A wasting, debilitating disease with uncertain aetiology affecting moose (Alces alces americana) in Eastern North America has been reported repeatedly ever since the 1910s. Despite the intensive studies during 1930-1960s the cause of the sickness could not be established. In the 1960s a parasitic nematode (Parelaphostrongylus tenuis) was reported as constituting a probable explanation for the sickness, although several clinical and pathological signs remained unexplained. In Sweden, a moose disease with similar signs, has been shown to be caused by molybdenosis resulting from a nutritional imbalance. The findings of this investigation were applied in Nova Scotia to determine trace element concentrations in tissues from indigenous moose. Co deficiency was found in about half of the cases and the investigation was complemented by determining the vitamin B12 level, which proved nutritional Co/vitamin B12 deficiency, further verified by an increased MMA (methylmalonic acid) level in plasma. Deficiencies were found mainly in the Tobeatic and Cape Breton Highland regions. No indications of molybdenosis or other trace element disturbances were found in Nova Scotia. Otherwise, extremely high Cd levels (148 mg Cd/kg kidney wet wt., maximum) were found, though probably not contributing to the moose sickness. The Cd burden of moose on mainland Nova Scotia was more than 50% higher than that of moose in Huntville and Alonquin (Ontario, Canada) and five- to six-fold is higher than the highest Cd levels found in Sweden. To counteract the bio-geochemical effects of Co deficiency in the moose environment, provision of Co-containing salt licks is suggested.