Mineral Supplementation of Dairy Cows:

An In-Service Training Seminar for Teagasc Advisers

 

by Phil Rogers MRCVS, Teagasc, Grange

 September 21, 2005

 

Introduction

This file is on WWW at http://homepage.eircom.net/~progers/tahip/dairy_min.doc and should be read in conjunction with references (2 and 3).  

Table 1 shows the mean mineral levels in Irish forages (pasture and grass silage) in the early 1990s (1). Values highlighted in yellow indicate abnormal national means for that element. 

Table 1: Mean mineral levels in Irish forages (pasture and grass silage) in the early 1990s.

Major elements (% DM)

 

Forage		Ca	P	K	Mg	N	Na	S
Pasture	Mean	0.65	0.40	2.83	0.20	3.51	0.29	0.39
	SD*	0.18	0.09	0.76	0.05	0.96	0.17	0.10
Silage	Mean	0.69	0.31	2.35	0.18	2.41	0.36	0.31
	SD*	0.16	0.07	0.62	0.04	0.56	0.15	0.11
		Trace elements (mg/kg DM)

 

Forage		Cu	Mo	Se	I	Zn	Mn
Pasture	Mean	9.22	2.49	0.09	0.26	30.8	119.8
	SD*	2.67	3.09	0.15	0.18	8.7	97.0
Silage	Mean	10.36	1.48	0.09	0.27	29.7	103.5
	SD*	5.26	1.17	0.13	0.18	10.5	60.1

*SD (standard deviation): 95% of values fall in the range (mean +/- SD*1), i.e. 95% of Irish herbage Ca values lay between 0.47 and 0.83 %DM; 99% of values fall in the range (mean +/- SD*2), i.e. 99% of Irish herbage Ca values lay between 0.29 and 1.01 %DM. 

The main imbalances found in Irish pasture (1) were:

• N, K and S and Mo were high in 65, 32, 80 and 42% of samples, respectively
• P, Mg, Na, Cu and Zn were subnormal in 32, 49, 19, 65 and 25% of samples, respectively
• Se and I were subnormal in 94 and 97% of samples, respectively
• High Se was found in 1.2% of pasture samples; endemic Se toxicity occurs on circa 50 farms in the Republic
• Mn deficiency was not a problem; only 2% of samples were subnormal
• Co levels are not shown, because much Co found on pasture (or silage) analysis is surface contamination from soil. However, Co deficiency is common in Irish herbage.

From these national data, it follows that optimal mineral nutrition of Irish cattle and sheep on forage-based diets involves routine supplementation to ensure balanced inputs of the essential major- and trace- elements to ensure that neither deficiencies (primary or secondary) nor toxicities occur.

For details on the methods of control of mineral imbalances in cattle, see the REFERENCES at the end of this paper, especially references (2 and 3).

1. FUNCTIONS OF THE ESSENTIAL MAJOR ELEMENTS

In this section, the clinical signs of mineral deficiency and toxicity were taken from WWW, and especially from Dr. Maurice E White’s “Cornell Consultant (4), adapted for conditions seen in Ireland. That free online software is most useful to vets and agricultural professionals who may have difficulty differentiating between different diseases in farm animals. BOOKMARK that resource (4).

 

Calcium (Ca) is the most common mineral in the body; 99% of it is in bones and teeth; the other 1% is in the blood and soft tissue. Adequate dietary Ca is critical to maintain a healthy skeleton and teeth. Ca also is necessary for:

o        neuromuscular transmission smooth and skeletal muscle contraction

o        cardiac automaticity

o        constriction and relaxation of blood vessels

o        nerve function

o        cell division and movement

o        cellular oxidative processes

o        signal for secretion of hormones, such as insulin

o        co-factor for "vitamin K-dependent" clotting factors in blood coagulation (needed to protect against fatal blood-loss after calving, wounds, surgery, etc)

o        Intracellular calcium is a second messenger in many intracellular responses to chemical and electrical stimuli and required by many enzymes for full activity

o        Many different calcium binding proteins have been described; two with well established functions are troponin and calmodulin. Troponin is involved in muscle contraction; calmodulin causes configurational changes to proteins and enzyme activation.

Ca levels in the blood and fluid surrounding the cells (extracellular fluid) must be kept within a narrow concentration range for normal physiological functioning. The physiological functions of calcium are so vital to survival that when calcium intake is inadequate the body demineralises bone to maintain normal blood calcium levels.

Hypocalcaemia (low blood Ca status) may cause milk fever: ataxia, muscle weakness, ruminal stasis (hypomotility or atony), downer cow (inability to stand), coma, circulatory shock and death. Other signs of hypocalcaemia include: abdominal distension, abnormal anal, perineal, tail reflexes, abnormal pupillary response to light, agalactia, anorexia, arrhythmia, ataxia, atrial fibrillation, bloat, cold skin, decreased amount or absent faeces, constipation, diarrhoea, dullness, dysmetria, dyspnoea, dystocia, excitement, fever, generalized weakness, grinding teeth, hyperesthesia, hypothermia, inability to open (trismus) and/or close jaw, increased respiratory rate, muffled, decreased, heart sounds, mydriasis, pulse deficiency, seizures or syncope, sinus tachycardia, tachycardia, tetany, tetraparesis, tongue protrusion, trembling, tremor and weak pulse.

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.

