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

Moose (Alces alces L.) affected by a disease with unknown aetiology were co mpared with healthy moose regarding trace element concentrations in liver a nd 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. Substant ially 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 hepa tic levels of Mo in the affected moose were 36% higher and Cu was approxima tely 60% lower than in reference animals collected in 1982. The most import ant clinical chemical changes were decreased concentrations of bilirubin, t hyroxine (T-4) and the liver-specific enzymes GLDH and g-GT. Also, the acti vities of the enzymes CuZn-SOD and CSII-Px in erythrocytes were decreased. Increases were recorded for free fatty acids (NEFA), the muscle-specific en zyme CK, but especially for urea and insulin. Changes in the plasma protein pattern were also discernible after electrophoresis on agarose gel membran es, indicating chronic immunostimulation. All the observed changes in trace element concentrations and clinical chemical parameters are compatible wit h molybdenosis and secondary Cu deficiency in ruminants and most of the par ameters are in agreement with those found in experimental copper deficiency and molybdenosis in the goat. It is, therefore, suggested that the moose d isease with previously unknown aetiology is mainly caused by molybdenosis. (C) 2000 Elsevier Science B.V. All rights reserved.