Schistosome infection in deer mice (Peromyscus maniculatus): impacts on host physiology, behavior and energetics.

Animals routinely encounter environmental stressors and may employ phenotypic plasticity to compensate for the costs of these perturbations. Parasites represent an ecologically important stressor for animals, which may induce host plasticity. The present study examined the effects of a trematode parasite, Schistosomatium douthitti, on deer mouse (Peromyscus maniculatus) physiology, behavior and energetics. Measures were taken to assess direct parasite pathology as well as potential host plasticity used to reduce the costs of these pathologies. Parasitized mice had increased liver and spleen masses, as well as decreased liver protein synthesis. Parasitism also led to increased gastrointestinal (GI) mass, either directly due to parasite presence or as host compensation for decreased GI function. No additional plasticity was recorded - infected animals did not consume more food, decrease in body mass or reduce their activity. Parasitism led to reduced thermoregulation during short-term cold exposure, indicating that there may be fitness costs of parasitism. There were no changes in the other measures of energetics taken here, namely basal metabolic rate (BMR) and cold-induced maximal metabolic rate (MR(max)). Together, the results suggest that many costs of parasite infection are largely ameliorated through physiological or morphological compensatory mechanisms.