Copper toxicosis in a dairy goat herd.

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, gamma-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.