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Trace element requirement of goats

  • Christopher Halpin, Scientific Officer, Department of Agriculture, "Attwood" Veterinary Research Laboratory, Westmeadows. Vic. 3047.

Animal tissues and feeds contain mineral elements in varied proportions. At present healthy livestock are believed to require approximately 22 essential minerals and these are classified as macrominerals or trace elements on the basis of the quantities required.

The macrominerals - required gram amounts - are important for structural purposes (calcium, phosphorus and sulphur), in the maintenance of osmotic balance (sodium, potassium and chlorine), nerve transmission and enzyme activities (magnesium). The trace elements - required in microgram amounts - act primarily as catalysts in enzyme systems (manganese, copper, zinc, molybdenum, selenium), hormones (iodone) and vitamins (cobalt).

Many producers are very conscious of the mineral requirements of their livestock. In the true perspective trace element deficiency is a minor cause of lost productivity in grazing livestock in Victoria when compared to protein and energy deficits, parasitism and inadequate shelter. However, in some districts specific deficiencies of iodine, selenium, cobalt and copper produce disorders and deaths in young stock and losses to individual producers have been significant.


Iodine is converted into the essential thyroid hormones with the thyroid gland. A severe deficiency of iodine causes this gland to swell producing a "goitre". Recently it has become recognised that low or marginal iodine nutrition of goats is a significant problem in the southern and mountain districts of Victoria. Iodine deficiency is endemic to the high rainfall districts of Victoria, and similar deficiencies occur along the Great Dividing Range throughout Eastern Australia. Goats seem to have a higher requirement for iodine than other livestock.

Iodine deficiency is only a problem in newborn kids. Adult goats appear able to tolerate seasonal deficits in iodine supply by using reserves stored in the thyroid gland. This reserve is not available to the developing foetus. Thyroid hormones are essential for growth and development of the foetus, particularly the brain, lungs, heart and hair follicles, and contribute especially to survival of the newborn kid. Iodine deficiency makes newborn kids very susceptible to cold, wet weather and mortalities may be very high.

Recent research at the Attwood Veterinary Research Laboratory has demonstrated that iodine nutrition of sheep and cattle has a marked seasonal cycle in Victoria. Intake of iodine from pasture is lowest in late winter when the requirements of pregnant animals are at a peak. Thus it has become a standard recommendation that pregnant does grazing in high rainfall areas receive a. drench of supplementary iodine once or, in some cases twice, during the last two months of their pregnancy. Treatment of affected kids with iodine or thyroxine tablets is rarely useful and it is far more effective to ensure adequate iodine nutrition of the foetus.

Drenches: The drench is made up by dissolving 28 gm of potassium iodide in one litre of water. Each doe should receive 10 ml. Iodine is highly volatile and it is important to mix the drench just before use. lodised salt licks and feed supplements containing iodine are not recommended in most situations because some goats always avoid licks and it is impossible to accurately gauge intake with these systems. Drenching is cheap and accurate and can even be combined with some worm drenches, although it is wise to check this with the manufacturer.

Injections: lodised oil injections have been used to prevent iodine deficiency in New Zealand quite successfully. The product is not registered for use in Australia.

Iodine deficiency may also be induced by goitrogens - substances within the feed which inhibit the utilization of dietary iodine. Goitrogens have been detected in some legumes and forage crops, but are considered unlikely to be a significant cause of goitre.


Selenium deficiency has been associated with a range of disorders in grazing animals. In its most serious form it causes white muscle disease, a myopathy which affects kids, lambs, calves and foals in some higher rainfall areas of Victoria.

Selenium deficiency has also been associated with illthrift and poor wool growth in sheep and reduced resistance to disease in a number of species. In New Zealand, selenium supplementation has resulted in significant improvements in lambing performance in low selenium areas. Similar responses have not been observed in a number of trials in Victoria.

Other factors are significant in the induction of white muscle disease: stress, mustering, increased levels of unsaturated fatty acids in spring pastures and poor vitamin E nutrition have been directly involved. Both selenium and vitamin E have roles in the prevention of muscle damage by oxidants produced during metabolism. White muscle disease occurring in weaner lambs grazing cereal stubbles, or dry autumn pastures, is responsive to vitamin E but not selenium supplements.

