Abstract

Chronic copper toxicity was diagnosed in a Jersey herd in the Waikato region of New Zealand following an investigation into the deaths of six cattle from a herd of 250 dry cows. Clinical signs and post-mortem examination results were consistent with a hepatopathy, and high concentrations of copper in liver and blood samples of clinically affected animals confirmed copper toxicity. Liver copper concentrations and serum gamma-glutamyl transferase activities were both raised in a group of healthy animals sampled at random from the affected herd, indicating an ongoing risk to the remaining cattle; these animals all had serum copper concentrations within normal limits. Serum samples and liver biopsies were also collected and assayed for copper from animals within two other dairy herds on the same farm; combined results from all three herds showed poor correlation between serum and liver copper concentrations.To reduce liver copper concentrations the affected herd was drenched with 0.5 g ammonium molybdate and 1 g sodium sulphate per cow for five days, and the herd was given no supplementary feed or mineral supplements. Liver biopsies were repeated 44 days after the initial biopsies (approximately 1 month after the end of the drenching program); these showed a significant 37.3% decrease in liver copper concentrations (P <0.02). Also there were no further deaths after the start of the drenching program. Since there was no control group it is impossible to quantify the effect of the drenching program in this case, and dietary changes were also made that would have depleted liver copper stores.Historical analysis of the diet was difficult due to poor record keeping, but multiple sources of copper contributed to a long term copper over supplementation of the herd; the biggest source of copper was a mineral supplement. The farmer perceived this herd to have problems with copper deficiency prior to the diagnosis of copper toxicity, so this case demonstrates the importance of monitoring herd copper status regularly. Also the poor correlation between liver and serum copper concentrations in the three herds sampled demonstrates the importance of using liver copper concentration to assess herd copper status.

Highlights

  • There are two forms of copper poisoning – acute and chronic

  • The aim of this paper is to present a case of sudden death due to copper toxicity seen in a dairy herd in the Waikato region of New Zealand, and to discuss appropriate diagnosis, management, and investigation of this condition

  • This herd had experienced deaths from copper toxicity, yet Cu(S) concentrations from healthy animals were within the normal range and did not show any correlation with Cu(L) concentrations

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Summary

Background

There are two forms of copper poisoning – acute and chronic. Acute copper poisoning can result from the accidental administration of large quantities of copper (often via oral copper salts, parenteral copper administration, or grazing pasture recently fertilised with copper) [1]. Ante-mortem blood samples and post-mortem kidney and liver samples were taken from each of the remaining three cows that died (cows 4-6) and assayed for serum GGT, serum GLDH, and copper concentration (liver [8], kidney [7] and serum) These results supported a diagnosis of copper toxicity (see Table 1). A lactating Jersey cow producing 20 litres of milk/day under reasonable New Zealand pasture conditions (normal iron, sulphur and molybdenum) has a daily copper requirement of approximately 136 mg [6] For this herd: Pasture = 13 kg DM @ 10 mg/kg DM = 130 mg Cu PKE = 3 kg DM @ 22 mg/kg DM = 66 mg Cu Mineral blend @ 5 g/cow/day = 370 mg Cu Total = 566 mg Cu/day giving an excess of 430 mg. Breed may play a role in making this herd vulnerable to copper toxicity; some data suggests that Jersey cows accumulated more copper in their livers than Holstein cows fed the same diet [12]

Conclusions
Findings
11. Alexander P
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