Neville Suttle talks to Veterinary Record about copper supplementation in cattle feed.
COPPER has a diverse range of biological roles in animals; there are many copper-dependent enzymes that are involved in energy metabolism, immunity, iron metabolism and coat pigmentation to name a few. Neville Suttle, of the Moredun Foundation and co-author of a recent paper1 in Veterinary Record that followed a herd of cows with high winter mortality and high liver copper, explains: ‘In the UK, grass, hay and silage are widely but erroneously believed to be low in copper and complimentary feeds are often supplemented with the essential element. Without supplementation, forages will commonly contain 5 to 12 mg Cu/kg DM, cereals 4 to 6 mg Cu/kg DM and protein sources 10 to 40 mg Cu/kg DM.’
The level to which complimentary feeds should be supplemented with copper is the subject of much debate. The difficulty lies in estimating the available copper in a complete diet consisting of components differing widely in copper concentration and not knowing how they interact with each other. Copper toxicity is becoming more common in the UK because copper availability is often underestimated and requirements are overestimated. EU regulations set the maximum permitted level for copper in complete cattle feeds at 35 mg Cu/kg at 88 per cent dry matter. The Advisory Committee on Animal Feedstuffs (ACAF) suggests that under normal conditions, and in the absence of antagonists such as molybdenum and sulfur, which reduce copper availability, the maximum addition should be 20 mg Cu/kg dry matter.2
In the winter of 2005/06, 13 of 46 female calves in a herd died at less than one month old. They had developed chronic, low-grade diarrhoea and failed to thrive, despite good quality care. Samples that had been submitted to the Edinburgh Disease Surveillance Centre (EDSC) detected Cryptosporidium and coronavirus in two samples but this did not explain the high mortality. Three of the later casualties were submitted for postmortem examination, which revealed high copper concentrations in the liver. At this point, the lead investigator Archie Hunter from the EDSC, sought advice from Dr Suttle, who recommended that copper supplementation be reduced and surveillance continued. Three healthy culled newborn male calves were promptly submitted for postmortem examination to establish a baseline for liver histopathology.
Inspection of the feeds showed that mineral supplements were providing approximately 60 mg Cu/kg DM for milking cows and 41 or 46 mg Cu/kg DM for dry cows, both exceeding the maximum permitted level. Despite there being no typical clinical signs of chronic copper poisoning, supplementation was reduced to 45 mg Cu/kg in milking cows and later to 16 mg Cu/kg. For dry cows, the supplementation was reduced to 28 mg Cu/kg. Calf mortality fell the following winter (2006/07) but rose again the next (2007/08). All supplements were withdrawn in 2008, including those in the milk substitute and creep feed, which had 10 and 35 mg Cu/kg added, respectively. Mortality once again dropped and stayed low for the following three winters, at which point the study ended.
Although many histological abnormalities were found in the livers of casualties, most were seen in equal abundance in the culled, healthy newborn calves, suggesting that chronic exposure of the unborn calf to high levels of copper caused changes in the livers of healthy calves. Other research has shown that depletion of liver copper can be exceedingly slow after the removal of copper supplements from mixed diets for lactating cows3; the results for culled newborn male calves in 2011 indicated that one cow still passed on high liver copper to her calves, five years after withdrawal of copper supplements began. If excess copper was still causing damage, where was it coming from? One possibility is that calf feeds were being continuously medicated with coccidiostat to control calf scours. The medication was killing off rumen protozoa, which normally keep copper availability suppressed by generating sulphide, a powerful copper antagonist; therefore, medicated calf feeds with no added copper could still provide too much copper.
Although association is not proof of causation, it seemed plausible that the reduction in copper supplements reduced calf mortality and liver disorders in young unweaned calves in this herd. The authors reasoned that the combination of high copper status and low-grade enteric infections were responsible for the history of liver disorder and calf mortality at birth.
As the extent of over-supplementing becomes more apparent in the UK, Dr Suttle commented: ‘I would like to see recommended rather than maximum permitted levels becoming the benchmark for copper supplementation and retrospective studies of calf mortality in previous outbreaks of copper poisoning, like the one reported recently in dry Jersey cows.’ 4, 5 He also emphasises that requirements vary, depending on levels of molybdenum and sulfur in the environment, which quench copper availability: ‘Fixed rate supplementation to cover worst case scenarios is asking for trouble with a cumulative poison such as copper.’
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