A review of the "mysterious" wasting disease in Swedish moose (Alces alces L.) related to molybdenosis and disturbances in copper metabolism.
The main purpose of this article is to review the previously published data on so-called "moose sickness" in the light of two case studies presented here. Molybdenosis and Mo-induced disturbances of Cu metabolism in moose are characterized by numerous severe lesions caused by reduced activity of Cu-containing enzymes such as ceruloplasmin, superoxide dismutase in blood, and myocardial cytochrome c oxidase. Consequences of such metabolic disturbances (e.g. glucose intolerance, insulin resistance, and non-insulin-dependent diabetes mellitus) were first reported in moose in 2000. This was corroborated by the detection of furosine, pentosidine, and Nepsilon-(carboxymethyl)-lysine in blood plasma and the kidney, indicating long-term hyperglycemia. Increased concentrations of insulin, glucose, and urea and reduced levels of phosphate, T4, and Mg in blood were also seen. Recently, a similar toxic endocrinopathy was reported in sheep treated therapeutically with thiomolybdates because of chronic Cu toxicosis. Two case reports illustrate the difficulty of diagnosing Mo-related disturbances of Cu metabolism in moose, as analyses of Cu and Mo have not proved entirely reliable because of interaction, accumulation, and the short biological half-life of Mo. The increased bioavailability of Mo is most probably the result of increased pH in the soil, caused, for example, by liming, making Mo accessible in forage plants consumed by moose. The etiology underlying the Swedish moose disease has been difficult to determine because of the complex clinical signs and unspecific pathological findings. However, a combination of clinical chemistry, trace element analysis, and biochemistry correlated with the pathological findings has corroborated molybdenosis and Mo-induced disturbances of Cu metabolism as the probable etiological factor. Alternative etiologies suggested for the moose disease, such as viral infection, starvation because of overpopulation, and/or shortage of forage as well as senescence and phytotoxic substances, are discussed.
Frank
Adrian
A
Department of Clinical Chemistry, Faculty of Veterinary Medicine and Animal Sciences, Swedish University of Agricultural Sciences, Box 7038, SE-750 07 Uppsala, Sweden.
D000818:Animals; D000835:Animals, Wild; D003300:Copper / Q000172:deficiency* / Q000378:metabolism; D003670:Deer; D003677:Deficiency Diseases / Q000662:veterinary*; D005260:Female; D006041:Goats; D008982:Molybdenum / Q000633:toxicity*; D013577:Syndrome; D019282:Wasting Syndrome / Q000662:veterinary*; D015431:Weight Loss
D003300:Copper; D008982:Molybdenum