For details on the control of parturient hypocalcaemia and milk fever, see references (5 and 6) and http://homepage.eircom.net/~progers/tahip/3control.htm#hypocal

Ca excess is rare in ruminants because they can handle huge amounts of dietary Ca by shutting down its absorption. However, cows can die during treatment for milk fever if Ca borogluconate is injected too rapidly intravenously.

Phosphorus (P) is the second most common mineral in the body; 85% of it is in teeth and bone; the other 15% is in body fluids and in the genetic material in cells. Adequate dietary P is critical to maintain a healthy skeleton and teeth. P also is necessary to:

• control blood pH; phosphate is a buffer in the blood but carbonate is more important
• deliver energy (via P in ATP, a triphosphonucleotide) to all body processes
• synthesise phospholipids
• synthesise RNA and DNA 

Hypophosphataemia (low blood P status) in cattle may cause: abnormal length oestrus cycle, agalactia, anoestrus, anorexia, dryness of skin or hair, female infertility, forelimb lameness, forelimb swelling, generalized lameness or stiffness, hindlimb lameness, hindlimb swelling, inability to stand, lack of growth or weight gain, pica, reluctant to move, rough hair coat, underweight, poor condition, thin, emaciated, unthriftiness, ill thrift and weight loss.

In Ireland, P deficiency in dairy 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. 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. For details on the control of P deficiency in cattle, see http://homepage.eircom.net/~progers/tahip/3control.htm#conp

Excess P is undesirable; it reduces the absorption of Ca and Mg. In calves, it can cause urinary stones that may obstruct male calves and require surgery.

 

Magnesium (Mg): Adequate dietary Mg is critical to prevent grass tetany and milk fever and for optimal dry matter intake and milk yield in dairy cows. Mg also is necessary:

• for neurotransmission
• to relax nerves and muscles
• to build and strengthens bones
• to maintain normal blood circulation

Hypomagnesaemia (low blood Mg status) may cause grass tetany (tremors, spasms, convulsions, ataxia, muscle weakness, recumbency and death; death may be sudden); reduced feed intake and lower milk yield in dairy cows; softening and weakening of bone, with increased risk of parturient hypocalcaemia and milk fever in cows; heart arrhythmia, irregular contraction, or increased heart rate; hypertension; imbalanced blood sugar levels; headaches. Other signs of hypomagnesaemia in cattle include: abnormal behaviour, aggression, changing habits, anorexia, change in voice, cold skin, coma, constant or increased bawling, dullness, dysmetria, dyspnoea, excessive salivation, excitement, fever, generalized lameness or stiffness, generalized weakness, grinding teeth, head pressing, hyperesthesia, inability to stand, increased frequency of urination, increased respiratory rate, nystagmus, opisthotonus, prolapsed third eyelid, propulsion, seizures or syncope, sudden death, tachycardia, tetraparesis, vomiting or regurgitation.

For details on the control of hypomagnesaemia and grass tetany, see reference (7) and http://homepage.eircom.net/~progers/tahip/3control.htm#conmg

Excess Mg is undesirable; it causes anorexia, cold skin, diarrhoea, reduced milk yield, dullness, generalized weakness, hypothermia, inability to stand and tetraparesis. In calves, it can cause urinary stones that may obstruct male calves and require surgery. Also, cows can die during treatment for milk fever or grass tetany if Mg salts (usually magnesium sulphate) is injected too rapidly intravenously.

Sodium (Na): Adequate dietary Na is critical to maintain normal fluid and electrolyte balance in blood and cells and. Na (as salt) also is essential:

• for muscle contraction
• for nerve transmission
• to maintain pH balance in cells
• to stimulate appetite and water intake
• to aid Mg absorption

 

Na (or salt) deficiency in ruminants may cause agalactia, anorexia, decreased or absent thirst, hypodipsia, adipsia, lack of growth or weight gain, oliguria or anuria, pica, polydipsia, polyuria, underweight, poor condition, thin, emaciated, unthriftiness, ill thrift and weight loss. For details on the control of Na deficiency in cattle, see http://homepage.eircom.net/~progers/tahip/3control.htm#conna  

Excess Na (or salt) is undesirable; it causes dehydration and may trigger hypertension; gross excess (especially if water intake is restricted) may poison stock. Salt toxicity and water intoxication in ruminants may cause: abdominal distension, anorexia, arrhythmia, ataxia, blindness, bloat in ruminants, colic, coma, diarrhoea, dullness, dyspnoea, excessive salivation, excitement, fever, generalized weakness, haemoglobinuria or myoglobinuria, haemoptysis coughing up blood, hyperesthesia, hypothermia, inability to stand, increased frequency of urination, increased respiratory rate, nystagmus, oliguria or anuria, opisthotonus, pale, polydipsia, polyuria, red or brown urine, seizures or syncope, stiffness or extended neck, sudden death, tachycardia, trembling and tremor.

2. FUNCTIONS OF THE ESSENTIAL TRACE ELEMENTS 

Copper (Cu): About 33% of total body copper is in skeletal muscle, 33% in brain and liver and 33% in bone and other tissues. As bile is the main excretion route for Cu, liver and gallbladder diseases may affect copper balance.