Low selenium areas of Victoria include the acid oils on and about the Great Dividing Range, particularly the Central Highlands, and the high rainfall areas of the west and south-east coastal fringe. It must be emphasized that selenium nutrition is subject to marked variation between years, between seasons, and even between soil types within farms and paddocks: specific regional information is available from your State Department of Agriculture Offices.

Selenium deficiency can be prevented by a range of treatments.

Drenches and Injections: Kids affected with white muscle disease are treated with intramuscular injections or oral drenches of selenium. Selenium injections can be administered with pulpy kidney-tetanus vaccines and mixed preparations have been registered commercially for use in sheep, but not as yet in goats. Selenium can also be combined with some worm drenches. It is wise to check compatibility with the drench manufacturers and these mixtures should always be used immediately. It is important that an assessment of selenium nutrition be made before animals are treated because selenium compounds are toxic. Selenium in excess is a poison and is therefore obtained only on veterinary prescription.

Bullets: Selenium bullets are administered to individual animals, lodge in the rumen and should provide the small requirements of selenium for the life of the animal. However, some batches of commercial bullets were shown to provide adequate selenium for only a few months.

Topdressing: A mixture of selenium and superphosphate from Pivot Fertilizers, Selecote, has now been registered for use in Victoria and similar products may be available from your fertilizer supplier. This has proved a useful alternative method of supplementing grazing livestock in low selenium areas. SelenIum in the fertilizer is encapsulated within water-soluble prills, which readily break down upon application to pasture. Selenium priIls penetrate the pasture canopy and must be absorbed back through the root system to increase herbage selenium concentrations. With the registered fertilizer mixtures there is very little possibility of animals receiving a toxic dose. The continual supply of organic selenium for 6 months, combined with reserve capacity of body tissues ensures adequate selenium nutrition for 12 months with the fertilizer; selenium drenches and vaccines are only effective for around 3 months.

Selenium deficiency mostly affects young animals in spring. It is therefore recommended that the fertilizer application be timed so as to optimise the selenium nutrition of these animals; an autumn application will benefit the developing foetus and ensure protection during spring.


Ruminant animals are unique in their ability to supply their own requirements of essential vitamin B12. In a classic example of symbiosis, microorganisms within the goat rumen utilize dietary cobalt to synthesize vitamin B12 which is then available to the host animal. Vitamin B12 is an essential coenzyme in the major pathway through which propionate and several amino acids are metabolized. Propionate, derived from rumen fermentation of plant celluloses, is the main precursor of glucose in the ruminant. The clinical signs of cobalt deficiency in ruminants are in fact, due to reduced tissue vitamin B12 concentrations and a breakdown of this glucose pathway.

Cobalt deficiency in ruminants causes unthriftiness, "weepy" eyes, severe wasting and eventually death if sufficiently severe and prolonged. Mild cobalt deficiency is easily confused with unthriftiness caused by underfeeding, heavy worm burdens or selenium-responsive illthrift. Cobalt deficiency can only be accurately diagnosed in livestock by tests for vitamin B12 in blood or tissues.

In Victoria, cobalt deficiency has been identified in sheep along the coastal fringe of western Victoria and southeast Gippsland, and isolated areas further inland. It commonly occurs also in coastal areas in other States. The disease has not been recognized in goats, but more recent studies indicate that specific areas of the southern mountain districts particularly, provide only marginal dietary cobalt for goats. In low cobalt areas, lambs are most sensitive to deficiency followed by ewes, calves and cows in that order. Severe signs are seen only rarely in cattle in Victoria. Cobalt deficiency can be cured and prevented by providing supplementary cobalt or vitamin B12:

Injections: Vitamin B12 must be given by injections, vitamin B12 drenches are not recommended. A 1-2 mg dose should last 2-3 months and is the preferred method of treatment.

Drenches: Cobalt sulphate must be given as a drench, and can be combined with some anthelmintics and other trace elements, copper and selenium. It must be administered weekly to be effective. A suitable drench recipe dissolves 15 g cobalt sulphate in 1 litre of water: Give goats 2 ml. Large doses of cobalt are poisonous.

