No reliable statistics are available from which to assess the economic losses caused annually in the UK or elsewhere by trace element deficiency diseases in farm livestock. However, data such as those provided by the Veterinary Investigation Diagnosis Analysis Service or by annual FAO/WHO Reports on Animal Health clearly indicate that, in many instances, the circumstances leading to the development of trace element deficiency diseases are neither effectively recognized nor anticipated.

By definition, the essential trace elements are required in very small amounts for optimum body function. The list of essential trace elements is steadily increasing, partly due to improved methods for the detection of very low concentrations and partly to the creation of experimental environments from which such elements can be excluded so that their essential properties can be demonstrated. However, this paper is considering field problems, and discussion will be limited to those elements which are known to be associated with disease in cattle and sheep. Pigs and poultry will be excluded because the major proportion are fed adequate amounts of the trace elements in compounded diets. In contrast, most of the sheep and a large proportion of the cattle population are heavily dependent on home-grown feeds, often only grass or grass products, and these animals are most at risk. Without supplementation, the intake of trace elements is dependent on the concentration in the herbage. It has been estimated that grassland provides almost three quarters of the total crude protein for ruminants in Britain and cereals provide another eighth. We must assume that home-grown feeds are a major contribution to animal diets.

The role of trace element deficiencies in the causation of clinical diseases is often questioned because of the poor correlations which are found between the trace element status of the animal or its diet and the incidence of disease. The most striking example is that relating to the copper (Cu) nutrition of sheep, in which concentrate diets containing 8 mg Cu/kg DM can cause poisoning (Hogan, Money and Blayney, 1968) while pastures containing twice as much Cu can cause a deficiency disease (swayback) to develop (Allcroft and Lewis, 1957; Alloway, 1973). Unidentified stress factors are often invoked to explain such anomalies. However, the poor relationships between nutritional status and disease incidence reflect the inadequacies of past methods of assessing the extent that a trace element is absorbed from the diet and its functional activity in the animal and the fact that requirements vary during an animal's life. The object of this paper is to re-emphasize the nutritional component of trace element disorders by looking at the quantitative and functional basis of trace element requirements, the factors which predispose animals to deficiencies and how these might be countered.

This paper reviews evidence showing that heredity is involved in the utilization of trace elements by animals. Underwood (1981) has stressed the importance of achieving dietary balance in the provision of minerals in animal nutrition and Howell (1983) has emphasized that although a small amount of a trace element may be essential for health a larger amount could be injurious. In these circumstances, information which can be used to meet the essential requirements for trace elements more precisely is likely to help in optimizing animal performance and avoiding risks to health and life. An understanding of the role of heredity in influencing trace element requirements is important in this context. Genetic variation in requirements also suggests the possibility that genetic solutions to trace element deficiency or toxicity problems may provide an alternative strategy to prophylaxis and other nutritional and management aids.

The soil and its parent materials are the primary sources of trace elements on which soil-plant-animal relationships are built. It is important to recognize, however, that anthropogenic inputs of trace elements, in particular heavy metals from industrial and urban sources, may add to and at times exceed those from natural geological sources. Both deficiencies and excesses of trace elements can result in serious nutritional or toxicological disorders, while less severe imbalances may result in sub-clinical effects and, possibly, in production and fertility problems. Where obvious visual symptoms are absent, sub-clinical effects are frequently not recognized, although the areas affected are thought to be large and there are obvious economic implications. This paper examines the influence of soil and geological factors on trace element disorders in livestock, including interactions between natural and man-made sources of trace elements, and illustrates the applications of regional geochemical maps in predicting areas in which disorders are likely to be found.

The symptoms of trace element deficiency arise from the combined effects of the different lesions provoked within the animal body. Since a variety of different lesions have been described, many of which affect inter-related systems, it is not surprising that diverse symptoms may arise even from the one trace element deficiency; nor that similar symptoms may be caused by deficiencies of different trace elements. The major effects of trace element deficiencies on body functions have been outlined in Table 3.2.1 (from Underwood, 1980).

A number of diseases of ruminants are related to deficiencies of vitamin E and selenium (Se). Nutritional myopathy or white muscle disease (Blaxter and Sharman, 1953; Oksanen, 1965; Allen, Bradley, Berrett, Parr, Swannack, Barton and MacPhee, 1975; McMurray and McEldowney, 1977) affects the young bovine. Crawley and Bradley (1978) have described a sudden death syndrome in Se-deficient, bucket-fed, calves, which disappeared when Se was added to the diet.