 

Cu is part of prolyl and lysyl hydoxylases, enzymes needed for collagen synthesis. Because of this, connective tissue-rich tissues such as capillaries, scar tissue, and bone matrix are most sensitive to copper status. Copper also functions at the catalytic site of the antioxidant enzyme superoxide dismutase (SOD). Also, the copper-containing plasma protein caeruloplasmin is integral to iron metabolism since it catalyzes oxidation of the mineral, which is required for its binding to proteins involved in absorption, transport, and storage. The redox potential of copper ions gives it a key role in energy metabolism as a component of the cytochromes that participate in electron transport.

Cu, molybdenum (Mo), sulphur (S), iron (Fe) and lush grass: All of these are inter-related in cow 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.

Hypocuprosis (clinical 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. Cu deficiency may cause skeletal abnormalities, reproductive difficulties, impaired nervous tissue function and changes in hair and skin pigmentation. Cu also helps to maintain bone mass.

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, I and Mn levels in herbage but increases the levels of Mo and Se. 

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, and 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, and 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. 

For details on the prevalence and control of Cu deficiency in cattle, see references (8) and http://homepage.eircom.net/~progers/tahip/3control.htm#cudef

 

Cu toxicity: Excessive Cu inputs easily poison sheep and pre-ruminant calves. Although adult cattle tolerate high Cu inputs, cases of Cu toxicity have occurred in cows in Ireland where grossly excessive Cu supplements were used. For details of Cu toxicity and methods of control, see reference (13).

 

Selenium (Se): Se functions in 4 main areas: antioxidant function, immunocompetence, prostaglandin synthesis and deiodination in the thyroid gland.

• Antioxidant function: Se is part of the antioxidant enzyme complex, glutathione peroxidase (GSH-Px or GPx). GSH-Px catalyzes the reduction of hydrogen peroxide and lipid hyproperoxide, preventing oxidative damage to body tissues. It is mainly responsible for reducing peroxide free radicals that include lipid peroxide formation in cell membranes. Reduction of peroxides formed by oxidation of membrane phospholipids breaks the auto-oxidative chain reaction that damages cell membranes. Se-dependent antioxidant protection of cell membrane phospholipids is synergistic with vitamin E. Reduced antioxidant capacity infers decreased immunocompetence and decreased tolerance of stress.
• Immunocompetence: Se is important for immune competence. Se deficiency can increase susceptibility to bacterial diseases, such as calf scours, shipping fever, metritis and mastitis.
• Prostaglandin synthesis: Se protects the oxidative state of lipid intermediates formed during cyclooxygenase reactions which determines the balance of the end products and whether proaggregatory, proinflammatory or antiaggregatory, antiinflammatory responses will dominate. Se deficiency can be associated with lazy calving, increased calf mortality and increased incidence of retained placenta in cows.
• Deiodination in the thyroid gland: Se is part of a second selenometalloenzyme, thyroid iodothyronine 5'-deiodinase, an enzyme that catalyzes the deiodination of thyroxine (T₄) to the more metabolically active triiodothyronine (T₃) in tissues. That deiodination step is crucial for proper iodine metabolism in thyroid hormones.

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 <42iu/g Hb) is widespread in Irish cattle. Se deficiency in sheep (flock mean GPx levels <84iu/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: 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. A differential diagnosis between Se deficiency and iodine (I) deficiency must be made because either deficiency may cause abortion/stillbirth/weak calves with enlarged thyroids. 

Se and vitamin E: Dietary intake of vitamin E may influence the effects of Se deficiency in ruminants or the effects of Se deficiency 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). For details on the prevalence and control of Se deficiency in cattle, see references (8) and http://homepage.eircom.net/~progers/tahip/3control.htm#conse  

Se 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.

 

For details on Se toxicity, and for methods of control, see references (9) and http://homepage.eircom.net/~progers/tahip/3control.htm#setox

 

Iodine (I): The thyroid needs adequate amounts of I for synthesis of thyroxine (T₄) and triiodothyronine (T₃), hormones that regulate energy metabolism, growth, development, lactation, and reproduction.. The thyroid gland stores about 60% of the body’s I pool. The rest is in the blood, ovary, and muscle.

 

I deficiency: 97% of Irish forages are subnormal in iodine and common feedstuffs (high-nitrate grass, clovers, brassicas, soyabean, etc) contain goitrogenic factors. Though non-clinical I deficiency is common, herds that do not receive an I supplement are at risk of developing clinical or subclinical signs of I deficiency.

 

Goitre is a non-inflammatory, non-cancerous thyroid enlargement, often caused by direct I deficiency, or due to plants which interfere with iodine metabolism, such as brassicas (kale, rape or turnips, mustards, etc), soybeans and peanuts. Thyroid enlargement is most common in young animals but can also occur in older stock. It is more common in endemic areas, especially in mountains, on peaty soils and on high-Ca soils. Heavy liming can precipitate goitre in stock if I supplements are not provided. Goitre also can arise in I toxicity, and in Se deficiency.

 

Textbook Signs of goitre in ruminants include: abnormal breathing sounds of the upper airway (due to the swollen thyroid pressing on the airway), abnormal length of oestrous cycle, abortion or weak newborns, alopecia, dryness of skin or hair, female infertility, generalized weakness, hyperkeratosis, lack of growth or weight gain, lack of libido or erection, laryngeal, tracheal, pharyngeal swelling, male infertility, neck swelling, skin scales, underweight, poor condition, thin, emaciated, unthriftiness, ill thrift, weight loss

 

Common signs of bovine I deficiency in Ireland include: infertility (anoestrus or repeat breeding), abortion, stillbirth, weak-calf syndrome (calf born alive but weak, slow to suck and high mortality in the first few days of life), lazy calving and retained placenta.

