Editor's note: An abbreviated version of this case study appears in the February Bovine Veterinarian. See the full version here.
Chronic copper toxicity has classically been associated with chronic overprovision of copper to sheep and there are few reports of similar cases in cattle. Bradley1 reported a case in dairy cows that were moderately oversupplemented (37.5 ppm copper on a dry basis in total ration) for two years before mortality occurred and Perrin et al2 reported a case also of dairy cows that were greatly oversupplemented (>300 ppm copper on a dry basis in total ration) for nine months before mortality occurred.
Both would seem to imply, as opposed to sheep, some degree of resistance to copper toxicity on the part of cattle. Marta Lopez-Alonso et al3 reported an increasing frequency of bovine copper toxicity. Two cases of presumed copper toxicity in young, growing Holsteins were recently presented to the Wisconsin Veterinary Diagnostic Laboratory.
The first case involved a group of approximately 40, 200-250kg Holstein heifers in a group pen that were fed a ration (fed as individual components) composed of hay, corn, oats and a mineral/trace mineral fortified pellet. Within several weeks of introduction, several animals displayed a vague clinical picture of anorexia and lethargy followed by death, typically within two to three days of onset. Clinical examination revealed only mild icterus and chocolate-colored blood, interpreted as methemoglobinemia. Respiratory distress was not observed, however.
Clinicopathologic findings were not available but reference was made to increased liver enzymes. Treatments with antiobiotics and methylene blue were unsuccessful as were attempts to document nitrate toxicosis. Field necropsies revealed “generalized icterus, yellow-orange liver discoloration and increased, coarse granularity of livers”.
ICP/MS analysis of liver copper performed in our laboratory yielded 1500ug/g dry wt. (440ug/g wet). Toxicity is thought to occur with wet values above 250ug/g4. Routine aerobic and anaerobic cultures of liver, kidney, lung and bile were negative.
Histopathologic examination of formalin fixed, H&E stained sections revealed the following in the liver: There was diffuse vacuolation of hepatocytes with extensive, random, single cell to coalescent hepatocyte necrosis. Portal tracts were markedly expanded by fibrous tissue, often with portal-portal bridging, accompanied by marked biliary hyperplasia. Most tracts contained low to moderate numbers of mononuclear inflammatory cells along with low to moderate numbers of prominent macrophages distended by light brown, coarsely granular, cytoplasmic material that stained brick red with rhodanine, indicative of copper, in this case likely complexed with lipofuscin.