The 'mysterious' disease in Swedish moose. Concentrations of trace elements in liver and kidneys and clinical chemistry. Comparison with experimental molybdenosis and copper deficiency in the goat.

Moose (Alces alces L.) affected by a disease with unknown aetiology were compared with healthy moose regarding trace element concentrations in liver and kidneys, as well as certain clinical chemical parameters of blood plasma. The diseased moose showed decreased hepatic concentrations of Cu, Cd and Mg. Renal concentrations of Cd, Co, Mg and Mn were also decreased. Substantially increased concentrations in both liver and kidneys were seen for Al, Ca, Fe, Pb and Zn, while Se and Mo were increased in liver tissue. The hepatic levels of Mo in the affected moose were 36% higher and Cu was approximately 60% lower than in reference animals collected in 1982. The most important clinical chemical changes were decreased concentrations of bilirubin, thyroxine (T4) and the liver-specific enzymes GLDH and g-GT. Also, the activities of the enzymes CuZn-SOD and GSH-Px in erythrocytes were decreased. Increases were recorded for free fatty acids (NEFA), the muscle-specific enzyme CK, but especially for urea and insulin. Changes in the plasma protein pattern were also discernible after electrophoresis on agarose gel membranes, indicating chronic immunostimulation. All the observed changes in trace element concentrations and clinical chemical parameters are compatible with molybdenosis and secondary Cu deficiency in ruminants and most of the parameters are in agreement with those found in experimental copper deficiency and molybdenosis in the goat. It is, therefore, suggested that the moose disease with previously unknown aetiology is mainly caused by molybdenosis.