Two sexually intact female silver-shaded domestic ferret siblings from
different litters were examined because of CNS depression and letharg
y. Ferret 1 was dehydrated and hypothermic, whereas ferret 2 was icter
ic and febrile and had serum bilirubin concentration > 12.0 mg/dl and
BUN of 59 mg/dl. Despite supportive treatment, the ferrets died within
days of evaluation. On necropsy, ferret 1 had chronic hepatopathy, wi
th diffuse vacuolation of hepatocytes. In ferret 2, the liver had cent
rilobular degeneration and necrosis, and hemoglobinuric nephrosis was
evident, with hemoglobin in the renal tubules. In both ferrets, Kupffe
r's cells and macrophages contained eosinophilic material in the cytop
lasm. Special staining revealed copper pigment in hepatocytes and phag
ocytic cells in both livers. Analysis of liver specimens revealed 850
and 700 ppm of copper in ferrets 1 and 2, respectively. Copper values
> 200 ppm in liver are considered evidence of toxicosis in most animal
species. Copper toxicosis was diagnosed on the basis of the findings
from histologic examination of the liver and high hepatic copper value
s. Lack of related illness in 11 other ferrets in the same environment
and fed the same diet, plus sibling relationship and same phenotypic
coat color in the affected ferrets, suggested that these ferrets had a
n inherited defect in their ability to metabolize normal amounts of in
gested copper.