Hepatic Lipodystrophy in Galloway Calves.

Hepatic lipodystrophy in Galloway calves is a fatal liver disease affecting a small proportion of the Galloway breed described in different parts of Europe and North America during the past decades. The clinical findings include a diversity of neurological signs. Clinical pathology findings frequently indicate hepatobiliary disease. Postmortem examination reveals an enlarged, pale yellow, and firm liver. Histologic lesions include hepatic fibrosis, hepatic lipidosis, and bile duct hyperplasia. To date, the etiopathogenesis remains obscure. Infectious causes, intoxications, and a hereditary origin have been considered. We describe hepatic lipodystrophy in Galloway calves from an extensively farmed cow-calf operation in southern Germany. Main clinical findings in 6 calves were consistent with hepatic encephalopathy. Clinical pathology findings in 5 of 6 tested animals revealed increased concentration of total bilirubin (maximum value [MV], 54 µmol/l; reference range [RR], <8.5 µmol/l), direct bilirubin (MV, 20 µmol/l; RR, <3.4 µmol/l), increased activity of gamma glutamyl transferase (MV, 162 U/l; RR, <36 U/l) and glutamate dehydrogenase (MV, 420 U/l; RR, <16 U/l). In addition, activity of glutathione peroxidase was decreased in all tested ( n = 5) animals (MV, 61 U/g hemoglobin [Hb]; RR, >250 U/g Hb). Postmortem examination in 6 calves revealed a firm, diffusely enlarged yellow liver with a finely nodular surface. Histologic lesions included hepatic fibrosis, hepatic lipidosis, and bile duct hyperplasia. Our findings add to the existing data on hepatic lipodystrophy in the Galloway breed and outline a protocol to aid in the diagnosis of this disorder.

Hepatic lipodystrophy of pedigree Galloway calves.

Hepatic lipodystrophy has been recognised in pedigree Galloway calves since 1965. Between 1975 and 1984 15 cases from five farms were examined. The calves initially appear normal and in good bodily condition but invariably die by five months of age. The characteristic clinical and neurological changes lead to body tremors, opisthotonus, and dyspnoea before the animals become recumbent and die. On postmortem examination the most significant finding in all cases was an enlarged, pale and mottled liver weighing up to 2.75 kg. Limited histopathological examinations of the brain and liver revealed changes suggestive of hepatic encephalopathy. Exhaustive investigations of the farms failed to reveal any significant findings and the small number of cases made it impossible to determine whether the disease was genetically determined; limited evidence suggests that a 'storage disease' cannot be excluded.