Teagasc Farm Nutrient Profile:
 Reference Information for Professionals

Phil Rogers⁽¹⁾, Tom Gately [deceased]⁽²⁾ & Tom Keating⁽³⁾,

(Re-edited for the WWW by Phil Rogers, Nov 22, 2000)

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Role of Nutrients & Minerals
Elements Essential for Plants & Animals / Support Information for Soil Test Results
Support Information for Forage Test Results / General Comments

Elements essential for plants and animals: Certain elements or minerals, sometimes called nutrients, are essential for optimal growth of plants and for health and optimal productivity in animals. There are two classes of essential elements: major elements and trace elements.

Major elements (macro-nutrients) are present in large amounts in the plant. Their levels are expressed as g/100 g plant DM (% plant DM). They include calcium (Ca), chlorine (Cl), magnesium (Mg), nitrogen (N), phosphorus (P), potassium (K), sodium (Na) and sulphur (S).

Trace elements (micro-nutrients) are present in plants in tiny amounts. Their levels are expressed as mg/kg DM (parts per million in plant DM). They include cobalt (Co), copper (Cu), iodine (I), iron (Fe), manganese (Mn), selenium (Se) and zinc (Zn). Plants also contain boron (B) and molybdenum (Mo). High levels of Mo in herbage are undesirable, as Mo reduces Cu absorption by cattle and sheep.

Essential elements and plant growth: Table 1 shows the elements needed for herbage and cereal/root-crop growth. If these elements are deficient in soil, or if other elements or soil conditions block their uptake by the plant root, the levels in the plant may be deficient. Deficiency of major elements can limit sward dry-matter (DM) production. Deficiencies of trace elements rarely if ever limit growth of herbage in Irish farms but they may limit growth of cereal and root crops.

Essential elements and animal health: Table 1 shows the elements needed for optimal health and productivity in ruminants (growth, fertility and viability of the young, lactation etc). If these elements are deficient in the feed, or if other elements block their absorption from the digestive tract or interfere with their uptake or utilisation by animal tissues, the levels in animal blood or tissue may be deficient.

Clinical and subclinical nutrient imbalance in animals: Severe imbalance of essential elements in animals can cause clinical or sub-clinical disorders that can limit animal production.

Non-clinical imbalance: Mineral imbalance, even when severe, can exist in non-clinical form (health and productivity are normal). Therefore, irrespective of the results of soil, feed or blood tests, performance may improve very little after trace element supplements if the herd was fully healthy (no clinical or subclinical problems) before the tests were done. However, the immunity of the herd may improve and the herd is likely to suffer less severely than would be the case if stress or changes in management and feeding are imposed later.

Fe deficiency does not occur in ruminants on green feeds or root crops, or in those with access to soil. Soil is usually high in Fe. High intake of soil or Fe may cause Cu deficiency in ruminants. Mineral mixes to ruminants should have zero or low Fe in that case.

Zn deficiency is rare in ruminants but may occur if high Ca intake blocks Zn absorption in the digestive tract. Mn deficiency is very rare in ruminants.

Soil analysis measures the level of nutrients available in soil. Feed analysis measures the levels of nutrients in the feed (herbage, silage, other fodder, meals etc). Herbage analysis is better than soil analysis for some nutrients (such as N, S) and most trace elements, except Co and I.

If sampling is well done, soil and herbage analyses can help in the assessment of the mineral status of a farm. If low levels of specific minerals, or high levels of antagonists to those specific minerals are found, this suggests that the mineral nutrition of livestock grazing that farm may be deficient in those minerals.

There can be large seasonal changes in the levels of nutrients in herbage and, to a lesser extent, in soil. For example, Mo can be low in spring herbage and high in autumn in the same field. Mg can be lower and P higher in spring grass than in summer grass. Thus, for critical assessment of the mineral status of herbage on a farm, it may be necessary to sample on 2 or 3 times (spring, summer and autumn).

Soil and feed tests need careful interpretation as mineral deficiency on blood test often occurs on farms where soil or feed tests show little or no abnormality. Many mineral deficiencies in ruminants are induced by known and unknown factors which antagonise the absorption or utilisation of specific minerals in the digestive tract or tissues. For instance, severe Cu deficiency on blood test often occurs on farms in which herbage/silage Cu and Mo are quite normal but where other factors, such as high intake of soil or high intake of sulphate from deep-bore water antagonise Cu metabolism. I deficiency in blood can occur on diets with normal I levels if goitrogenic feeds are used. High Ca levels in the diet, by reducing Zn absorption by the animals, can cause secondary Zn deficiency in blood, even if the feed has normal Zn levels. Mg deficiency in blood can occur on feed with "normal" Mg levels if Mg antagonists (lush grass, high K, high fatty acids etc) are present.

Therefore, one does not rule out the possibility of mineral deficiency in ruminants on the basis of normal levels of the mineral in soil or feed. In general, if there is a problem with animal health or productivity, blood analysis (from the problem group and at the onset of the problem) is more reliable than feed or soil analysis in assessing the mineral status of animals.

If the clinical history, or soil or feed tests suggest mineral deficiency in stock, blood tests can be used to confirm this and as a guide to the selection of the best methods of control. Where mineral deficiencies cause serious ill-health in the herd or flock, the average level in the blood of unsupplemented animals is usually very low. Marginal or moderately low values in unsupplemented animals are seldom of clinical significance.

In herds with unsolved clinical or subclinical disorders, possible mineral deficiency should be confirmed by blood analysis before supplementation strategies are designed and before money is spent on mineral supplements which may not be the best ones to solve the problem.

