Molecular mechanism

Copper toxicosis is an inherited disorder of copper metabolism that causes excessive copper accumulation within the liver, leading to progressive liver damage. Affected dogs are often clinically normal when young despite increasing hepatic copper levels, with signs such as lethargy, vomiting, weight loss, jaundice and behavioural changes developing as liver disease progresses (Su et al., 1982; Washabau, 2013). Histological changes are initially absent despite copper accumulation, making early disease difficult to detect without genetic testing or liver biopsy (Washabau, 2013). Forman et al., (2005) identified a 39.7 kb deletion associated with copper toxicosis in Bedlington Terriers. The deletion is located on canine chromosome 10 (CFA10), spanning approximately 65.3091–65.3489 Mb and affecting intron 1 and intron 2 of the COMMD1 gene.

Copper Toxicosis is inherited in in an autosomal recessive pattern and the COMMD1 test is a well-established cause of copper toxicosis in Bedlington Terriers (Forman et al., 2005). Genetic testing identifies affected and carrier dogs and remains an important breeding tool. However, not all cases of copper toxicosis in Bedlington Terriers are explained by the COMMD1 deletion, so a normal result does not exclude all forms of the disease (Haywood et al., 2023).