Bullets: Cobalt bullets are administered to individual animals, lodge in the rumen and continuously release the trace quantities of cobalt required. Recent evidence indicates that bullets are effective for only 14 weeks in sheep.

Topdressing: Cobaltised superphosphate is a suitable method of treating grazing goats. It is not definitely known if autumn applications always provide sufficient cobalt for the following spring’s kids and close monitoring is advised. Pastures can also be sprayed with dilute solutions of cobalt sulphate (140 g/ha) as an interim treatment.

Licks: Cobalt salt licks should contain up to 100g/t cobalt sulphate and should be provided in the ratio of 1 block per 50 goats. Some animals, usually those most in need, fail to lick the blocks and do not get their requirement.


Copper is essential for optimal pasture growth, as well as animal health, and is unique for its interactions with other essential element. Excesses of both molybdenum and sulphur can induce copper deficiency in animals receiving an otherwise adequate dietary copper concentration.

Copper deficiency is most remembered for its association with "steely" wool in sheep - the wool harsh-handling, unevenly crimped and is weaker than normal. Deficiency may cause a variety of other symptoms in sheep and cattle - anemia, illthrift, scouring, bone abnormalities, and reproductive disorders - some of which have been detected in goats receiving inadequate dietary copper.

Copper toxicity is also a significant animal health problem, particularly in sheep. Toxicity can be induced in 3 ways:

  • Overdosing with copper supplements.
  • Prolonged grazing on clover-dominant pastures.
  • Prolonged grazing on heliotrope (contains a liver toxic alkaloid).

Extreme caution should be used with copper supplementation, and any producer who suspects that stock are suffering from copper deficiency should seek specialist advice from a veterinary practitioner or the Department of Agriculture.

Copper is more available to livestock from dry pastures and hay. Hence, copper deficiency in Victorian livestock has a definite seasonal cycle. Problems are worse in the winter-spring period and are often resolved over summer-autumn even with no supplementary copper.

Historically, copper deficiency has often occurred in conjunction with cobalt deficiency. - "Coast Disease" - and many affected areas have received copper fertilizer applications. In contrast to cobalt however, copper fertilizers appear to provide adequate pasture copper for many years (at least 15 years according to one source) and problems of copper deficiency in livestock in more recent times are usually introduced or secondary to excessive intakes of molybdenum, sulphur and possibly other elements such as iron. Molybdenum toxicity (molybdenosis, molybdenum-induced copper deficiency) may be due to naturally occurring molybdenum pastures (e.g. peat swamps), can be a result of application of molybdenum fertilizers to pasture and has been associated with the application of lime fertilizers to pasture to treat soil pH.

In districts that have shown any signs of copper deficiency in goats, cattle or sheep, advice should be sought from the Department of Agriculture on need for copper fertilizer or copper treatment of livestock, especially if contemplating the use molybdenum to boost pasture production.

Topdressing: The most practicable means of control of copper deficiency in goats is by topdressing pastures with fertilizers that are fortified with copper oxide. Copper is normally applied at from 0.5 to 2 Kg per hectare every one to seven years respectively on part or all of the farm.

Injections: An organic copper injection (Cujec) which lasts for some months is available for sheep, but its safety in goats is uncertain. Problems associated with injectible copper compounds have included abscesses at the site of injection due to poor technique, and toxicity. Injectible copper therapy is suitable for both primary and conditioned (i.e. molybdenum induced) forms of copper deficiency, and a single treatment provides adequate copper for 2-3 months.

Drenching: Oral drenching with an aqueous solution containing copper sulphate is useful in primary copper deficiency only. Copper sulphate may be mixed with levamisole-based and oxfendbendazole anthelmintic drenches, and should be used within 24 hours. Copper is not compatible with many other drenches. With primary copper deficiency, a single oral treatment is adequate for 1-4 weeks. However for copper deficiency due to excess molybdenum, weekly treatments may be required, making form of treatment generally impractical. Copper-containing salt licks may be used where individual animal treatment is impractical.

Treatment over the period from mid-winter to spring is usually sufficient for all but the most severely deficient animals. Treatment should be aimed at providing adequate copper nutrition for at least six weeks prior to kidding.

New treatments such as copper oxide needles and glass bullets have been developed and are being tested prior to commercial release.

© 1985 A.C.G.A.