• Blood samples from 10 animals in the problem group are best to assess the role of mineral imbalances in an ongoing clinical or subclinical problem, such as infertility.
• Blood samples from 10 unsupplemented weanlings in autumn or from cows in late pregnancy are best to assess the underlying trace-element status of the herd.
• Blood samples from 10 unsupplemented cows in late pregnancy are best to assess the trace-element status near calving in problems of retained placenta, stillbirth, weak calves or death of young calves.

The correct blood sampling kits are available to your vet.

As many mineral deficiencies on blood test cause no health problems or loss of productivity (i.e. are non-clinical) one can expect that some problem herds may show marginal or low levels of trace elements that are coincidental rather than causal. Correction of such deficiencies does not cure the initial production problem if the cause is something else. For instance, if Leptospirosis or Salmonellosis is the primary cause of calf losses (abortion, stillbirth, weak-calves), a marginal to low Cu, Se or I status may have little relevance to the problem. Or if the primary cause of herd infertility is poor detection of heat or poor quality silage, mineral supplements will not correct the problem, irrespective of blood (or feed, or soil) test results.

Tables 2 and 3 summarise the tests available in Teagasc and indicate their relative importance in the investigation of nutrient imbalances.

The general fertility of soils can be assessed when the soil pH (or Lime Requirement (LR)) and the P and K contents are known. The pH gives an indication of the need for lime while the P and K values indicate the need for these elements to enable the soil to realise its full potential. The suitability of soils for different crops is a function of many variables and good husbandry demands that physical, chemical and biological properties of the soils be taken into consideration.

The range of pH, P and K that would be suitable for grazing conditions are as follows:

More N, P and K are required for silage making than for grazing, as silage does not recycle the minerals removed, whereas grazing animals return a lot of nutrients to the soil via dung and urine. If needed, extra N, P and K are supplied by means of fertiliser. Depending on the over-wintering system for cattle, this may be supplemented with slurry or farmyard manure.

Thus soil analysis tells if large dressings or else maintenance levels of lime, phosphate (P) or potash (K) are necessary for the herbage or crops to be grown in the fields from which the samples were taken. In some cases, no dressing may be needed for 1-2 years. Thus, if farms are soil-sampled every 3 years or so the results can help farmers to save money on unnecessary use of fertiliser.

Soil pH is a measure of soil acidity/alkalinity. The main influence of soil pH is on the availability of nutrients for uptake by plant roots. Low pH favours the less productive grasses. Soil pH values are not usually measured as such but are expressed as Lime Requirement (LR). LR is the amount of lime in tons per acre required to raise the soil pH to 6.8. It is not a firm recommendation but should be interpreted for the particular soil and the particular crop.

LR is a better measure than soil pH as to how much lime to use because it takes the texture of the soil into account. Since Mo availability increases with increasing pH, and as high Mo induces Cu deficiency in cattle and sheep, the pH on high-Mo containing soils should not be raised >6.2 unless the farmer is prepared to supplement the stock with adequate Cu supplements. In the case of soils with a pH of 6.8 or more (no lime requirement (LR = 0) or excess lime (LR = XS)), the possibility of Mo-induced Cu deficiency in young cattle should be considered. On soils with a pH >6.8, pastures would need to be monitored for Mo content.

Soil phosphorus (P) levels have been built up in Irish fields over the past forty years. Today, fertiliser applications are applied more often to maintain soil reserves rather than to give big yield increases. However, there are still many grass fields where the soil test levels are low.

The following guidelines are used to interpret soil P levels for grassland and silage areas:

High soil phosphate levels can interfere with uptake and utilisation of zinc, inducing a deficiency in plants. Use regular soil tests to monitor P levels, as there are very big variations in the rate of depletion of soil reserves. Too much phosphate in soil leads to excessive runoff into surface water, with consequent eutrophication (algal blooms, 'greening') of water in rivers and lakes.

Serious potassium (K) deficiency for plant growth is now likely to arise only on K- fixing soils which occur mainly in parts of Kildare, Meath, Dublin, Carlow and Offaly. Deficiencies are also possible in fields where silage or hay is removed and on very light soils. On K-fixing soils and very sandy soils, fertiliser K should be applied in the spring for grazing and before each cut for silage. Care should be taken not to apply excess fertiliser K for grazing in the spring as it may reduce Mg uptake, resulting in grass tetany in lactating cows and ewes. Application of K in autumn is preferable to application in spring: it reduces the risk of grass tetany.

The following guidelines are used to interpret soil K levels:

Frequent soil testing is necessary to monitor soil K levels, especially in fields under silage, or on light or K-fixing soils.

The use of magnesium (Mg) for herbage growth usually is necessary only on sandy soils. Soil Mg levels <25 mg/kg are very low for herbage growth and <50 mg/kg are low for herbage growth.

If there is a local source of magnesian limestone which contains at least 9% Mg, it may be used to raise the soil Mg level whenever the soil is being limed. Where no lime is required, magnesian compounds may be applied at a rate of at least 75 kg Mg/ha (60 units Mg/ac) as calcined magnesite or kieserite.

A good level of Mg in light sandy soils may raise herbage Mg levels slightly. This may help to lower the risk of grass tetany in lactating cows and ewes. However, hypomagnesaemia and tetany can occur on soils and herbage of normal Mg status. Application of Mg to soil usually is not effective in preventing grass tetany, as it is very difficult to raise herbage Mg levels sufficiently to overcome the Mg antagonists present in tetany-prone pasture. Oral Mg supplements at the correct level are the most reliable way of preventing tetany.

Soil tests for sulphur (S) are unreliable in assessing S requirements for pasture growth, as temperature and rainfall influence the availability of S to plants. It is better to rely on herbage analysis. Where soil or plant S is low, as is the case on about one third of our soils (especially light soil being used for silage) S should be applied in the spring and for each silage cut and at least once (in April) for grazing.