 

I (like Cu, Se, Co, Zn and Vit E) is important for a competent immune system in calves and cows. I deficiency renders a herd more prone to bacterial and protozoal infection, including calf scours, pneumonia, metritis and mastitis.

 

Though severe I deficiency can reduce milk yield and growth rate, these effects are uncommon in Ireland. For details on the prevalence and control of I deficiency in cattle, see references (8, 10, 11) and http://homepage.eircom.net/~progers/tahip/3control.htm#idef

 

I toxicity can arise if grossly excessive I supplements are used. It can cause: agalactia, anorexia, chemosis (exophthalmos, swelling and redness of conjunctival & scleral membranes of the eyelids and eye surface, coughing, dryness of skin or hair, excessive salivation, female infertility, fever, increased respiratory rate, lack of growth or weight gain, lacrimation, mucoid nasal discharge, rough hair coat, skin crusts and scales. Severe toxicity can cause abortion or stillbirth of calves with a toxic goitre.

 

Cobalt (Co): Co is part of cobalamin (Vit B₁₂). Cattle do not need a dietary source of vitamin B₁₂ because ruminal microorganisms synthesize B₁₂ from dietary Co. About from 3-13% of dietary Co is converted to vitamin B₁₂ in the rumen. Co also is needed for ruminal microbial synthesis of thiamine (Vit B₁) and for optimal digestion of carbohydrate by ruminal microorganisms.

Two forms of Co deficiency occur:

(a) Primary Co deficiency in soil and herbage occurs especially on peaty soils, calcareous soils derived from sea-shells and soils derived from granite and sandstone rocks (most of the mountainous areas of Ireland).

 

(b) Secondary Co deficiency occurs on soils with adequate Co but high manganese (Mn). High soil Mn blocks herbage uptake of Co from soil. Mn-induced deficiency is very common in limestone soils that stretch from counties Meath and Dublin, across the midlands to Counties Roscommon and Galway. Also, heavy liming of soil can precipitate Co deficiency in stock grazing that area.

 

Common signs of bovine Co deficiency: Co deficiency often is non-clinical but may cause subclinical and clinical signs in sheep and cattle (more often in sheep). Effects in cattle (especially in calves on peaty soils) include reduced feed intake, poor appetite or anorexia, poor condition, poor thrive or decreased growth, emaciation, rough appearance (rough hair coat) and a markedly reduced vitamin B12 status in serum and liver.

 

Other signs include: agalactia, anaemia or pale mucosae, rapid heart rate, female infertility, anoestrus, diarrhoea, dullness, exercise intolerance, generalized weakness and pica.

 

Co (like Cu, Se, I, Zn and Vit E) is important for a competent immune system in calves and cows. Co deficiency renders a herd more prone to roundworm infestation, especially ostertagiasis. For details on the control of Co deficiency in cattle, see reference http://homepage.eircom.net/~progers/tahip/3control.htm#codef

 

Co toxicity in cattle and sheep: On farms where Co deficiency occurs, it is common to supplement ruminants with Co at 5-10mg Co/d (adult cattle) or 1-2mg Co/d (adult sheep). Gross overdosing can kill. The lethal dose is extremely high, about 6.6-22mg/kg LW in cattle and 44-66mg/kg LW in sheep. Diagnosis is by dietary history and liver and kidney cobalt levels.

 

Clinical signs of Co toxicity include: agalactia, anorexia, dullness, inability to stand, polydipsia, polyuria, sudden death, underweight, poor condition, thin, emaciated, unthriftiness, ill thrift, weight loss.

 

Zinc (Zn): Zn is a cofactor for >100 enzymes in the body. Zn-dependent enzymes are needed to metabolise protein, nucleic acid, carbohydrate, fat and alcohol. Zn is important for normal immune system development and function. Zn also is essential for protein synthesis, integrity of cell membranes, skin and hoof health, maintenance of DNA and RNA, tissue growth and repair, wound healing, taste acuity, prostaglandin production, bone mineralization, proper thyroid function, blood clotting and cognitive functions. Considering its role in growth and development, Zn is an integral mineral for foetal development and sperm production.

 

Two forms of Zn deficiency occur: (a) Primary Zn deficiency is uncommon in Irish ruminants, even though 25% of Irish forages have subnormal Zn levels (Table 1). (b) Secondary Zn deficiency (due to excessive intake of Ca) occurs occasionally. Cattle on high-Ca feeds should receive a generous Zn supplement (750mg Zn/cow/d).

 

Clinical signs of Zn Deficiency include: small testes/scrotum, alopecia, anestrus, anorexia, cracked skin, decreased mobility of forelimb joint, defective growth of nail, claw, hoof; dryness of skin or hair, dullness, excessive salivation, female infertility, forefoot pain, forelimb swelling, foot lameness, generalized weakness, hindfoot pain, hindlimb swelling, hyperkeratosis, inability to stand, kyphosis, lack of growth or weight gain, lack of libido or erection, lacrimation, male infertility, matted or dirty hair, oily skin, hair or feathers, greasy, opisthotonus, pale mucosae, parakeratosis (thickened skin), pica, pruritus, rough hair coat, skin crusts, skin erythema, skin pain, skin scales, skin ulcer, splitting nail, claw, hoof, tachycardia, trembling, underweight, poor condition, thin, emaciated, unthriftiness, ill thrift and weight loss.

