Nutritional and Metabolic Diseases

White Liver Disease

White liver disease, a manifestation of cobalt deficiency known for some time in sheep, has been reported in goats only in New Zealand and Oman, though it may be underdi­agnosed in other regions where cobalt-deficient soils occur.

Etiology and Pathogenesis

Cobalt deficiency in ruminants is a well-known condition associated with grazing of cobalt-deficient soils. It results in chronic wasting with anemia and hypoproteinemia. However, the specific manifestation of white liver disease apparently occurs only in sheep and goats.

Cobalt is used in the rumen by microflora to produce cyanocobalamin, or vitamin B₁₂, which serves as a coen­zyme to methylmalonyl-CoA mutase in the citric acid cycle, facilitating the conversion of propionic acid to glu­cose via succinate in the liver. When small ruminants are cobalt deficient or are fed high-carbohydrate diets that exceed the capacity of the liver to convert propionate to succinate, these animals may accumulate methylmalonyl- CoA or methylmalonic acid in the tissues and convert it to branched-chain fatty acids that accumulate in hepatocytes. This conversion to branched-chain fatty acids does not occur in cattle or deer, and white liver disease as a manifes­tation of cobalt deficiency is not observed in these species (Black et al. 1988).

Epidemiology

Cobalt deficiency in livestock associated with cobalt-deficient soils has been reported from New Zealand, Australia, Europe, and northeastern North America. Ovine white liver disease has been specifically reported from New Zealand, Australia, Brazil, the United Kingdom, the Netherlands, Switzerland, and Norway. For a long time, caprine white liver disease had been reported only from New Zealand (Pearson 1987; Black et al.

Reported cases of white liver disease from New Zealand involve young Angora or Angora cross goats between 4 and 18 months of age, but mostly between 4 and 6months of age. Grass pastures appear to be more conducive to deficiency in goats than are legume pastures, and lush pasture may also predispose to the condition. The diagnosis in Oman derived from slaughterhouse samples of goat livers that showed hepatic lipidosis and low cobalt concentrations. The man­agement of these goats while alive was unreported.

Clinical Findings

The principal complaint in cobalt deficiency is chronic ill- thrift. Affected goats are thin, weak, and listless, with decreased appetite, pale mucous membranes, and subman­dibular edema. Diarrhea may be seen. White liver disease in sheep is associated with photosensitization, but this has not yet been reported in goats.

Clinical Pathology and Necropsy

A macrocytic normochromic anemia and hypoalbumine- mia are common findings. The cases of caprine white liver disease reported from New Zealand were confirmed on the basis of serum vitamin B12 levels ante mortem or liver lev­els at necropsy using normal values established for sheep. Adequate serum levels are reported as more than 400 pmol/L and adequate liver levels as more than 200 nmol/kg. In Oman, confirmation was based on analy­sis of liver cobalt concentrations, which in affected goats were 0.08 ± 0.02 parts per million (ppm) dry matter com­pared to 0.53 ± 0.11 ppm dry matter in livers of normal con­trol goats. Standard reference values for liver cobalt in normal goats are not reported. In cattle and sheep, the nor­mal range is 0.15-0.20 ppm dry matter and 0.02-0.06 ppm dry matter in cobalt-deficient animals (Johnson et al.

Necropsy findings include an emaciated carcass and a pale-colored liver. Histologically, there is widespread fatty change in the liver, with many hepatocytes containing sin­gle large fat globules in the cytoplasm, mild to moderate bile duct proliferation, portal fibroplasia, and sinusoidal accumulations of macrophages containing periodic acid- Schiff (PAS)-positive ceroid material.

Diagnosis

All causes of prolonged weight loss must be considered in the diagnosis, as discussed in Chapter 15. Because young goats often have gastrointestinal helminthiasis that appears clinically similar, cobalt deficiency as a concurrent or underlying condition should not be neglected, even when evidence of helminthiasis is found on fecal flotation or necropsy.

Treatment

For young stock, intramuscular injection of vitamin B₁₂ at a weekly dose of 100 μg, or for adults 300 μg, has been used to ameliorate signs of white liver disease in affected herds. Also, sheep respond to daily oral supplementation of cobalt at 1 mg/head/day (or 7 mg/head/week), given until there is noticeable improvement.

Control

Deficient pastures may be top dressed with cobalt as cobalt sulfate at a rate of 350 g/ha annually, but animals should be supplemented nutritionally in the short term, because pas­ture uptake is not immediate. When pasture treatment is not possible, cobalt should be supplemented in the diet.

For sheep the recommendation is 0.1 mg/head/day. Commercially available cobalt pellets given orally to sheep provide continuous release of cobalt for as long as three years, as long as they remain in the rumen (Kimberling 1988). They are of particular value in extensive grazing systems, where pasture top dressing of cobalt or regular feed sup­plementation is impractical.