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Navigating the Mineral Minefield
By P. Bone & S.B. Telfer,
There are twenty-three identified mineral elements that are essential but possibly toxic, which interact with one another in a soil, plant, animal relationship as illustrated by Dyer (fig 1). Handling the problems that arise from these complex interactions can feel like treading through a minefield. Two of the most important interactions when considering fertility and reproduction, are iron/molybdenum/sulphur and selenium/iodine.
Influences on Fertility and Production.
Fertility and production can be influenced by management, forage, energy, protein, soil, disease and even the water supply. The effects of management, energy, protein and disease are well documented, but less is known about the forage, soil and water connection. Problems arise from diet, soil and water in relation to their mineral composition and the interaction of those minerals in the animal. Looking at your cows can provide information about the occurrence of both good and harmful interactions; however, not all of these problems will be visible.
Interactions between iron, molybdenum and sulphur
Rumen microbes take up these elements from the food and water consumed by the animal and produce iron/sulphur and molybdenum/sulphur (thiomolybdate) compounds. Both compounds try to react with copper. In terms of quantity, iron intake is likely to be significantly more abundant than molybdenum and probably ten times greater than copper; hence the formation of iron/sulphur/copper compounds is greater and the amount of copper in the rumen is depleted to a negligible level. This leaves the thiomolybdate (molybdenum/sulphur) molecules unable to find copper to react with. The consequence is that the thiomolybdate is absorbed into the animal and moves into the blood stream. It seeks out active copper molecules in the body, usually within enzymes, deactivating and poisoning them – i.e. thiomolybdate toxicity. The outward sign of this deactivation of copper enzymes is the clinical symptoms that have been wrongly attributed to a “deficiency” of copper: spectacles, coat discolouration etc (fig 2). The clinical diagnosis, however, would show that the copper levels (blood and liver) are normal and that as well as outward visible symptoms, the affected animals also show poor oestrus behaviour, reabsorption of embryos and reduced energy utilisation seen as reduced milk yield and/or growth rate. Black cows show coppery coloured coats, 'spectacles' around the eyes and bare ears when suffering from thiomolybdate toxicity. These symptoms are usually, incorrectly, attributed to copper deficiency; high levels of copper supplement could prove fatal.
The prevention/cure of thiomolybdate toxicity is achieved by supplying copper into the rumen to leave enough available for both the iron/sulphur molecules and the thiomolybdate to react with. The copper must be available in the rumen in the first instance to block the passage of thiomolybdate into the animal. Unfortunately, a misleading and erroneous message has been propagated that fertility can be improved by feeding more copper in the diet and that the effect is achieved by the animal absorbing this extra copper into its body.
The work being carried out by Mike Kerby of Delaware Vets (Table 1) illustrates how this feeding of extra copper is resulting in severe problems. Farm S lost a significant number of cows to copper toxicity (excess copper in liver - Table 1), but the animals are still suffering from the clinical symptoms seen in Figure 2 which is confirmed by the blood analysis from University of Nottingham (NUVETNA). Low CP/PL ratios and depressed SOD activities (Table 1) confirm the presence of thiomolybdate toxicity. The results from Mike Kerby's work show that excessive absorption and retention of copper in the body will not prevent the animals suffering from thiomolybdate toxicity – the symptoms, previously defined as those of “copper deficiency” are still evident!
The copper has to be available in the rumen to stop the thiomolybdate toxin passing into the bloodstream and forms of copper such as copper oxide, dietary protected copper and injectable copper cannot fulfil this role. The unique form of soluble glass copper in CoseIcure and Cosecure provides a constant supply into the rumen to neutralise the toxic thiomolybdate that is produced continuously by the microbes. Improved fertility has been seen in cattle treated with Cosecure compared to multi-element treatments that utilise copper oxide (needles or matrix boluses) and copper injections (Black & French, 2004 Vet Record, page 652) and New Zealand suckler cow trial 2007.
Iodine is key in maintaining a normal metabolic rate through its role in producing the hormone thyroxin (T4) from the thyroid gland. An iodine problem usually arises in the first instance in young calves at birth or soon after. However, this does mean that the cow herself may have been short of iodine or that there had been an adverse interaction between elements. The common clinical signs that might indicate an iodine problem are hairlessness in newborn calves, weak, sickly or dead calves, which on post mortem reveal large goitrous thyroid glands. The presence of a goitre is the only clear indication of an iodine deficiency.
Lack of selenium and vitamin E can cause problems that are well recognised, although the mechanisms differ between the element and the vitamin. The symptoms most frequently encountered are those of retained placentas, calving difficulties and young calves and lambs being stiff and dopey, with the larger animals frequently dropping dead. Less obvious is the impaired immune function, although this can still cause significant losses.
Selenium and Iodine interaction
An effect exclusive to selenium and unrelated to vitamin E, is the connection between iodine metabolism and this element. In order to produce active thyroxin in the thyroid gland, a selenium dependent enzyme is necessary. Therefore, a lack of selenium reduces thyroxin levels and can result in calves seeming iodine deficient. These supposed iodine deficient calves have no goitres (enlarged thyroids) and the cure is supplemental selenium, not iodine.
Negotiating your way through this mineral minefield requires patience and care.
Clinical signs are without doubt helpful, but they need proper interpretation. The lack of the trace minerals selenium (along with vitamin E) and iodine, as well as the iron/ molybdenum/sulphur interactions can have significant deleterious effects and adverse financial consequences on the fertility and productivity of ruminant animals.
The VLA has reported a very low incidence of true iodine deficiency in cattle in the UK; therefore, it is essential that diagnosis is correct and it has to be established whether problems are due to the interactions between the elements or due to deficiencies. A full mineral analysis of forage, feed and water is a good starting point, especially in relation to thiomolybdate toxicity as the levels of iron, molybdenum, copper and sulphur will give a good indication of the severity of the problem. This information will also be necessary in defining the mineral input necessary to aid in the correction of the problem. Where thiomolybdate toxicity is diagnosed the in-feed dietary mineral is an essential ingredient, but the animals also require supplemental copper, which will be available in the rumen constantly. Therefore, as part of the prevention and/or cure of these mineral imbalances Telsol offers advice on dietary mineral supplementation as well as Cosecure boluses: copper, selenium and cobalt and now, where required, CoseIcure boluses that have iodine in addition to the other three elements.
For further information contact Peter Bone (Tel: 07785 368591) or Stewart Telfer (0113 226 0666)