 

Skin lesions of Zn deficiency have been produced experimentally and suspected clinically when there was low Zn in the diet associated with high Ca. Horn growth can be inhibited. Clinical disease is uncommonly recognized in the field. Blood samples for Zn levels can easily be contaminated by needles, bottles or rubber stoppers. For details on the control of Zn deficiency in cattle, see reference http://homepage.eircom.net/~progers/tahip/3control.htm#conzn

 

 

“Protected Zn” versus Inorganic Zn?: Although anecdotal, and without a firm scientific basis, some Irish farmers reported that outbreaks of hoof-lameness in their cows that failed to respond to inorganic Zn supplements (usually Zn sulphate) cleared up within weeks of including “protected Zn” supplement, usually Zn-methionine. For more details on causes and control of lameness in cows, see reference (12).

 

Lethal Trait A 46, Parakeratosis, Zn Deficiency in Calves is a rare, progressive and sometimes fatal disease of calves characterized by oozing and crusting lesions associated with hair loss, especially of the lower limbs, head, and neck. There can be associated delayed wound healing and pneumonia. The condition is due to an autosomal recessive gene causing an excessive Zn requirement due to an inability to efficiently absorb Zn from the gastrointestinal tract. Onset of signs is at 2-6 weeks of age, with diarrhea usually the earliest clinical sign. Affected calves may have diminished suckling ability; difficulty in curving their tongues around the nipple causes a chewing and pulling motion with their tongues flat against the nipple to ingest milk. A 'spectacled' appearance, like that seen in Cu deficiency, can occur. The condition is reported in Friesian, Danish Black Pied, Angus, and Shorthorn breeds. Clinical signs include: abnormal lung or pleural sounds, absence of skin, alopecia, anorexia, chemosis, congestion oral mucous membranes, conjunctival, scleral, injection, conjunctival, scleral, redness, corneal edema, coughing, cracked skin, decreased hair pigment, diarrhea, dryness of skin or hair, dullness, dyspnea, excessive salivation, fever, hyperkeratosis, increased respiratory rate, lack of growth or weight gain, lacrimation, moist skin, hair or feathers, mucoid nasal discharge, oily skin, hair or feathers, greasy, oral mucosal ulcers, vesicles, pruritus, purulent nasal discharge, rough hair coat, skin crusts, skin erythema, skin pain, skin scales, tongue ulcers, vesicles, underweight, poor condition, thin, emaciated, unthriftiness, ill thrift and weight loss.

 

Zn toxicity from excessive amounts of Zn in animal feeds or minerals is very rare in Ireland.

However, cattle in New Zealand are drenched with Zn oxide slurry to prevent facial eczema. This has a low margin of safety and can induce hypocalcemia, which in some cases can lead to clinical paresis.

 

Clinical signs of Zn oxide toxicity include: agalactia, anorexia, cold skin, dehydration, diarrhea, generalized weakness, inability to stand, tachycardia, tetraparesis and weak pulse.

 

Also, several incidents of Zn toxicity in cattle and sheep occurred in USA. Sources of Zn included: accidental addition of Zn oxide to cattle feed, galvanized wire and troughs, heavy use of Zn-containing fertilizers and fungicides, and milk replacer containing large amounts of a Zn supplement. Clinical Signs included: abdominal distention, agalactia, anorexia, arrhythmia, bloat in ruminants, chemosis, colic, constant or increased vocalization, decreased amount of stools, absent feces, constipation, dehydration, diarrhea, dullness, exophthalmos, generalized weakness, grinding teeth, icterus, lack of growth or weight gain, nystagmus, pale, pica, polydipsia, polyphagia, polyuria, rough hair coat, seizures or syncope, skin edema, sudden death, tachycardia, underweight, poor condition, thin, emaciated, unthriftiness, ill thrift and weight loss.

 

Manganese (Mn): Mn is part of the enzymes pyruvate carboxylase, arginase and superoxide dismutase (SOD). It also activates hydrolases, kinases, transferases and decarboxylases. Of the many enzymes activated by Mn, only glycosyltransferases are known to require it specifically.

 

Mn requirements for reproduction are higher than for growth and skeletal development. The recommended concentration for breeding cattle is 40 mg/kg DM.

 

Mn deficiency in early pregnancy has caused a few outbreaks of chondrodystrophy, a congenital developmental defect. Affected calves are born dead, or born as dwarfs with domed heads, cleft palate, abnormal limbs, etc. It also can cause abortion or weak newborns, anoestrus, female infertility, and male infertility. Other signs include: abortion or weak newborns, anestrus, female infertility, male infertility, small litter size (pigs and sheep).

 

Fortunately, though described, Mn deficiency is rare in Ireland. In USA, 50mg Mn/kg TDMI is advised as the minimum recommended level. Experimental Mn underfeeding caused anestrus and infertility in cattle. Cattle supplemented with manganese in a deficient area had increased fertility. For details on the control of Mn deficiency in cattle, see reference http://homepage.eircom.net/~progers/tahip/3control.htm#conmn

 

3. SUPPLEMENTATION RATES FOR THE MAJOR ELEMENTS AND TRACE ELEMENTS Regional (between- and within- county) differences in mineral deficiencies in cattle are known. For example, before widespread routine adoption of mineral supplementation in dairy herds, counties Clare and Carlow had the lowest bovine blood levels of I and Se in the Republic. Also, Mo-induced Cu deficiency is especially common on shale soils and in pastures reclaimed from Bord na Mona cut-over peat soils.

