ArticleFrontiers in veterinary science2026
Case Report: Fatal copper-associated hepatopathy in a Belgian Shepherd Malinois dog initially investigated as suspected malicious poisoning.
Article in Frontiers in veterinary science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Copper-associated hepatopathy (CAH) is a recognized cause of severe liver injury and acute hepatic decompensation in dogs and may present as chronic hepatitis, cirrhosis, or peracute death. This report describes a fatal case of CAH in a 9-year-old, 30-kg female Belgian Shepherd Malinois dog that was initially investigated as suspected malicious poisoning because of sudden death, tongue protrusion, and bloody feces at the scene. At forensic necropsy, approximately 55 mL of blood-tinged pleural effusion and 10 mL of blood-tinged ascitic fluid were present, the spleen was markedly enlarged, and both kidneys showed multiple dark cortical foci, whereas the liver lacked striking gross abnormalities apart from increased fragility. Histologically, the liver showed multifocal to coalescing hepatocellular degeneration and necrosis with abundant coarse brown intracytoplasmic pigment, raising suspicion of copper accumulation. Rhodanine staining confirmed copper-associated pigment within centrilobular hepatocytes, and toxicologic screening of stomach contents, liver, and kidneys was negative for common exogenous toxicants relevant to malicious poisoning. Quantitative analysis by inductively coupled plasma optical emission spectrometry (ICP-OES) yielded a hepatic copper concentration of 887.4 μg/g wet weight, corresponding to approximately 3176.4 μg/g on a dry-matter basis (estimated, not directly measured) when an assumed hepatic dry-matter content of 28% is applied. This estimated dry-weight concentration exceeds the commonly cited toxic threshold of >1,000 μg/g dry weight and, considered together with the histologic lesions and copper-specific staining, was interpreted as supportive evidence of copper-associated hepatopathy contributing to the fatal outcome. This case highlights CAH as an important differential diagnosis in dogs that die suddenly with hemorrhagic findings, even when the liver is grossly unremarkable and the initial forensic suspicion is malicious poisoning. It also emphasizes the diagnostic value of integrating necropsy, histopathology, copper-specific histochemistry, toxicologic screening, and quantitative copper analysis in veterinary forensic investigations.
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