Cobalt (Co) is not required by herbage but is essential for nitrogen fixation in clover and legumes. Also Co is not required by cattle or sheep themselves, but is essential for rumen microorganisms. These are essential for efficient digestion of carbohydrate, as they digest cellulose and manufacture proprionic acid, which the ruminant uses in its energy metabolism. Rumen microbes also synthesise B vitamins (especially B1 and B12).

Disturbed rumen function can cause deficiency of B vitamins. Metabolism of carbohydrate can be disturbed and appetite can be depressed. Growth, lactation, wool production and reproduction can be impaired. Thus, Co deficiency may cause illthrift, pining, weakness, scour and emaciation in lambs and calves and, sometimes in adults. It also weakens the resistance of sheep to parasites. Reduced rumen function and feed intake predispose to depraved appetite and fat mobilisation to the blood and liver, ketosis and circling disease (cerebrocortical necrosis) and infertility (anoestrus and/or repeat breeders). However, Co deficiency rarely, if ever, has been confirmed as a cause of bovine infertility in Ireland.

Soil cobalt and manganese levels: Soil Co levels usually are low in granite, sandstone, limestone soils, calcareous coastal soils and peats. Soil Co tests are better that feed Co tests because soil Co level can be 50-100 times higher than plant levels and 1 gram soil contamination on 500 grams of herbage could double the level of Co found on plant analysis. Soil tests for Co are of little value unless accompanied by parallel analyses for total manganese (Mn). Regardless of soil Co level, a high (>500 mg/kg) total Mn level in soil can restrict plant uptake of Co and result in low Co levels in herbage. To assess the Co status of a forage-fed herd, soil tests for Co and Mn are more valuable than plasma vitamin B12, or forage Co, tests. Guidelines to assess the Co status of a forage-fed herd are:

*Even if soil Co is normal or high, a soil total Mn >500 mg/kg may restrict plant uptake of Co. If soil Mn is >700 mg/kg, low or very low Co levels are likely in herbage.

Ignore plasma vitamin B12 and forage Co levels in assessing Co status of ruminants? Artefacts in the assay of vitamin B12 in may return abnormally low values in ruminants. Those values bear no relationship to the real Co or B12 status; thus the B12 test in ruminants is largely worthless. Herbage should not be submitted for Co analysis unless guaranteed free of soil contamination, for instance samples of regrowth, grown under special cages. Silage usually has some soil contamination. In plant samples free of soil, plant Co levels <0.10 and 0.07 mg/kg DM are deficient for cattle and sheep respectively.

Copper (Cu) is essential for herbage growth and also is required by ruminants. Soil levels of 3-10 mg/kg are normal.

Induced Cu deficiency in animals is more common and more important than simple Cu deficiency. Dietary factors that antagonise animal Cu status include molybdenum (Mo), iron (Fe), sulphur (S), zinc (Zn) and others, such as factors in lush grass. Soil is high in Fe, and cattle and sheep ingest a lot of soil (and Fe) when grazing bare pastures, or when fed on soil-contaminated silage, or whole-crop fodderbeet silage.

Simple Cu deficiency in forage and unsupplemented animals eating that forage: Simple deficiency in pasture occurs mainly on peaty soils or on reclaimed hills and on coarse textured soils, sandstones and granites. This usually occurs when Cu levels are <6 mg/kg dry matter (DM) but can sometimes happen at levels <10 mg/kg DM) Animal problems due to simple Cu deficiency (Cu low in soil and herbage and no Cu antagonists present in the feed) are quite rare. They seldom are as severe as Cu deficiency induced by Cu antagonists in the feed.

Soil tests for Cu are of little value to assess the Cu status of forage or animals, as soil Cu levels correlate poorly with those in plant or animal tissue. Plant Cu uptake is variable and Cu antagonists in the diet can markedly depress Cu absorption and metabolism by animals, even if the feed has normal Cu status. Marginal or normal Cu levels in soil may be associated with low levels of Cu in plants and animals. However, blood and feed tests are more reliable to assess Cu status of animals and feed.

Herbage grown on soils containing high Mo may induce Cu deficiency in animals even when the soil and herbage Cu levels are relatively high. In high-Mo areas, increased intake of herbage Mo increases the risk of Mo-induced Cu deficiency. Increased soil moisture (after rain, or on low-lying or poorly drained land), liming and a high clover content of pasture increase herbage Mo levels and intake. For safety of animal Cu status, herbage Mo levels should be <2 mg/kg DM, herbage Cu should be >10 mg/kg DM, and the Cu/Mo ratio should be >4/1.

Soil tests for Mo are of little value to assess plant Mo, or animal Cu, status, as plant Mo levels relate more to soil pH and soil moisture than to soil Mo level. Blood and feed tests are more reliable to assess the Cu and Mo status of animals and forage. However, soil tests for Mo and lime requirement (or pH) may help to assess the Mo risk and are a guide as to whether the full LR should be applied.

Se deficiency: Se is not needed by plants but is needed by animals. To fulfil EU Animal Feed Legislation, optimal feed levels for ruminants are 0.22-0.57 mg/kg DM. Soil Se tests are of little value in diagnosing Se deficiency in animals. Blood and feed tests give a better assessment of animal Se status. However, soil Se levels help in the investigation of Se toxicity.

Se toxicity: In Se-toxic Irish fields, soil Se averages 21 mg/kg (range 3.2-132.0 mg/kg, with occasional values >132 mg/kg; 50% of values are >9 mg/kg and 90% >5 mg/kg. Herbage levels in endemic Se toxicity in animals are >3.0 mg/kg DM in 90% of cases and >6 mg/kg in 50% of cases.

Iodine

Iodine (I) is not needed by plants but is needed by animals to form thyroid hormones which help control metabolic rate, calf / lamb viability, growth, milk yield and fertility. Soil tests for I are more useful than feed I tests (see below).