 

However, for many reasons, it is impractical for the feed mills and mineral-mix trade to try to formulate regional mineral mixtures because, for example, Kerry feeds are sold in Monaghan and vice-versa. Therefore, we must be content with NATIONAL feed- and mineral-mix- formulations that supply generous but safe levels of the essential major and trace minerals in the daily allowance to cattle.

 

Suggested national targets for supplementary major and trace elements for cattle and sheep are in tables 3 and 4 of “Control of Mineral Imbalances in Cattle and Sheep: A Reference Manual for Advisers and Vets” at http://homepage.eircom.net/~progers/tahip/3control.htm

 

Targets extracted from those tables for cows are:

Table 3. Suggested optimum supplementation levels of Major Elements for stock. The supplementation level of Ca, P and Mg for cows is usually in the range 0-50% of minimum daily requirement. That of Mg rises to 100% in the tetany season. That of Na is usually 20-40% but may be 140% or more if salt is supplied ad libitum.

Recommended supplement of major elements (g/cow/d)

(*) The optimal Ca and Mg supplements for Dry Cows on silage or grass are 0 and 15 g/cow/d, respectively.

(**) The higher Mg supplements (20-50 g/d for calved cows) are for use in the tetany seasons. Otherwise a Mg supplement of 5-10 g/d for cows is enough in lactation.

Table 4. Suggested optimum supplementation levels of Trace Elements for stock. Except for Cu in sheep and Fe in all stock, the minimum supplementation level of trace elements is set at 100% of minimum daily requirement, i.e. it ignores background levels in forage.

Recommended trace element supplement (mg/cow/d)

The lower levels are for routine continuous use. With the following exceptions, the higher levels are advised for national use in the Teagasc 5-month mineral programme for cows (1 month prepartum to 5 months postpartum; see Addendum: “Comparative costs of mineral supplements for cows from 1 month pre- to 4 months post- calving” [ http://homepage.eircom.net/~progers/tahip/3control.htm#costs ], or as needed in groups of cattle at risk of severe deficiency:

^ Some authorities advise much higher Mn supplements (up to 980 mg/cow/d) in herds with severe infertility due to suspected Mn deficiency. A pro-rata dose for ewes would be up to 98 mg Mn/d.

* Give Cu to sheep only on veterinary confirmation of Cu deficiency.

** Within 5 miles of known Se-toxic farms, reduce the Se supplement to about 50% of the lower level, unless blood test confirms Se deficiency in the group.

*/** Ionophores (monensin etc) increase the retention rate of Cu and Se by ruminants. If ionophores are fed, avoid the higher levels of Cu and Se supplements, unless blood test suggests that higher levels are needed.

*** Zn supplement of up to maximum is advised if high-Ca diets are fed.

4. MINERAL SUPPLEMENTATION METHODS (see references 2 and 3 for details)

 

These will be discussed in relation to:

(a) Fixed rate supplementation (best method) and

(b) Ad libitum supplementation (second class; hit-and-miss; many cows unprotected and some take far too much).

 

(a) Fixed rate supplementation (best method)

• (a1) Fixed rate supplementation IN FEED
• (a2) Fixed rate supplementation ON FEED
• (a3) Fixed rate supplementation IN WATER
• (a4) Fixed rate supplementation VIA DRENCHING [impractical in cows]
• (a5) Fixed rate supplementation via veterinary products

 

(b) Ad libitum supplementation: This uses commercial mineral blocks or licks, or DIY mixtures, such as 50:50 calcined magnesite:molasses, or high-magnesium pasture mineral + molasses. Though better than no supplementation, ad libitum supplementation is second rate. It should be considered only in marginal areas for herds whose managers cannot use a better fixed-rate supplementation method. The main problem with ad libitum methods huge variation in intake between cows. Intake can vary from 0-400g/cow/d. Even at a narrower range (10-300g/d), the variation between cows can be 30-fold. Also, intake is not random; some cows consistently take too much and some take little or none.

 

5. ADVANTAGES AND DISADVANTAGES OF THE DIFFERENT METHODS OF SUPPLEMENTATION

These will be discussed in relation to:

• Safety and efficacy: Fixed-rate supplementation is the best and safest;
• Cost: High-spec minerals IN FEED or ON FEED is the cheapest and best;
• Pasture Nuts: Low-level (1, or 2, or 3kg/cow/d) high-spec pasture-nut fed until 4 months after calving is a very effective way to guarantee normal mineral status in the critical stage of milk yield and early pregnancy.
• Simplicity of use and labour involved:
• Water medication with Mg and trace-elements via proportioner pumps is the handiest but the NZ Water Medication Dispenser is the best.
• Mayo Healthcare Water Medication Tablets include Aquadyne (420mg I), Aquasel (35mg Se) and Aquacopp (840mg Cu), all developed in cooperation with Grange Research Centre.. The tablets are suspended below the water-line in the trough and release their trace elements into the water. The recommended dose rate of Aquadyne and Aquasel is 1 tablet/7 cows/d. In serious Cu deficiency, one may need a dose of 3-4 tablets/7 cows/d. The tablets are simple to use and cost-effective.
• Veterinary Products for Trace Element Supplementation: Some veterinary products are excellent; others are not. Before they are used, deficiency of the specific mineral(s) should have been confirmed by blood or other tests.

