TY - JOUR
T1 - A review of the "mysterious" wasting disease in Swedish moose (Alces alces L.) related to molybdenosis and disturbances in copper metabolism
AU - Frank, Adrian
PY - 2004
Y1 - 2004
N2 - 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 N-epsilon-(carboxymethyl)-lysine in blood plasma and the kidney, indicating long-term hyperglycemia. Increased concentrations of insulin, glucose, and urea and reduced levels of phosphate, T-4, 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.
AB - 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 N-epsilon-(carboxymethyl)-lysine in blood plasma and the kidney, indicating long-term hyperglycemia. Increased concentrations of insulin, glucose, and urea and reduced levels of phosphate, T-4, 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.
KW - ruminants
KW - moose
KW - molybdenosis
KW - Cu-containing enzymes and proteins
KW - disturbed Cu metabolism
KW - endocrinopathy
KW - liming
KW - ruminants
KW - moose
KW - molybdenosis
KW - Cu-containing enzymes and proteins
KW - disturbed Cu metabolism
KW - endocrinopathy
KW - liming
UR - https://res.slu.se/id/publ/5302
U2 - 10.1385/BTER:102:1-3:143
DO - 10.1385/BTER:102:1-3:143
M3 - Review article
C2 - 15621935
SN - 0163-4984
VL - 102
SP - 143
EP - 159
JO - Biological Trace Element Research
JF - Biological Trace Element Research
IS - 45660
ER -