Low I levels in herbage are likely if soil I levels are <5 mg/kg. However, I deficiency in animals can occur on soils with normal I status if I uptake by plants is reduced, or if the diet contains goitrogens. (See section on forage I). Note that the plasma inorganic iodine (PII) test is the most sensitive test to assess the I status of animals.

Guide values to assess soil I levels in relation to plant levels are:

* Regardless of soil I levels, plant I levels usually are severely deficient for lactating ruminants in Ireland. Routine provision of generous I supplement is advisable before parturition and before and during the breeding season.

Factors such as soil type and rainfall can predispose to simple I deficiency by increasing the rate at which I is leached from the soil. The counties in which human goitre was endemic in the early part of this century included Tipperary, Carlow, Kilkenny, Meath, Cavan and Sligo. Use of iodised household salt has eliminated simple I deficiency in humans in the last 50 years but a high proportion of animals receive no I supplement.

Soil I levels in coastal areas are replenished constantly by sea-spray on the prevailing on-shore winds. However, low levels of I in soils, plants and/or animals have been found within 3 miles of the coast.

Protein requirements of ruminants are met by absorption of amino acids from the small intestine. The amount of these amino acids depends on (a) the degree to which dietary protein and non-protein N is degraded and converted to microbial protein in the rumen and (b) the amount of dietary amino acids which escapes unchanged through the rumen to be absorbed in the small intestine. The quality of dietary protein is not very critical, as rumen bacteria convert non-protein N to true protein that is used by the animal. Microbial protein synthesis requires energy. Thus, the value of a protein source depends on the amount of energy available for microbial growth.

High yielding dairy cows need more amino acids than rumen microbes can supply, even at high rates of synthesis. Thus, the diets of high yielders should be balanced to include proteins of low rumen degradability. Such proteins escape breakdown in the rumen and reach the small intestine intact.

Feed N level can be converted to crude protein (CP) by the equation CP = N X 6.25. N levels in pasture range from 1.0-5.7% DM (CP 6.3-35.6% DM). High levels of CP, soluble carbohydrate and a low content of fibre in young spring grass means that the feeding value of such herbage is never limited by its protein content. At the other extreme, with advancing maturity, herbage (especially that saved as hay) may be inadequate to maintain the animal in a positive N balance through the combined effects of inadequate intake of energy and of digestible protein.

Cattle can utilise up to 33% of the total N in the ration as non-protein N such as urea or ammonia. Lactating cows need a dietary CP level of 14-16% DM but lower levels (11-12% DM) are adequate for dry cows and heifers.

Excess protein and non-protein N in the diet can be harmful: if cows before calving are fed a gross excess of protein (>19% DM), as occurs when feed N exceeds 3% DM, their subsequent fertility may be reduced. Early in the grazing season, much of the N in lush grass is present as non-protein N. This may also depress conception rates by 15-25 percentage points over a 3-6 week period, after which, conception rates may recover spontaneously. Excess N is degraded to ammonia and is eliminated from the body and is therefore wasteful.

The desirable level of herbage potassium (K) for pasture production is 2.5% DM. Lower levels suggest poor soil fertility and/or poor pasture quality. The requirements of feed K for growth and milk production are controversial but minimum levels of 0.5 to 1.0% DM are recommended for lactating cows. Feed K levels >3.0% DM may predispose to grass tetany by inhibiting Mg uptake by herbage. Lush grass, by decreasing transit time of feed in the digestive tract and by causing digestive upset/grass scours, may reduce the absorption of many minerals, including Mg and Cu.

In Ireland, sulphur (S) deficiency in grassland occurs mainly on light textured soils with a high sand and ash / low organic matter content. S levels <0.20% DM can adversely affect production and quality of grass. Herbage N/S ratios >15/1 may be associated with reduced herbage production. S levels <0.16% DM may reduce protein digestion by ruminants.

High S levels in feed reduce the absorption and utilisation of Cu in sheep. Thus, feed S levels >0.30% DM are regarded as suspect with regard to Cu deficiency in sheep.

High S levels in grass silage may indicate use of silage additives with sulphuric acid. Such additives can reduce Cu status in cattle if they do not contain added Cu. Additives with adequate amounts of added Cu have not this effect: they have the same effect on Cu status of cattle as those with formic acid or molasses or no additive. Apart from sulphuric acid, other forms of S (use of S fertilisers or S fed direct to animals) has little or no effect on the Cu and Se status of cattle in Irish trials but very high levels of S may reduce the Se status of cattle.

Each litre of milk removes 1.1-1.4 g of calcium (Ca) and high yielding cows have a requirement for dietary Ca of 0.45-0.65% total feed DM. Deficiency of feed Ca (feed Ca <0.45% DM) is very rare in cattle on green feeds. Most plants are efficient at taking up Ca into their leaves and stems.

Ca supply may be low in stock on low-Ca feeds, such as straw, fodder beet and roots without supplementary mineral feeding. In such cases, signs of protein or energy deficiency may appear, rather that signs of hypocalcaemia, as animals have a very efficient hormonal mechanism to maintain blood Ca levels irrespective of dietary intake.

Hypocalcaemia and Milk Fever: Low blood Ca level (hypocalcaemia) in the period 1 day before to 1 day after calving (parturient hypocalcaemia) can predispose to milk fever in cows calving for the third time or more. Blood Ca remains remarkably stable in cows, except within 1 day of calving and in periods of severe stress (anorexia or starvation, marked loss of body heat, as in subzero temperatures, or cold, wet, windy weather etc). There is little value in blood tests for Ca outside of these times: values are likely to be normal. Stress stimulates release of adrenalin and cortisone and burns up body fat. This mobilises fat into the blood and liver (fatty liver syndrome) and creates Ca and Mg soaps in blood. Hypocalcaemia may occur under stress (fasting, transport, harsh weather) but the period of greatest risk is at calving and for 36 hours after that, when cows may get milk fever.