The correct dose or frequency of administration of each product must be used. If the dose is inadequate or is not given frequently enough, otherwise excellent products can give poor results. For example, because of the severity of challenge to Cu status (high Mo in feed or high soil/Fe intake), the required dose rate of Cu (or its frequency of use) in Irish herds is often 2-3 times the dose or frequency that is recommended in the United Kingdom. If excessive doses are used, there may be a risk of toxicity, especially with Cu products.

Excellent veterinary products that supply a single trace element include:

o        CuO capsules (24 g CuO orally gives 2-4 months protection in cattle);

o        Cu-EDTA injection (100 mg Cu (subcutaneous) gives 6-12 weeks protection in cattle, but is a less preferred way to supplement with Cu).

o        All Cu-injections are irritant. If possible, avoid the use of Cu injections in animals destined for slaughter, as abscesses and scarring of tissues can follow injection. Avoid especially Cu-EDTA or other irritant injections during or less than 1 month before the breeding season. Local reaction to irritant compounds may depress conception rates by up to 20 points. If Cu is needed, oral CuO capsules or other oral Cu supplements are preferable at this time.

o        Barium selenate injections (100 mg Se/100 kg LW (subcutaneous) gave disappointing results after a change of manufacturer in 1991, but gave satisfactory results in later years. [Sodium selenate or selenite injection (up to 10 mg Se/100 kg live weight, s/c) is much cheaper than barium selenate, but is short-acting. Protection lasts only 4-6 weeks. Depending on the herd-health history, frequent sodium selenate / selenite injections may be needed].

o        If only one trace element deficiency (say Cu or Se deficiency) exists in a herd, effective veterinary products have advantages over oral supplements. However, some are expensive if used at the dose or frequency of administration needed in Irish herds.

o        Bullets that supply 3 or more trace elements are available on the Irish market. They are given orally by a special bulleting gun. The products include "Cosecure" and the post-1991 "Alltrace". The special glass matrix of the bullets is slowly soluble in the reticulo-rumen and releases its supplement over a period of about 6-10 months. "Cosecure" and the new "Alltrace" are similar as regards control of Co, Se and Cu deficiencies. "Ionox" is a new bolus, released on the Irish market in autumn 1996. The bolus was developed in cooperation with Teagasc, Grange.

o        Multiple trace element deficiency often occurs in Irish herds. Therefore, at least Cu, Co, Se and I supplements are advisable during a 5-month period, from 1 month before calving to 4 months after calving. Also, a high Mg supplement (30g Mg/cow/d) is needed during the tetany season and a moderate Mg supplement (15g Mg/cow/d) is needed for 1 month pre-calving. In that case, routine use of multiple veterinary products can be very expensive. Even if "Cosecure", "Alltrace" or "Ionox" bullets can be used, oral mineral supplements may be considered as a good alternative on economic grounds because at least many bullets/cow/year are needed under Irish conditions. For example:

o        Alltrace boluses (Agrimin, UK) have no Mg. The following table shows that, depending on the element of interest, 4-15 boluses per cow would be needed every 8 months to release the same amount of trace element daily as would be provided in the medium Teagasc-recommended daily targets:

	Medium Teagasc Target (mg/cow/d)	Quantity (mg) in each Alltrace bolus	Daily supply per bolus over 240 days	Boluses needed every 240 days to supply medium Teagasc Target
Se	4	251	1.045	3.8
Cu	300	16379	68.2	4.4
Co	7.5	236	0.98	7.6
Zn	543	13382	55.8	9.7
Mn	375	8326	34.7	10.8
I	30	497	2.07	14.5

o        Cosecure boluses (Telsol, UK) have no I or Mg. Most Irish herds would need an I supplement + Mg supplement (at least) in addition to Cosecure. The following table shows that, depending on the element of interest, 2.4-4 boluses per cow would be needed every 6 months to release the same amount of trace element daily as would be provided in the medium Teagasc-recommended daily targets:

	Medium Teagasc Target (mg/cow/d)	Quantity (mg) in each Cosecure bolus	Daily supply per bolus over 180 days	Boluses needed every 180 days to supply medium Teagasc Target
Cu	300	13400	74.4	4.0
Co	7.5	500	2.78	2.7
Se	4	300	1.67	2.4

o        Ionox boluses (Bayer, UK & Ireland) have no Cu or Mg. Most Irish herds would need a Cu supplement + Mg supplement (at least) in addition to Ionox. The following table shows that, depending on the element of interest, 1.6-4.2 boluses per cow would be needed every 196 days to release the same amount of trace element daily as would be provided in the medium Teagasc-recommended daily targets:

	Medium Teagasc Target (mg/cow/d)	Quantity (mg) in each Ionox bolus	Daily supply per bolus over 196 days	Boluses needed every 196 days to supply medium Teagasc Target
I	30	3500	17.9	1.68
Se	4	500	2.55	1.57
Co	7.5	350	1.79	4.20

Poor veterinary products: Under Irish law, veterinary surgeons may prescribe any permitted product that they think fit. Most products are effective and safe if the correct dose is used in the correct circumstances. However, some are less effective than others: the manufacturer's recommended dose is too small to release the amount of required active ingredient per day to meet the animal's needs.

