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Selenium in Animal Production

  • Dr. M K Hill. Dean of the Faculty of Rural Science. UNE Armidale NSW (from Mohair Australia Newsletter Vol 7 # 3 Sept 1998 Technical Issues)

Selenium is an interesting non-metalic element (atomic weight 79) which occurs in a variety of forms and is probably better known for its use in Xerox copiers, light metres, electrical equipment and in the manufacture of glass. It has the curious property of being photoconductive, which means its electrical conductivity increases when light is shone on it, and one could be forgiven for thinking that such a substance would have little involvement in the nutrition of animals.

In the 1930's however, it was finally realised that the peculiar condition of "alkali disease", which causes loss of hair and hoof deformities in horses on the rangelands of South Dekota, Wyoming and Nebraska, was due to an excess of selenium in fodder plants. For the following 25 years, interest in selenium as a component of the diet focussed on its toxic effects and it was not until 1957 that it was, in fact, recognised as an essential ingredient of the diet.


The discovery that selenium is an essential element in the nutrition of animals was made in the United States by workers who sought to explain why rats, fed brewer's yeast, did not develop a liver disease seen in those fed other types of yeast.

At about this time, New Zealand scientists began to focus their attention on a newly-recognised, widely-distributed disease of lambs, called "white muscle disease". In 1958, following further American studies on selenium, dosing trials were commenced, and a major advance in animal nutrition was initiated.

Since that time selenium has been shown to affect sheep, cattle and most probably goats in a variety of ways. It was shown to be involved in the prevention of white muscle disease, in fleece growth, in fertility, in the survival and growth of the young and even in the loss of molars and occasionally, incisor teeth. In chickens, rats and pigs various expressions of selenium deficiency have been firmly established and in man, it has been suggested that an insufficiency of selenium might be involved in such diverse conditions as Kwashiorkor (a quite common form of malnutrition in children in parts of Africa), cancer, and in "bad backs".


Of the dozen or so "trace elements" known to be required in minute amounts in the diet of grazing animals, only four are likely to become deficient in the diet - iodine, copper, cobalt and the latest addition, selenium. It is an odd quirk of nature that the concentration of each of the others in plant material never falls below that required in the diet of animals. There is still much to be learned about mineral metabolism in animals and this is particularly true for selenium.

We do, however, now have a fairly clear picture of selenium deficiency in the diet of sheep and it is likely that time will reveal a similar picture in the goat. The various expressions of selenium shortage can be summarised as follows:

  1. White Muscle Disease (Muscular Dystrophy).

    White Muscle Disease (WMD) is most commonly seen in lambs between two and six weeks of age after forced exercise, such as that associated with marking. Animals walk stiff-legged, with an arched back and mortality may reach levels of 20-25%. Unlike arthritis (which commonly occurs 9-10 days after marking), symptoms appear within 24 hours of stress and joints are not hot and swollen. At post-mortem, muscles of the heart, limbs, shoulders and back show varying degrees of degeneration with whitish streaks of extensive calcification being evident, particularly in the left ventricle of the heart - hence the name "White Muscle Disease".

    It is now apparent that the condition can occur at any stage during the first year of life, indeed it may occur prenatally. It is, however, very rare in mature animals. There are, nonetheless, three periods during the first year of life when the risk of WMD is apparently greatest. The first is the neo-natal period. This so-called "congenital WMD" describes a condition in which the young die within the first few days of post-natal life, exhibiting the usual muscular degenerative changes. The second period involves the 3 - 6 week-old lambs previously described, and the third involves hoggets between 9 and 12 months of age. It is probable, however, that this apparent age sensitivity is nothing more than a reflection of pasture conditions coincident with these ages and that the disease may affect as animal at any stage during the growth phase, dietary conditions permitting.

    The disease, in one form or another, has now been recognised in most sheep producing countries of the world and is widely distributed in Australia, having been first recognised in Victoria in 1954. The mortality and debility associated with WMD represents serious economic problems to producers and for many years the only known preventive measure was the administration of Vitamin E, which was used commercially before the advent of selenium in 1957.

  2. Selenium Responsive Ill-Thrift.

    Curiously, a varying proportion of lambs in a selenium deficient flock do not exhibit the classical symptoms of WMD and in some cases the proportion may be so high that the WMD problem goes unnoticed. Growth rate and general thrift may, however, be adversely affected, with no apparent cause. Selenium deficiency can, therefore, vary in degree from a total imperceptible reduction in rate of growth to a severe deficiency associated with high levels of mortality. "Ill-Thrift" - depressed growth of young without obvious cause - is a major problem in all forms of animal production and it is now evident that selenium contributes importantly to this problem in grazing animals, particularly after weaning.

  3. Fertility.

    While adult ewes rarely develop WMD, they are, nevertheless, susceptible to selenium deficiency, which manifests itself in an increased incidence of barrenness. In some parts of New Zealand, later shown to be selenium deficient, lambing percentages had been observed to decline over a period of years following a phase of pasture development and only the occurrence of WMD among the lambs which managed to survive, provided some clue as to the cause. It was soon apparent that selenium deficient ewes cycled and mated normally but the embryo failed to implant within the uterus. Embryonic death, 3-4 weeks after joining, perhaps repeated in a second or third cycle thus resulted in an incidence of barrenness proportional to the degree of the deficiency.