Factors that predispose to hypocalcaemia: In the month before calving, major predisposing factors to a high incidence of parturient hypocalcaemia are:

• high Ca intake (root tops, high-Ca mixes);
• low Mg intake (silage Mg 0.15-0.19% DM);
• deficient or excessive energy intake (leading to thin-cow syndrome or fat cow/fatty liver syndrome);
• stress, especially subzero temperatures.

Other predisposing factors are gut stasis or anorexia on the day of calving; increasing age and genetics (some breeds and lines are more susceptible). Factors which may cause hypocalcaemia at other times include low feed intake, anorexia, low Ca availability, intestinal stasis, gross excess of dietary P or Mg, reduction of Ca release from bone, fat mobilisation (fatty acids in blood forming Ca soaps), acidosis and oxalic acid poisoning.

Average Ca levels in most Irish herbage and grass silages are 0.50-1.40% DM. Thus, feed Ca levels usually exceed the recommended pre-calving Ca intake for dairy cows. The result is a high incidence of milk fever in autumn-calving cows that have spent the dry period at grass. Although Ca levels in grass silage may exceed the recommended pre-calving level for dairy cows, the incidence of milk fever decreases once cows are housed and put on a silage based diet, as intake of silage DM (and Ca) is less than that of grass DM (and Ca).

Hypocalcaemia, even in the absence of milk fever, can weaken the contractions of the uterus at parturition. This may prolong calving and may cause dystocia, stillbirth, weak calves and retained placenta and metritis. Thus, hypocalcaemia, with or without Mg deficiency can influence fertility indirectly via its effect on the uterus and consequent metritis.

Each litre of milk removes 0.9-1.24 g of phosphorus (P) and high yielding cows have a high requirement for dietary P, at least 0.36% DM (preferably 0.40-0.45% DM). Average P levels in Irish forages are: herbage 0.43; early- cut silage 0.38; late-cut silage 0.33; hay 0.24% DM. Forage P <0.36% DM is rare on well fertilised herbage but many silages contain P levels below that. Silage often has 20-25% less P than herbage on the same farm. Thus, mild deficiency of P can arise in high-yielding cows on silage plus dairy ration if the ration is not balanced or if inadequate mineral supplements are fed. Many hays contain too little P for high-yielding cows. Other low-P forages, such as straw, pressed pulp, fodder beet and roots without supplementary mineral feeding also may cause P deficiency in stock. In such cases, signs of protein or energy deficiency may be apparent also.

Clinical signs of P deficiency usually are confined to cattle grazing over poorly fertilised peaty soils, marginal hill land or run-down farms. Signs include weak bone, joint-lameness, abnormal hoof growth, depraved appetite, anorexia and severe illthrift in young-stock. Reduced appetite may create nutritional stress. This may reduce fertility (anoestrus and repeat breeders) in cows and delay puberty in heifers.

In Ireland, P deficiency in cows is rare, due to routine use of phosphate fertiliser and feeding of supplemented concentrates. Serious P deficiency is unlikely until feed P falls <0.20% DM.

Ca and P in lactation: After calving, high Ca and P levels in milk almost double the Ca and P requirements. Recently calved high yielding cows are usually in a negative Ca and P balance. Such cows maintain blood levels by mobilising skeletal reserves. Provided this negative balance is not unduly prolonged, it should have no adverse effect.

Dietary Ca/P ratio: The ideal ratio of Ca/P in feed for milking cows is about 1.4/1. However, ratios of 1/1 to 3/1 are acceptable and ruminants can tolerate ratios as high as 6/1 provided the absolute levels of Ca, P and vitamin D are adequate. While a ratio of Ca/P <2.4/1 in diets fed pre-calving is recommended by some authorities, increasing the P level in feed pre- calving has little effect in preventing milk fever. A ratio <1/1, i.e. an excess of P over Ca in the diet, can reduce Ca absorption.

Low blood Mg levels can give rise to grass tetany in calved cows. Hypomagnesaemia also can reduce feed intake, even in the absence of tetany. This may cause nutritional stress and reduced fertility. Decreased feed intake can lower milk yield by 10-20% in the herd. Mg shortage pre-calving can reduce turnover of Ca from bone to blood, thereby increasing the risk of milk fever in cows calving for the third time or more. Therefore, Mg deficiency can influence fertility indirectly, by influencing Ca metabolism at parturition (see section on Ca deficiency above) and also by reducing feed intake in lactation.

In the absence of Mg-antagonists in feed (as on summer grass or winter diets supplemented with concentrates), Mg absorption from the digestive tract averages 25-35% of intake. The minimum dietary Mg level needed to prevent grass tetany in lactating cows and ewes is 0.20% DM. Levels of 0.25-0.30% DM are preferable for high-yielding cows. Many silages have low levels of Mg (0.10-0.19% DM). Feed Mg <0.20% DM and low blood Mg levels are common in unsupplemented cows on spring grass or autumn aftermath. Thus, deficiency of Mg can arise in high-yielding cows on silage + dairy ration, or on spring herbage or autumn aftermath, unless the diet is well balanced or adequate mineral supplements are fed.

Lush grass: Mg antagonists in the feed include factors in lush, rapidly growing grass (heavily fertilised with N and K), high dietary fat or fatty acids in grass. Such factors often arise in tetany-prone pasture. They reduce Mg absorption to 5-17% and increase the dietary Mg requirement of high yielding cows from 0.20% DM to 0.30-0.40% DM or more.

Reduced Mg absorption on tetany-prone swards and low ability to mobilise Mg stored in bone, means that cows or ewes, especially those losing Mg in milk, need high Mg intakes on a regular basis (every 1-2 days).

