Mortality, hepatopathy and liver copper concentrations in artificially reared Jersey calves before and after reductions in copper supplementation

Abstract

High winter mortality (28 per cent) in female Jersey calves (<one month) characterised by mild hepatopathy and enteropathy was investigated. Liver copper (Cu) was very high in casualties, but also high in culled, newborn males (19.2 ± 1.54 and 12.0 ± 2.74 sd mmol/kg dry matter (DM) respectively). Serum glutamate dehydrogenase (GLDH) was >80 IU/l in healthy females aged 3-24 weeks, and correlated with serum aspartate transaminase (AST). Copper supplementation of total mixed rations during lactation was excessive (40-60 mg added Cu/kg DM) and reduced to 16-28 mg Cu/kg, but supplementation of milk replacer and creep feed (10 and 35 mg added Cu/kg DM, respectively) continued. The syndrome recurred two years later, and liver Cu remained high in casualties (13.6 ± 2.6) and culled cows (6.38 ± 2.38 mmol/kg DM) prompting withdrawal of all Cu supplements. Mortality remained low (6-9 per cent) thereafter. Three years after removal of all Cu supplements, six culled newborn were examined postmortem; five had normal liver Cu (4.5 ± 1.73), but a sixth had 11.65 mmol/kg DM. In live, healthy calves (1-6 months old) sampled at the same time, GLDH and AST increased with age to levels found five years earlier, indicating possible subclinical hepatopathy. Causative links between Cu supplementation, high calf mortality and hepatopathy are plausible, and reductions in Cu supplementation may prove beneficial in other dairy herds.

A controlled trial on the effect of feeding dietary chestnut extract and glycerol monolaurate on liver function in newborn calves

“…GLDH is considered to be a liver‐specific enzyme and effective biomarker of acute hepatic injury with activity in hepatocytes ten times higher than in other tissues. It is released in cases of hepatocellular necrosis (Thomas, ) and therefore of great value for indication of liver disease in adult cattle as well of liver dystrophy in calves (Hunter et al., ). The significant increase in serum GLDH activity in calves from group C and CG indicates acute hepatic injury.…”

Copper Supplementation, A Challenge in Cattle

“…Overall, copper requirements in cattle will range in practical conditions from 5 to 20 mg/kg DM. However, in the total mixed ration (TMR) [ 21 ] and concentrate based diets [ 18 , 54 ], copper concentrations no higher than 5 mg/kg DM have been demonstrated to be sufficient to maintain an adequate copper status, while in situations with a large influence of copper antagonists copper concentrations up to 20 mg/kg DM are needed to prevent copper deficiency. The range may also be higher in situations of extreme exposure to copper antagonists, and the EU legislation allows for copper supplementation up to 30 mg/kg feed (88% DM), which equates to 40 mg/kg of the total dietary DM.…”

“…In fact, monitoring studies carried out on numerous samples from culled cattle collected in slaughterhouses and/or diagnostic laboratories have demonstrated that a large number of cows have hepatic copper concentrations well above the adequate/normal/physiological levels, and that they are at risk of chronic copper toxicity in many countries such as the UK [ 9 , 11 ], New Zealand [ 12 ], the USA [ 13 , 14 , 15 ], the Netherlands [ 16 ] and Spain [ 17 , 18 , 19 , 20 ]. Dairy cattle are most affected, particularly Holstein Friesian [ 11 , 15 ] and Jersey cows [ 12 , 21 ], and available temporal data show an alarming tendency for an increasing incidence of cases [ 12 ]. These trends are undoubtedly due to copper supplementation aimed at preventing copper deficiency, as dietary copper intake from pasture alone is unlikely to cause such accumulation in liver tissue [ 22 ].…”

Reducing the risk of copper toxicity in dairy cattle

“…The ‘availability baby’ was thrown out with the bathwater of commercial practice, which ignored ration components of high availability. Most total mixed rations may need no more than 5 mg Cu/kg DM (Hunter and others 2013). Updated guidelines on copper availability and requirements are available (Suttle 2010).…”

“…Plasma Cu may be raised by infection but an appropriate follow‐up test (eg, haptoglobin) can refine diagnosis. Newborn calves and replacement heifers, as well as cull cows, should be monitored because they are also being overloaded with copper, possibly to their detriment (Hunter and others 2013). Acute overload can also cause problems: copper injections before artificial insemination can lower fertility (Hawkins 2014) and should only be given to cows in the ‘deficient’ category.…”