. Assuming a TDMI of 3% LW/d, these doses would equate with 0.4-3.0% NO₃^- (or more) in feed DM. If the daily allowance of these feeds is eaten rapidly (especially in 1-2 feeds per day), or is eaten more slowly by stock unused to high-NO₃^- feeds, acute poisoning of cattle, sheep and horses could occur on feeds with >1.5% NO₃^- in DM and subacute or chronic poisoning could occur on feeds with 0.5-1.5% NO₃^- in DM.

Kemp et al (1978) and Guerink et al (1982) found that 0.75-1.0% NO₃^- in DM of hay or wilted silage (eaten over the whole day) could be tolerated by cows; freshly-cut grass with up to 1.5% NO₃^- in DM could be fed safely indoors and grass with up to 2% NO₃^- in the DM could be grazed safely outdoors. However, care must be taken in interpreting guidelines for safe and toxic levels. For example, in 803 forages analysed during outbreaks of death in cattle from suspected NO₃^- poisoning in Oklahoma, 59% of samples were >0.6% DM and 80% <1.4% DM; the mean NO₃^- level was 1.37% DM (Edwards & McCoy 1980). Assuming a TDMI of 3% LW/d, this corresponds to a mean NO₃^- dose of 411 mg NO₃^-/kg LW, or 247 g NO₃^- /d for cows of 600 kg LW.

In contrast to these data on toxic doses, a recent article on the Internet (Kvasnicka & Krysl 1998, at http://www.forages.css.orst.edu/Topics/Pastures/Species/Grasses/Animal_issues/NO3.html) suggests that feeds with 0.56-0.94% NO₃^- in DM should be restricted to <25% of the total ration for cattle and that water with >220 mg NO₃^- /l should be avoided and that water levels >656 mg NO₃^- /l should be regarded as lethal.

Clinical signs: While the main signs are due to met-Hb conversion and tissue anoxia caused by NO₂^-, other signs are due to the direct caustic irritant effects of NO₃^- in the digestive tract and arterial hypotension and peripheral circulatory failure due to NO₂^-.

Signs of poisoning occur very rapidly (within 0.5-5 hours) after ingestion of pre-formed NO₂^-. While death in NO₃^- poisoning often occurs within 12-24 hours of exposure, it may occur within 0.5-4 hours of exposure in peracute cases. Signs may be delayed for a few days after access to high-NO₃^- feed, as rumen microbes need this time to adapt in favour of the NO₂^--producers.

There are five types of poisoning: peracute (lethal), acute (severe), subacute (moderate), chronic (mild) and sub-clinical.

In peracute poisoning, animals are found dead, without warning. Acute (severe) signs, usually with met-Hb conversion to 80-90% include cyanosis (with mucous membranes brown to black), severe respiratory distress with rapid respiration and rapid weak pulse, weakness, recumbency, coma and death. Some cases may be blind. Acute cardiac and circulatory failure without other signs can occur also. Subacute (moderate) signs, due to the irritant effects of NO₃^-, include salivation, lacrimation, grinding of the teeth, vomiting, abdominal colic and diarrhoea. Weakness, ataxia, muscle tremor, convulsions, rapid heart rate and breathing difficulty occur also. Chronic (mild) signs include listlessness, lethargy, depressed feed intake, growth rate, fertility and milk yield. Some authors claim that prolonged ingestion of sub-lethal doses of NO₃^-/NO₂^- has no obvious effect on productivity. Sub-clinical poisoning may show no obvious signs except brownish mucosae, due 10-20% conversion of Hb to met-Hb.

Abortion/stillbirth: Many authors found that pregnant cows aborted between 2-21 days after the onset of NO₃^- poisoning in the herd. Some cows which aborted did not show any other signs of poisoning. Haliburton & Edwards (1978) reported an abortion rate of 12.6% (range 6-71%) in cows exposed to high-NO₃^- forages (mean 0.8% NO₃^- in forage DM). Nicholls & Miles (1980) reported an abortion rate of 15-25% of cows which had survived an outbreak of NO₃^- poisoning about 1 week earlier. Clinical signs of NO₃^- poisoning in pregnant heifers and cows were not associated with abortion in other studies. Prolonged calving, stillbirth and birth of weak (soft) calves can also occur in cattle with acute, sub-acute or chronic NO₃^- poisoning.

Treatment: Once NO₃^-/NO₂^- poisoning is suspected, the source should be withdrawn and veterinary help should be sought immediately. Methylene blue (5-20 mg/kg LW intravenously, as a 1-4% aqueous solution in saline or in 5% glucose or 1.8% sodium sulphate solution in ruminants or 1-2 mg/kg LW as a 1% solution in horses and pigs) reduces met-Hb to oxy-Hb within 1 hour. Daily oral doses of tungsten (as sodium tungstate) can prevent reduction of NO₃^- to NO₂^- in the rumen but more research is needed on safe dose rates. Vasoconstrictors (adrenalin) and cardiac/respiratory stimulants (etamiphylline camsylate) can save lives in acute cases (Cawley et al 1977; Malone 1978). Treatment may need to be repeated in severe cases.

