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Copper toxicosis in a dairy goat herd

Jennifer Cornish DVM, DACVIM1, John Angelos DVM, PhD, DACVIM2, Birgit Puschner DVM, PhD, DACVT3, Grant Miller DVM4, and Lisle George DVM, PhD, DACVIM5
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  • 1 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616
  • | 2 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616
  • | 3 California Animal Health and Food Safety Laboratory System, University of California, Davis, CA 95616
  • | 4 Sonoma Marin Veterinary Service, 1120 Industrial Ave, Ste 13 and 14, Petaluma, CA 94952
  • | 5 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616

Abstract

Case Description—A closed herd of 400 mixed-breed dairy goats was examined because of a decrease in milk production and increase in mortality rate. Nine animals had died within a 1-month period.

Clinical Findings—Clinical signs were evident only in lactating goats and included anorexia and recumbency. In the most severely affected goats, signs progressed to neurologic abnormalities and death. Serum aspartate aminotransferase activity, γ-glutamyltransferase activity, and total bilirubin concentration were high in clinically affected does, but no evidence of hemolysis was found. A diagnosis of copper toxicosis was made on the basis of high liver and kidney copper concentrations and histologic evidence of hepatic necrosis. Goats were found to have been fed a mineral mix containing 3,050 ppm copper for 9 months prior to the onset of copper toxicosis. Overall, there was no consistent relationship between serum hepatic enzyme activities, serum copper concentration, and liver copper concentration.

Treatment and Outcome—Clinically affected goats were treated with penicillamine, ammonium molybdate, sodium thiosulfate, and vitamin E. Penicillamine increased urine copper excretion in treated does versus untreated control animals. An increased incidence of infectious disease was identified in the herd 9 months later. Liver vitamin E concentration was low in 10 of the 12 goats that underwent necropsy.

Clinical Relevance—Findings suggested that penicillamine may be an effective treatment for goats with copper toxicosis. Production losses months after the diagnosis was made suggested that the intoxication had a prolonged animal welfare and economic impacts.

Abstract

Case Description—A closed herd of 400 mixed-breed dairy goats was examined because of a decrease in milk production and increase in mortality rate. Nine animals had died within a 1-month period.

Clinical Findings—Clinical signs were evident only in lactating goats and included anorexia and recumbency. In the most severely affected goats, signs progressed to neurologic abnormalities and death. Serum aspartate aminotransferase activity, γ-glutamyltransferase activity, and total bilirubin concentration were high in clinically affected does, but no evidence of hemolysis was found. A diagnosis of copper toxicosis was made on the basis of high liver and kidney copper concentrations and histologic evidence of hepatic necrosis. Goats were found to have been fed a mineral mix containing 3,050 ppm copper for 9 months prior to the onset of copper toxicosis. Overall, there was no consistent relationship between serum hepatic enzyme activities, serum copper concentration, and liver copper concentration.

Treatment and Outcome—Clinically affected goats were treated with penicillamine, ammonium molybdate, sodium thiosulfate, and vitamin E. Penicillamine increased urine copper excretion in treated does versus untreated control animals. An increased incidence of infectious disease was identified in the herd 9 months later. Liver vitamin E concentration was low in 10 of the 12 goats that underwent necropsy.

Clinical Relevance—Findings suggested that penicillamine may be an effective treatment for goats with copper toxicosis. Production losses months after the diagnosis was made suggested that the intoxication had a prolonged animal welfare and economic impacts.

Contributor Notes

Address correspondence to Dr. Cornish.