Sodium (Na) deficiency may reduce milk yield. It may occur in milking cows if feed Na is <0.15% DM. Na deficiency also reduces Mg absorption. To prevent Na deficiency and to improve Mg absorption on tetany-prone feeds, Na levels in the feed of in milking cows should be >0.20% DM.

Feed K/Na ratio: Feed K/Na ratios >20/1 may increase the risk of grass tetany. For example, if feed K level is 4.0% DM, feed Na should be >0.20% DM.

Copper (Cu), molybdenum (Mo), sulphur (S), iron (Fe) and lush grass are taken together because of their inter-relationships in animal nutrition. Cu antagonists in the feed interfere with absorption and/or utilisation of Cu. Mo is a powerful Cu-antagonist in cattle and sheep. Other Cu-antagonists include high Fe intake (from soil, mineral supplements too high in Fe or from Fe-rich water) and high sulphate intake from deep-bore wells. High stocking rates and high soil intake also can lead to induced Cu deficiency via high Fe intake. High levels of feed S antagonise Cu in sheep.

Cu deficiency in stock, especially that induced by high Mo levels or other antagonists in feed, can cause loss of productivity and ill- health. While calves and yearling cattle are particularly susceptible, cows, adult cattle, sheep and lambs can be affected also. Induced deficiency is more common and much more important economically than simple Cu deficiency.

Normal levels of dietary Cu for cattle are 10-30 mg/kg DM. Levels of Cu in herbage >10 mg/kg DM are rarely attained, especially in pure ryegrass swards. Old pastures which contain clovers, herbs and weeds usually have higher levels of Cu than pure ryegrass but overall do not compare with them in stock carrying capacity. Feed Cu levels of 7.0-9.9 mg/kg DM are marginal for cattle, 5.0-6.9 are low and <5 mg/kg DM are very deficient in the absence of Cu supplements. Although simple Cu deficiency occurs in Ireland, low herbage Cu levels rarely affect grass production and many herds have moderate to severe simple Cu deficiency without obvious clinical or sub-clinical effects.

Sheep need less feed Cu than cattle. In the absence of Cu-antagonists, Cu levels of 7-15 mg/kg DM are optimal. Levels >15 mg/kg DM may poison sheep and <7 mg/kg DM are deficient.

Dietary Mo levels: Normal levels are 0.4-2.0 mg/kg DM. Elevated levels in feed reduce the utilisation of dietary Cu in ruminants. The higher the feed Mo levels, the greater the blockage of Cu metabolism and the more Cu supplement is needed to overcome the deficiency. Feed Mo levels >2 mg/kg DM are suspect and >3.5 mg/kg DM are high.

Mo toxicity: Dietary Mo levels >10 mg/kg DM may be toxic, depending on Cu intake in feed or supplements. Signs may include early embryonic death (day 6 to day 14) with return to oestrus in 18-24 days. Anoestrus or suboestrus may occur. Abortion, stillbirth, lowered immunity, death in young calves, severe scouring, faded coats, stiffness, lameness, poor thrive in growing cattle can arise also. Severe scouring, ill thrift, lowered milk yield, emaciation and death, even in cows, can arise in very severe cases.

Herbage Mo levels may need to be checked at least twice in the season, as they depend on soil moisture. Herbage sampled in wet weather may have 5 to 15-fold higher Mo levels than samples taken from the same area in dry weather. Thus, normal or only marginally elevated Mo levels in herbage sampled in dry weather do not exclude Mo-induced Cu deficiency at other times of the year.

Cu/Mo ratio: A Cu/Mo ratio in the diet of at least 3/1 is needed to prevent Cu deficiency and to avoid Mo toxicity. A ratio of at least 4/1 may be necessary to prevent low blood Cu levels in sheep. Cu/Mo ratios <2/1 are low and <1.5/1 are very low. Low Cu/Mo ratios can cause severe Cu deficiency in the absence of Cu supplements.

Liming: Liming decreases Cu, Co and Mn levels in herbage but increases the levels of Mo and Se. (See section on soil LR, above).

Lush grass and fertilisers: Cu deficiency can arise on feeds with Cu >10 mg/kg DM and Mo <2 mg/kg DM. For example, N, P, K fertilisers influence Cu status in herbage and animals. Application of N, especially when combined with P and K, can produce lush grass (high N, P, K). This can reduce transit time of feed in the digestive tract and cause digestive upset/grass scours. Thus, factors in lush grass may reduce the absorption of minerals, including Cu and Mg. Feed tests for N, P, K can suggest high intakes of these elements. Lush or rapidly growing grass (N >3.0% DM; K >3.0% DM; P >0.4% DM) has a laxative effect and may reduce the rate of absorption of some minerals, including Cu.

Also, the effect of N fertiliser has paradoxical effects on Cu levels in herbage. The effect depends on the initial soil Cu status. If soil Cu levels are high, N raises the herbage Cu content but if soil Cu levels are low, N reduces herbage Cu levels.

Dietary Cu and S: In other countries, high intake of S in feed (feed S >0.30 and especially >0.40% DM) or of sulphate ion from deep-bore water has exaggerated Cu deficiency. Feed tests for S may be useful to explain Cu deficiency in cases that arise in the absence of other obvious causes. As mentioned under feed S levels above, ideal S levels are 0.16-0.30% DM. Feed S levels >0.30% may induce Cu deficiency in sheep or increase their requirement for dietary Cu. Under Irish conditions, sulphate ion, such as in sulphuric acid additive with no added Cu, can depress Cu status in cattle but high S levels in herbage, or feeding flowers of S for long periods have little effect on Cu status in cattle. (See section on forage S, above).

In most other countries, a selenium (Se) intake of 0.10-0.18 mg/kg DM in total feed (depending on vitamin E content) is recommended to maintain Se levels in blood above the minimum normal level. Our cattle seem to need higher Se levels in feed, at least 0.24 mg/kg DM, to maintain normal Se status in blood. The discrepancy between our results and those of other countries is under investigation. EEC legislation allows a total feed Se level up to 0.50 mg/kg DM.