Three products of questionable value in cows are: Mg bullets (to prevent hypomagnesaemia), "Alltrace" bullets (to prevent deficiency of Mn, Zn or I) and Iodine injection (to prevent I deficiency).

Mg bullets: To give 20-40 g Mg/cow/d from Mg bullets that release 1 g Mg/d/bullet would require 20-40 bullets/cow. The usual dose of 2-4 bullets/cow is too small by a factor of 10. Mg bullets may be considered for use in suckler cows on outfarms but 4-6 bullets/cow are advisable every 4-5 weeks.

Alltrace boluses: These Agrimin boluses do not release enough Zn, Mn or I (see the Alltrace table, above) to make them effective supplements if those elements are seriously deficient in a herd.

Iodine injection: [Lipiodol is not registered as a veterinary therapeutic product by the National Drugs Advisory Board]. Oil-based I injections (such as Lipiodol, 40% I) sometimes are used to supply I in I-deficient herds. The oil-based products are slow-acting and we are unaware of controlled work published in refereed scientific journals that shows that they prevent neonatal problems in cows. We are also aware of failure of I injection to prevent stillbirth in calves, which was controlled within days by oral I supplements.

In conclusion, Irish forages (pasture and grass silage) have multi-imbalances of major and trace minerals. These imbalances sometimes (but not always) cause clinical or subclinical problems.

Optimal mineral nutrition of Irish cows on forage-based diets involves routine supplementation to ensure balanced inputs of the essential major- and trace- elements to ensure that neither deficiencies (primary or secondary) nor toxicities occur. Most cow farmers should supplement for 5 months (1 month before calving to 4 months after calving).

Supplementation outside of that 5-month window may be needed in special cases, for example in abortion due to I deficiency, or in tetany outside of the normal risk period.

 

Serious dairy farmers should use fixed-rate methods of mineral supplementation, IN FEED, ON FEED, or IN WATER.

Farmers using mineral mixes need at least THREE different mineral formulations:

1.       Dry Cow Formula usually sprinkled on silage at 100g/cow/d for circa 1 month prepartum;

2.       Lactation Formula, usually included at 125-150g/cow/d in dairy concentrate, fed at 6-7 kg/cow/d indoors;

3.       High-Mg (tetany control) formula, with high trace-elements, usually included at 140-170g/cow/d in a pasture nut, fed at 1, or 2, or 3 kg/cow/d.

Farmers feeding a lot of maize-silage, or fodder-beet need special mineral balancers for those feeds.

For details on methods of control of bovine mineral imbalances, see the REFERENCES, especially references (2 and 3).  

REFERENCES [further reading]

1.       Rogers PAM & Murphy W (2000) Levels of Dry Matter, Major Elements (Ca, Mg, N, P, K, Na and S) and Trace Elements (Co, Cu, I, Mn, Mo, Se and Zn) in Irish Grass, Silage and Hay. http://homepage.eircom.net/~progers/tahip/0forage.htm

2.       Rogers PAM & Gately T (1993) Control of Mineral Imbalances in Cattle and Sheep: A Reference Manual for Advisers and Vets. http://homepage.eircom.net/~progers/tahip/3control.htm

3.       Rogers PAM (2003) Optimal Mineral Nutrition of Cattle and Sheep on Irish Farms. http://homepage.eircom.net/~progers/tahip/bov_ov_min_nutr.htm

4.       White ME (2005) Cornell Consultant: Online Veterinary Diagnostic Software. http://www.vet.cornell.edu/consultant/Consult.asp?

5.       Rogers PAM (2001) Hypocalcaemia & Milk Fever in Cows. http://homepage.eircom.net/~progers/tahip/milkfeve.htm

6.       Rogers PAM (2000) Mineral-Vitamin Mixes for Cows and other Cattle. http://homepage.eircom.net/~progers/tahip/mins_bov.htm

7.       Rogers PAM (2004) Magnesium Supplements for Cows. http://homepage.eircom.net/~progers/tahip/mgsupbov.htm

8.       Rogers PAM (2001) Copper, Iodine and Selenium Status in Irish Cattle. http://homepage.eircom.net/~progers/tahip/abattoir.htm

9.       Rogers PAM, Arora SP, Fleming GA, Crinion RAP & McLaughlin JG (1990) Selenium toxicity in farm animals: treatment and prevention. http://homepage.eircom.net/~progers/tahip/setoxicity.htm

10.    Rogers PAM (2001) Iodine Supplements for Livestock. http://homepage.eircom.net/~progers/tahip/iodsupp.htm

11.    Rogers PAM (1999) Iodine supplementation of cattle. End of Project Report: Project No. 4381. http://homepage.eircom.net/~progers/tahip/i_report.htm

12.    Rogers PAM (2001) Herd Lameness and Laminitis. http://homepage.eircom.net/~progers/tahip/lamebov.htm

13.    Rogers PAM (2001)  Control of Copper (Cu) Poisoning in Sheep. http://homepage.eircom.net/~progers/tahip/cutox.htm

14.    Rogers PAM (2003) Online Technical Notes for Vets, Advisers & Nutritional Consultants. http://homepage.eircom.net/~progers/tahip/tecnotes.htm

15.    Rogers PAM, Gately TF & Keating T (2000) Teagasc Farm Nutrient Profile: Reference Information for Professionals. http://homepage.eircom.net/~progers/tahip/2manual.htm