Ovine white liver disease in a yearling ewe

Dominique Comeau

Animal Health Laboratory, University of Guelph, Guelph, ON

AHL Newsletter 2025;29(3):9.

A yearling ewe was submitted for postmortem examination at the Animal Health Laboratory following a history of anorexia, depression, and weight loss lasting several weeks, eventually leading to euthanasia. Discharge around the eyes and mouth was also described as the clinical condition progressed. Several animals had died sporadically in the past year with a similar presentation, and variable underlying causes including parasitism and mineral imbalances were identified. On gross examination of this ewe, the blood was thin and watery, supporting anemia, and the mucus membranes were off-white with no evidence of jaundice. There was severe effusion in the abdomen, thorax, and pericardium with at least three liters of serous fluid in the abdomen. The liver was diffusely pale and very firm. Histologically, this correlated with severe bridging fibrosis effacing up to 50% of the liver parenchyma. Abundant lipid vacuolation was noted in the remaining hepatocytes, along with ceroid pigment and scattered neutrophils (Fig. 1). In addition, there was hypertrophy of astrocytes (neuronal support cells) in the brain, suggestive of early hepatic encephalopathy (Fig. 2).

Ancillary testing was performed to investigate possible parasitism or metabolic disease. A small burden of nematodes was found, but was not considered sufficient to be a major cause of the pathologic findings. A mineral panel performed on liver found that copper levels were within normal limits, ruling out copper toxicity. This was an important differential diagnosis; however, it was considered less likely due to the lack of jaundice, yellow discoloration of the liver, or dark discoloration of the kidneys. This ewe had cobalt levels too low to be detected. The normal reference interval for this mineral in sheep is 0.025-0.085 ug/g, and the lower limit of detection for our laboratory method is 0.006 ug/g. This result, together with the histologic findings, was considered diagnostic for ovine white liver disease.

Cobalt is an essential trace element in sheep and other ruminants, and it is required for the synthesis of vitamin B12 by the ruminal flora. Low levels are typically associated with sandy or high pH soil, or intensive cropping leading to leaching of the soil. Studies have demonstrated reduced activity of several vitamin B12-dependent enzymes within hepatocytes of lambs with experimentally-induced white liver disease, which hinders the oxidation of fatty acids and is the probable cause of lipid accumulation and secondary hepatocellular injury in this disease. Lesions of hepatic encephalopathy, as noted in this ewe, are occasionally reported in cases of white liver disease. Liver damage leads to increased levels of circulating ammonia, causing injury to the brain.

Figure 1. Bridging fibrosis throughout the liver (pale areas) with marked vacuolar change throughout (clear spaces). Inset shows higher magnification of vacuoles with intermingled inflammatory cells. H&E stain.

Figure 2. Section of the cerebrum showing swollen and clustered astrocytes (circled). H&E stain.

References

1. Kennedy S, et al. Histopathologic and ultrastructural alterations of white liver disease in sheep experimentally depleted of cobalt. Vet Pathol 1997;34(6):575–584.

2. Ulvund MJ. Ovine white-liver disease (OWLD) pathology. Acta Veterinaria Scandinavica 1990;31(3):309–324.