Se deficiency: Se deficiency on blood test (herd mean GPx levels <60 iu/g Hb) is widespread in Irish cattle. Se deficiency in sheep (flock mean GPx levels <100 iu/g Hb) occurs less often than in cattle. Most of these herds and flocks are (probably) in the non-clinical and sub-clinical categories.

Clinical signs of Se deficiency include late abortion/stillbirth/weak calves or lambs with enlarged thyroids, retained placenta, low immunity to infection in all ages of cattle and reduced fertility in bulls. Se deficiency may also cause muscular stiffness, recumbency, difficult breathing and poor weight gains in younger cattle. Early embryonic death (day 6 to 14) may occur, with return to oestrus in 18-24 days. Anoestrus or suboestrus may occur.

Clinical signs usually do not arise unless blood Se is near or <50% of normal blood Se levels but sub-clinical signs and lowered herd immunity to infection may arise at higher levels. Decreased immunity in animals is linked with deficiency of Se, Cu, Co, Zn, I and vitamins (especially Vits A and E). Lowered resistance to disease may increase somatic cell counts and the incidence of mastitis and metritis. Increased incidence of pneumonia, scours and joint-ill may increase mortality in calves and lambs.

Se-responsive disorders may arise if feed Se or herd mean blood GPx falls <67% of the lower limit of the normal range. Marginal Se deficiency on blood or feed test seldom cause loss of productivity but may be involved in lowered immune status.

Differential diagnosis of Se and I deficiency in perinatal problems: As iodine (I) deficiency also may cause abortion/stillbirth/weak calves with enlarged foetal thyroids, a differential diagnosis between Se and I deficiency must be made. Very low Se status in animals can interfere with thyroid function and I metabolism. Blood tests for GPx and plasma I can be used to check this.

Selenium and vitamin E: The effects of Se deficiency in ruminants may be influenced by dietary intake of vitamin E and may be independent of Vit E. Clinical and/or subclinical signs of Se deficiency often occur at pasture (rich in Vit E) or on silage (in which some Vit E may be destroyed).

Selenium toxicity: In selenium-toxic Irish pastures, herbage Se averages 18 mg/kg DM (range 1.6-140 mg/kg DM, with a few values above this; 50% of values are >6 mg/kg DM and 90% >3 mg/kg DM). Feed Se levels >3 mg/kg DM have been recorded also without adverse effect on stock.

Clinical signs of Se toxicity include severe lameness, horizontal grooves, cracks and sloughing of hooves, loss of appetite, loss of hair from the tail and eventually, death. High-Se pastures occur in Ireland, notably in Meath and parts of Carlow, Dublin, Kilkenny, Limerick and Tipperary. Interaction between Se and S, a closely related element, may occur: heavy applications of gypsum can reduce herbage Se levels and high S levels in the diet can reduce Se utilisation in animals.

Iodine (I) deficiency may be simple or induced (secondary). It may cause poor milk yields, poor weight gains in young stock and low immunity to infection in all ages of stock. Clinical signs include a high incidence of retained placenta and infertility (anoestrus, suboestrus or delayed puberty). Early embryonic death (day 6 to 14) with return to oestrus in 18-24 days may occur. Reduced fertility may occur also in bulls and rams. Calves and lambs from I-deficient dams may die before, during and after birth (late abortion/stillbirth/weak calves or lambs). Swollen thyroid glands, usual on post-mortem of I-deficient young-stock, are not diagnostic of I deficiency. As Se deficiency may also cause placental retention, abortion, stillbirth, and weak calves with enlarged thyroids, a differential diagnosis between Se and I deficiency must be made. A blood test for GPx (see section on Se deficiency, above) is most useful in this respect.

Simple I deficiency is due to low I in soil and feed. Heavy application of organic fertiliser (human sludge, animal slurry, poultry manure) or of inorganic fertilisers, especially N, reduces the I level in herbage. Liming has little effect. In contrast to popular myth, I deficiency has been confirmed in herds within three miles of the coastline.

Requirement for dietary I: There is controversy on the minimum requirement for dietary I. We use the American (NRC) standards for high yielding cows: 0.4-0.8 mg/kg DM. If goitrogenic feeds are used, the requirement may rise to 1-4 mg/kg DM. Irish herbage rarely concentrates I >0.30 mg/kg DM. The level of I in our pasture ranges from 0.03-0.35 mg/kg DM, with a mean value close to 0.25 mg/kg DM. Therefore most Irish ruminant feeds fall far below the I requirement for high yields. Low I levels in feed (feed I <0.4 and usually <0.2 mg/kg DM) suggest I deficiency.

Feed tests for I are not as useful as blood or soil tests. As soil I levels tend to be in the range 2-20 mg/kg (i.e. 10-100 times higher than herbage levels), herbage levels >0.5 mg/kg DM are ascribed to incorrect sampling and/or contamination by soil or other I sources. Soil contamination of herbage or silage samples may overestimate the real dietary I levels. Thus, "normal" feed I levels (0.4-0.8 mg/kg DM) do not exclude the possibility of simple I deficiency and may not overcome the effects of secondary deficiency induced by goitrogens in the feed.

Secondary I deficiency is due to goitrogenic substances (such as thiocyanate) in feed or to the presence of severe Se deficiency (which interferes with thyroid function and I metabolism)). Goitrogenic feeds include cabbage, kale, rape, sprouts, cauliflower, turnips, swedes, linseed, rapeseed, some clovers and soya beans. The diet should be checked for presence of goitrogens and for severe Se deficiency. If goitrogenic feeds are used, I supplements are advised routinely in late pregnancy, in breeding animals and in rapidly growing young-stock.

