When Using Zinc to Prevent Facial Eczema,
Remember Its Effect on Copper
The value of zinc in protecting against facial eczema (FE) is well known. High level dosing with zinc (usually as zinc oxide) is commonly used to prevent the problem in dairy cows. But one of the downsides of high zinc dosing is that it can interfere with copper uptake and storage. And this tends to happen just as cattle need to be accumulating liver copper reserves to see them through the winter. So if you have to drench with zinc over the FE period, how do you manage this antagonism between zinc and copper?
The antagonism between zinc and copper differs from that of molybdenum, sulphur and iron. Molybdenum, sulphur and iron, form insoluble complexes with dietary copper which prevent the copper being made available for transport across the gut to the blood stream. By contrast, zinc competes with copper for sites of absorption on the gut wall, rather than tie it up in insoluble complexes. High zinc intake can virtually block any absorption of dietary copper.
It is often recommended to discontinue copper supplementation while drenching with zinc for FE. This is partly because it’s seen as a waste of copper, but also because of concerns that free copper ions in the liver may increase the toxicity of the FE toxin, sporidesmin.
But such recommendation does not help maintain liver copper reserves as winter approaches. During a long FE risk period, cattle can be deprived of copper just as their demand for the mineral is increasing.
There are three options to counter this dilemma. The first is to ensure the herd’s liver copper reserves are adequate before high zinc dosing commences. This may require appropriate supplementation to ensure average liver levels are in the range of 500-1500 umol/kg by January. These reserves will carry them over the zinc drenching period until supplementation can be resumed.
The second is to maintain supplementation during zinc drenching, but with a form of copper that is not markedly antagonised by the zinc. Only copper in the amino-acid complex form seems to offer this characteristic. Copper is primarily absorbed from the gut linked to an amino acid. So too is zinc, and so competition for absorption sites can occur. But copper that is already complexed to an amino acid provides an advantage for its absorption compared to zinc in the form of zinc oxide or zinc sulphate. The zinc ions from the oxide or sulphate must first dissociate, and then find a free amino acid to link to within the gut. As copper complexed with an amino acid is already in the form required for absorption, it can successfully be absorbed despite the high inorganic zinc levels present. Research conducted during last year’s FE period indicates that copper amino acid supplementation during high zinc dosing does not seem to enhance the toxicity of sporidesmin.
The third option is to check herd liver levels immediately after the FE risk period and supplement accordingly, either with appropriate oral supplementation, copper needles, or injection of copper.
The main point is to recognise that high zinc dosing can markedly affect copper uptake, especially from inorganic salts such as copper sulphate. If prolonged zinc dosing is necessary to protect against FE, then you should consider the impact this may have on copper levels. If ignored, inadequate copper levels over winter may jeopardise the health and well being of the developing calves as well as their dams, and contribute to health problems at calving.
By the way, only liver biopsies give an accurate measure of liver copper reserves. Estimating copper reserves from blood samples can be very misleading. And it is preferable to take biopsies from the milking herd rather than to gauge levels from the livers of cull cows. This is more precise, and can cost little more than getting information from cull cows. |