Abstract
There exist widely accepted hypotheses that (1) parasitic lungworms (Parelaphostrongylus tenuis), carried by white-tailed deer (Odocoilesus virginianus) but pathogenic to moose (Alces alces), cause population declines in moose and (2) habitiat refuges are responsible for maintaining local moose populations in enzootic areas. However, data cited to support the first hypothesis are the same data that generated it. Also, the interpretation of those data is confounded by a lack of adequate controls on the effects of changes in habiitat and the effects of deer apart from their role as vehicles of P. tenuis transmission. Spatial aggregations of moose infected and not infected with P. tenuis are inconsistent with the second hypothesis. Further, for "refuges" to function, moose should shift habitat use from habitats used by infected deer, but habitats "contaminated" by deer feces apaprently are not avoided by moose. Habitat overlap is low in spring and summer because deer leave habitats they share with moose during winter, while moose remain. A present, there is little evidence that the mortality of moose caused by P. tenuis has necessarily resulted in the effects on moose populations and habitat use ascribed to it. Closer adherence to hypothetico-deductive, rather than retroductive, methodology should eventually help disentangle the relative importance of the effects of habitat alteration, food competition, and other sources of mortality besides P. tenuis on moose populations.