Blood tests (especially plasma inorganic I (PII) and GPx) in late pregnancy, are needed for accurate differentiation of I and Se deficiency. PII values <20 ng/ml are classed as very low; 100-300 ng/ml is normal and >300 ng/ml is high. I deficiency in cattle and sheep is common on blood PII test in unsupplemented animals. Cows on balanced dairy ration or iodised mineral mixes have higher PII values than unsupplemented cows in late pregnancy.

Milk I (MI) tests: Low MI values in milk may also be used to detect I deficiency but I supplements and teat-dips or disinfectants containing I can give "normal" MI readings, which can mask serious deficiency in unsupplemented dry cows. Many herds with low PII values are non-clinical.

Routine I supplements advisable: Regardless of plant I levels, routine provision of generous I supplements to ruminants is advisable before parturition and before and during the breeding season. Youngstock and growing animals may also need an I supplement on many farms.

The requirement of ruminants for dietary Zn ranges from 7-58 mg/kg DM. Zn absorption is under genetic control and certain lines may have a requirement >100 mg/kg DM. High Ca intakes depress Zn absorption. Secondary Zn deficiency (associated with Ca intakes >0.7 and especially >1.0% DM) occurs occasionally.

Signs of primary Zn deficiency are very rare unless feed Zn is <25 mg/kg DM. Irish forages usually contain 27-55 mg Zn/kg DM. Levels <25 mg/kg DM have been found in 1989-90 in some counties, notably Waterford and Wexford. However, clinical signs of primary Zn deficiency are very rare in Ireland.

Zn deficiency in cattle may cause reduced feed intake, poor growth, epithelial defects (including the uterus and digestive tract, delayed wound healing), skin lesions (thickened, itchy, scaly skin, poor hair quality, loss of hair), lameness and reduced immune status and increased mortality in calves. It may reduce fertility by increasing the risk of metritis in females and by testicular atrophy and poor spermatogenesis in males and may cause difficult births in heifers and increased perinatal mortality in calves. This rarely, if ever, has been confirmed in Ireland. Other effects of Zn deficiency in cattle are stiffness, swelling of the coronets, hocks and knees, fluid swellings behind the hind fetlocks, haemorrhage around the teeth and ulcers of the dental pad and teat lesions. Zn storage is poor in young animals, which can develop clinical signs within 2 weeks of going onto a deficient diet.

Normal Zn levels in feed do not exclude Zn deficiency associated with genetic malabsorption syndrome or deficiency induced by Zn-antagonists, such as high dietary Ca. Soil tests for Zn are of little value in assessing Zn status of animals; blood and feed tests give a better assessment.

Mn deficiency has been associated with infertility (anoestrus, small inactive ovaries and/or repeat breeders) in cows and with poor semen quality in bulls in other countries. It rarely, if ever, causes infertility in Ireland. Other effects of Mn deficiency in cattle include skeletal deformities (especially knuckling of the fetlocks; swollen, twisted joints) and poor growth in calves. Suckler calves on Mn- deficient farms are most at risk, as cows' milk is very low in Mn.

Alkaline soils and liming are associated with reduced levels of Mn in herbage. Some authorities state that herbage with less than 50 mg/kg DM is incapable of supporting normal bovine fertility. Irish forages usually contain normal Mn levels (30-400 mg/kg DM). Low Mn levels (<25 mg/kg DM) are very rare.

High quality home-grown feeds save money: Herbage (fresh or conserved) and home-grown crops (roots, cereals and other plant crops) are the cheapest source of feed for ruminants. In particular, top grassland management and high-quality silage are the keys to high animal yields. Aim for silage with a DMD of 75%. Maximising production and conservation of home-grown feeds increases net profit for farmers by reducing their dependence on purchased feeds.

Nutrient imbalance in feeds: Many home-grown feeds are imbalanced in nutrients and some may be of poor quality. These defects may cause illhealth or reduce the productivity of livestock.

Keeping stock health at optimum levels: Ultimately, farmers are responsible for the health and welfare of their livestock. Veterinary surgeons are responsible for the diagnosis / treatment of animal disorders and professional agricultural advisers can give very useful help in the investigation, control and prevention of a wide range of animal problems.

If there is evidence of ill-health or poor performance in your stock, all aspects of grassland management/conservation, animal husbandry, feeding, parasite control, infection etc should be examined closely. Please consult with your veterinary surgeon and Teagasc adviser.

If poor soil fertility, nutrient imbalances or errors in feeding, husbandry, grassland management are confirmed as causes of reduced health or productivity, Teagasc advisory and research staff can suggest methods of rectifying the errors and can formulate a programme for long-term control or prevention of the problem.

Which mineral supplements?: If the history, clinical findings or lab tests indicate a need for mineral supplements, they may be given in many ways (oral supplements, foliar dusting or spraying, veterinary products or mineral application to soil). Please note that mineral mixes for dry cows, calved cows and dry-stock have different formulations, i.e. there is no mineral mix which is properly balanced for all types of cattle and it can be dangerous to feed cattle formulations to sheep.

If a mineral problem has been confirmed in your animals, ask your adviser or vet to consult the Teagasc manual Control of mineral imbalances in cattle and sheep, on the WWW at 3control.htm or on request. This gives detailed advice on the various methods of supplementation. Whichever method is chosen, the correct dose or application rate is essential for best results. We suggest that you choose the best method for your animals and your feeding system in consultation with your Teagasc adviser and veterinary surgeon.

Further notes on mineral-related problems in cattle and sheep are available on the Grange Blood Lab Page at /bldlab.htm#notes on the WWW.

ACKNOWLEDGEMENT: We thank James Crilly MRCVS, Teagasc Headquarters, Sandymount Avenue, Dublin 4 for help in computerising the reporting system.