    Selenium has also been shown to affect the incidence of twinning among females. In this instance, the effect is likely to be an indirect one, operating through the known association between ovulation rate (hence the lambing percentage) and live-weight at the time of mating. Selenium administered to deficient stock, particularly during their first year of life, could significantly increase live-weight at first joining, hence the apparent stimulatory effect on the incidence of twinning.

  4. Fleece Growth.

  5. Selenium has also been shown to significantly improve fleece weight and fleece quality in deficient animals of all ages. These benefits are likely to arise from direct and indirect influences, the indirect effect being mediated through an increase in live-weight, the direct effect through an influence on follicle function. The fleece is probably one of the most sensitive monitors of the adequacy of selenium in the diet, though variation in fleece weight within a flock makes this difficult to validate in experimental work.


Not surprisingly, research into the biochemical role of selenium has lagged behind demonstrations of its importance in nutrition but it is clear that selenium is involved in enzyme systems, including one called glutathione peroxidase. This enzyme influences a variety of functions within the organism. It is this wide range of processes that explains the diversity of symptoms of selenium deficiency in livestock.

Recent developments in the measurement of these enzymes in blood give promise of a simplifying procedures for recognising selenium deficiency in animals in Australian agriculture.


The primary cause of selenium deficiency in growing livestock is a deficiency in selenium (Se) in the pasture. Selenium deficient areas in Australia have not yet been adequately mapped and while light soils and lush legume-dominant pastures are most often associated with selenium responsive conditions in animals, there are many exceptions.

Pasture improvement programs have certainly aggravated the position. Pasture species capable of very high rates of growth, the use of sulphur-containing fertilisers (which tend to suppress selenium uptake by plants) and high stocking rates (which tend to result in reduced availability of selenium in the soil) have all exacerbated the problem.

Climate also exerts a very significant effect on the incidence of selenium deficiency, mainly through the influence of rainfall on pasture growth. In conditions of rapid growth, the rate of selenium uptake tends to fall, and later, as the plant grows older, selenium becomes further depleted, hence problems may arise both during the active phase of pasture growth and later, when it matures.

For these reasons selenium deficiency in livestock is often spasmodic, perhaps appearing only in extraordinary good seasons. The combination of factors which have been described help to explain the rather perplexing situation in which poor animals are seen in the midst of abundant, high-quality pasture.

Much work is still to be done to define selenium deficient areas in Australia and in marginal areas it will always be difficult to predict seasons in which problems are likely to arise. The only certain way to identify selenium deficiency is to conduct a simple experiment in which some (preferably 20 or more) animals are treated and some are left as "controls" and measuring their relative performance over a period of 8-12 weeks, preferably during a period of rapid pasture growth.


Selenium is potentially an extremely toxic substance and must be administered with care. Normal pasture contains about 0.06 parts of selenium per million of dry matter which, assuming an intake in sheep and goats of one kilogram of dry matter per day, represents an intake of 22 milligrams of selenium per year. The fact that this represents about one quarter of the amount of iodine consumed in a year underlines the minute amount of selenium needed by grazing livestock.

Its toxicity, together with problems of even distribution on pasture, restrict the incorporation of selenium into fertilisers and there are only three particular ways of administering selenium to animals - oral dosing, injection or administration of heavy pellets with lodge in the rumen and dissolve over a period of months. Of these, perhaps the simplest and most convenient is drenching, using a solution of either sodium selenate (Na2 SeO4. 10H2O, M.Wt. 369) or sodium selenite (Na2SeO4, M.Wt. 172). The normal dose rate for sheep, beyond 12 weeks of age is 5 milligrams of Se. Hence a 100 gram bottle of sodium selenate (costing approximately $10 in 1970) would suffice for 4,280 doses at 0.23c each. Thus 4.6g of sodium selenate or 2.2g of sodium selenite, dissolved in one litre of distilled water, administered at the rate of 5ml per dose, provides 200 doses each with the required 5mg of Se. One millilitre of this solution is recommended for lambs less than 12 weeks of age.

The time at which selenium should be administered to sheep in selenium deficient areas can be summarised as follows:-

  1. Five milligrams of Se to ewes one month prior to joining.
  2. Five milligrams of Se to ewes one month before lambing.
  3. One milligram of Se to lambs (or 5mg to ewes) at marking (at four weeks).
  4. Five milligram of Se to lambs at weaning (16 weeks) and further doses 3, 6, 9 and 12 weeks later as necessary up to joining age.

Such a program of dosing could be expected to prevent all conditions of selenium deficiency described. If dosing times are made to coincide with other handling operations, labour costs can be reduced and, in deficient areas at least, very profitably.


Although some Angora producers in known deficient areas have used selenium in their husbandry, there is no good research data available on the effects of selenium on Angora goats. Therefore caution should be used in applying sheep research findings to the goat. If you decide to use selenium, follow the routine above closely and make sure beforehand that you are in an area thought to be selenium deficient.

(Editor's note. Sodium Selenate and Selenite are class S7 drugs - extremely toxic and can only be supplied in original sealed containers to vets and stock feed manufacturers. At very least you will need a veterinary prescription to obtain the chemicals. Selenium is otherwise available in vaccines, some worm drenches and as rumen bullets.)

© 2000 Mohair Aust Ltd