| Summary: | A severe vitamin E deficiency was observed in a captive moose (Alces alces) population that was maintained on a pelleted ration during 9 months per year. During 1998 only 10 of 17 calves identified in utero using ultrasonography at the Moose Research Center (MRC), Alaska, were born alive. An additional 3 calves exhibited posterior lameness within 3 weeks following birth and 2 of the 3 subsequently died. These symptoms have been previously associated with white muscle disease. White muscle disease results from both vitamin E and selenium deficiencies. While whole blood and liver selenium levels in 3 animals with white muscle disease were above recommended levels, serum vitamin E (α-tocopherol) levels for MRC calves were lower than levels observed in free-ranging neonatal calves in interior Alaska (Tanana Flats). Furthermore, mean serum vitamin E levels in adult cows during March at the MRC (0.08 μg/ml) were alarmingly lower than free-ranging Tanana Flats moose (2.8 μg/ml). We observed vitamin E deficiencies in animals fed diets with 5 IU/kg feed. Our data suggest that clinical symptoms of vitamin E deficiencies in adult moose may be difficult to detect, unless animals are reproducing. Following supplementation of vitamin E to 220 IU/kg in our pelleted ration during 1999, we observed no abortions and only 1 cow had still-born twin claves, but this was attributed to dystocia. Indeed, during 1999 only 2 of 16 calves identified in utero died of nonpredation causes. Although a vitamin E deficiency in free-ranging moose is unlikely, low selenium levels have been observed in free-ranging ungulate populations. Mean whole blood selenium levels in Tanana Flats moose (0.12 μg/g) were significantly lower than MRC adult cows (0.16 μg/g) fed a supplemented diet. More importantly, 8 of 10 animals from the Tanana Flats had selenium levels ≤ 0.085 μg/g and were below recommended levels for domestic cattle. Given the lack of data on soil selenium levels in Alaska, deficiency-related neonatal losses may occur that are attributed to other causes of mortality. It will be difficult to quantify in utero and neonatal calf losses resulting from selenium and vitamin E deficiencies if blood or tissue samples from study locations are not examined.
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