Despite the extensive knowledge of animals' dietary requirements for trace elements and detailed research into the uptake by plants of nutrients from the soil, it is surprising that the production of animal feedstuffs, having an appropriate trace-element content, still presents a considerable challenge to the agronomist. The present paper draws attention to some of the problems involved, using data from the many years of field-experiment research at the Macaulay Institute for Soil Research. These experiments have been largely restricted to the system of intensive agriculture prevailing in north-east Scotland, where heavily-grazed pasture and conserved herbage are the principal components of animal diets. The 6-7 year crop rotation most commonly practised includes a 3-4 year period of grass ley. The factors discussed have a wider relevance although their relative significance under conditions of low stocking rates, for instance on the rough or natural grazing on hill-land in the U.K. and other countries, will clearly be different.

Dietary manipulations or other oral treatments are, in many cases, the most efficient solution to the problem of trace element deficiency diseases in farm animals. Such approaches are particularly effective against chronic primary deficiencies where there is simply not enough of the required element in the diet to satisfy the animal's needs.

In some situations, however, notably severe and acute deficiencies, parenteral injections of a supplement provide the best methods of restoring normal mineral concentrations in the deficient animal's tissues. Parenteral supplements are also particularly effective against many secondary deficiences in which factors in the diet convert apparently adequate dietary concentrations of the required element into an unavailable form: their effectiveness arises because absorption from the alimentary canal is bypassed. Injectable trace element supplements have also proved particularly useful for short term supplementation during periods when there is a great demand for the element, for instance during pregnancy. One further advantage of the parenteral route of supplementation is that a known amount of the element is introduced into the animal's system.

Oral treatment of trace element deficiencies of livestock has a long although not always distinguished history. It has generally been the method first employed following the discovery of a trace element deficiency. Thus, Robert Fraser (1794) used oral dosing with soil to counteract the effects of cobalt (Co) deficiency in sheep; Hunter, Eden and Green (1945) dosed ewes with copper (Cu) for the control of swayback; McLean, Thomson and Claxton (1959) obtained significant growth responses following selenium (Se) supplementation of unthrifty lambs and Dynna and Havre (1963) used oral dosing with zinc (Zn) as part of the treatment of cattle suffering from a combined Zn-Cu deficiency in Northern Norway.

The opening sentence of the toxicology section of a recent veterinary pharmacology and therapeutics text reads “Everything is poisonous” (Hatch, 1977). Such a generalization reinforces the fact that this paper is concerned with the toxicity of essential trace elements which are necessary for the proper functioning of body cells and are usually thought of in their role as essential components of a diet. Thus, there is the apparent paradox of certain trace elements being both necessary for and damaging to the proper functioning of cells and of the animals that are composed of these cells. It has been said that there are not any toxic elements but that there are toxic concentrations of elements and the paradox of essentiality and toxicity is resolved if we consider that it is the concentration of the element within the biological system that determines the type of action that occurs. Very low concentrations of trace elements are required for the proper functioning of enzymes, cells and tissues. Increasing concentrations can be tolerated by cells but, at a particular concentration, the homeostatic mechanisms can no longer handle the element and cells are damaged. It has been suggested that there are three zones of action of trace elements, (i) the biological action zone, (ii) the inactive zone and (iii) the pharmacotoxicological action zone (Venchikov, 1974).

In a nation intensively and widely industrialized and with a varied geology exploited by mineral workings in the past and present, farm animals are exposed to a wide variety of inorganic environmental pollutants. What is surprising is that so little loss arises overall. Often in incidents where there is harm to livestock, the risk is isolated to the vicinity of a single factory and may affect only one farm or one field. On the first occurrence, the cause and source may become clear and action can be taken to prevent recurrences and so they are self-limiting. These cases are difficult to anticipate and can only be dealt with as they arise. They include accidental discharge of a wide variety of materials to water courses, or dust contamination of pastures from adjacent works.

The effects of season and husbandry on the selenium (Se) status of four flocks, located in areas of Dyfed in Wales, were monitored over a 16-month period. The Se status of each flock was assessed from the activity of the Se-dependent enzyme glutathione peroxidase (EC 1. 11. 1. 9, GSH-Px), determined at 30°C in individual blood samples. The survey was initiated in January 1981 and samples were collected at monthly intervals from 18 ewes per flock.