Prevention: Ruminant diets should contain low levels of NO₃^- and NO₂^-, preferably below 0.6% NO₃^- or 0.12% NO₂^- in DM. With the exception of grazed herbage (in which up to 2% may be tolerated), feeds with >1.5% NO₃^- (>0.34% NO₂^-) are unsafe for ad libitum feeding. All feeds with >0.7% NO₃^- (>0.14% NO₂^-) in DM (for instance Brassicas or beet tops) should be regarded as high-NO₃^- feeds. They should be fed in restricted amounts (a little and often), preferably spread over 12 hours or more of each day. High-NO₃^- feeds can be diluted with low-NO₃^- feeds to reduce the NO₃^- intake and spread it over a long period of each day. Maize yields respond to very heavy applications of slurry. There have been no problems of NO₃^- poisoning from maize, which is normally fed as silage (Jones 1981).

Ruminants likely to be exposed to NO₃^- should get adequate carbohydrate in the diet. Travelling or hungry animals should not be allowed access to dangerous plants.

Water (from rain-water storage tanks, wells or condensation in animal houses) or whey fed to animals should contain low levels of NO₃^- or NO₂^-. Poisonous water can be made safe by prolonged boiling.

Monensin should not be fed with diets high in NO₃^-.

Fertilisers and chemicals containing NO₃^- or NO₂^- should be stored, used and disposed of properly. Spillage should be cleaned up or dispersed as it arises. Pasture should be rested for an adequate time before grazing or cutting after N-application. To minimise plant NO₃^- levels, forage should be cut for conservation on dry, bright days, if possible. If sewage sludge or animal slurries are applied at high levels, use of inorganic N fertilisers should be reduced or eliminated accordingly.

Prevention using mucous membrane colour as an early-warning sign: Twice daily inspection of the mucosae (for instance in dairy cows at milking time) can be used as an early-warning of NO₃^-/NO₂^- toxicity. The mucous membranes of healthy ruminants are salmon-pink. They are inspected easily by everting the conjunctiva or parting the lips of the vagina. Changes in blood colour from light brown to black (corresponding to 20-80% conversion of Hb to met-Hb) are seen easily by inspection of the mucous membranes in cattle. At 20% conversion, the mucosae are a light or grey-brown colour. At this point, signs of poisoning are usually mild or absent.

Removal or reduction of the NO₃^-/NO₂^- source and/or treatment of animals with brownish mucosae can prevent further development of poisoning (Guerink et al 1982).

REFERENCES

• Anon (1977) Protein and non-protein nitrogen for ruminants. Proceedings Meeting of the Agricultural Commission of the U.N. (Geneva, Jan 10-13). Pergamon Press. 182 pp.
• Anon (1978) Nitrate poisoning. Veterinary Record, 102, 183 and 103, 386.
• Bartik M. & Piskac A (1981) Veterinary Toxicology. Elsevier, Amsterdam. 346 pp.
• Blood DC, Henderson JA, Radostits OM, Arundel JH & Gay CC (1979) Veterinary Medicine: a textbook of the diseases of cattle, sheep, pigs and horses. 5th Edition. Balliere Tindall, London. 1135 pp.
• Cawley GD, Collings DF & Dyson DA (1977) Nitrate poisoning. Veterinary Record, 101, 305-306.
• Clarke EGC & Clarke ML (1975) Veterinary Toxicology. Balliere Tindall, London. 438 pp.
• Edwards WC & McCoy CP (1980) Nitrate poisoning in Oklahoma cattle. Veterinary Medicine / Small Animal Clinician (March), 457-458.
• Guerink JH, Malestein A, Kemp A, Korzeniowski A & van't Klooster ATh (1982) Nitrate poisoning in cattle. 7. Prevention. Netherlands Journal of Agricultural Science 301, 195-113.
• Haliburton JC & Edwards WC (1978) Nitrate poisoning in Oklahoma cattle during the winter of 1977-1978. Veterinary & Human Toxicology 20, 401-403.
• Jones TO (1981) Nitrate poisoning in ruminants from forage crops in the East Midlands of England and in the Netherlands. Proceedings of the British Cattle Veterinary Association (1980-81), produced by Beecham Animal Health, 159-166.
• Kemp A, Guerink JH, Malestein A. & van't Klooster ATh (1978) Grassland Production and nitrate poisoning in cattle. Proceedings of 7th General Meeting European Grassland Federation, Gent. 9.1-9.15.
• Malone P (1978) Monensin sodium toxicity in cattle. Veterinary Record, 103, 477-478.
• Nicholls TJ & Miles EJ (1980) Nitrate/nitrite poisoning of cattle on ryegrass pasture. Australian Veterinary Journal 56, 95-96.
• Purcell DA, Raven AM & Thompson RH (1971) High nitrogen grass cubes as a source of nitrate poisoning in cattle. Research in Veterinary Science 12, 598-600.
• Setchell BP & Williams AJ (1968) Plasma nitrate and nitrite in chronic and acute nitrate poisoning in sheep. Australian Veterinary Journal 38, 58-62.
• Sinclair KB & Jones DIH (1967) Nitrate toxicity in sheep. Research in Veterinary Science 8, 65-70.