Until the early 1970s, selenium (Se) status in livestock had been assessed by the chemical measurement of the element Se. For example, the Watkinson (1966) method requires solubilizing Se by inorganic acids, forming a chemical complex, solvent extraction and fluorimetric detection. By contrast, erythrocyte glutathione peroxidase (GSH-Px), a Se-containing enzyme, is readily assayed in blood haemolysates on automated enzyme analyzers. This enzyme activity is usually related to dietary Se intake during preceding months. For both cattle and sheep, a correlation between erythrocyte GSH-Px and whole blood Se was shown (Anderson, Berrett and Patterson, 1978).

Deficiencies of selenium (Se) and vitamin E can result in myopathies in cattle and sheep but the mechanics have not been clearly described. Both Se, as a component of the enzyme glutathione peroxidase, and vitamin E as a radicle scavenger, are involved in the protection of cells against the toxic effects of oxygen. In young calves, Se/vitamin E deficiency can result in the death of the animals due to a focal myopathy occurring in heart muscle; focal lesions are also found in skeletal muscle. In older calves, a more diffuse myopathy is usually confined to skeletal muscle and usually occurs when cattle are turned out from winter housing to spring pasture. However, low Se/vitamin E status will not invariably result in clinical symptoms of myopathy and other factors may be involved. This report describes some of the biochemical changes which can occur during the onset of clinical myopathy in Se/vitamin E-deficient cattle.

We found recently that sodium hydroxide, when used as a grain preservative, will rapidly destroy vitamin E in barley (McMurray, Blanchflower and Rice, 1980). This observation has been applied experimentally to make diets deficient in vitamin E which are already naturally deficient in selenium (Se). Such barley, when supplemented with other essential minerals and vitamins plus either soya bean protein or urea, will allow moderate growth (0.7 kg/day) when fed to young ruminants.

As the initial part of a research programme to assess the importance of geochemical factors in livestock production, a survey has been conducted on the copper (Cu) content of whole blood samples from cattle analyzed by the Veterinary Investigation Service over the period 1977-1980 inclusive. The area covered was restricted to England and the Welsh borders; data for Wales were not included, as they were not of a strictly comparable form, being based on plasma rather than on whole blood analysis.

Observations were made, from 1970 to 1975, of the liver copper (Cu) levels of lambs reared on various feeding regimes and of lambs which were stillborn or died within the first 7 days of birth in what was considered to be a normal healthy flock.

Artificially reared Finnish Landrace × lambs were fed on reconstituted milk substitute and a concentrate containing 4 and 8 mg Cu/kg DM, respectively. Liver Cu levels were determined when lambs were slaughtered at 4/5 months of age. In one group, liver Cu levels varied from 500 to 1600 mg/kg DM without any evidence of Cu toxicity in any lambs, whilst, in another group, levels ranged from 50 to 600 mg/kg DM.

The conventional criteria of copper (Cu) status in ruminants, liver and blood or plasma Cu concentrations, show rapid reductions during depletion while the animal remains clinically normal. Criteria which change less rapidly in response to depletion might be more closely correlated with clinical and sub-clinical condition. Among such criteria are superoxide dismutase (SOD), which occurs as Cu- and Zn-containing enzyme in erythrocytes, and hair or fleece Cu. We have examined the temporal relationships between these different criteria of Cu status in two experiments, in which steers and lambs had been depleted of Cu, to assess their diagnostic value.

Although it is well established that changes in dietary iron (Fe) intakes can influence copper (Cu) metabolism in animals, little attention has been paid to their importance in causing Cu deficiency in ruminants. The realization that silages frequently contain large amounts of Fe, mainly as a soil contaminant, prompted us to assess the potency of Fe as a Cu antagonist and to compare its effects with those of molybdenum (Mo).

In one experiment, 27 male Friesian calves, aged about 3 weeks, were allocated to three treatment groups and given a milk-substitute ration containing 2.5 mg Cu and 50, 250 or 500 mg Fe (as FeCl3.6H20)/kg DM. Liver biopsies were taken after 8 weeks and analyzed for Cu and Fe. As expected, tissue Fe increased by as much as 50% with increasing Fe intake. However, there were no effects of Fe on hepatic Cu retention in these pre-ruminant calves (liver Cu was 343, 372 and 390 mg/kg DM, respectively: SEM = 40).