Acclimatization modulates energy metabolism in an aquatic amphipod under exposure to ciprofloxacin and thiacloprid.
TL;DR
It is suggested that ciprofloxacin primarily impaired nutrient assimilation through abundance shifts in multiple bacterial classes of the gut microbiome, and thiacloprid reduced feeding potentially through neurophysiological mechanisms, with secondary effects on the microbiome.
Abstract
Microbiome-host interactions are key determinants of organismal health, yet their role in mediating chemical stress in aquatic invertebrates remains poorly understood. We investigated how antibiotic and insecticide stress individually affect gut microbiomes and physiology in the freshwater amphipod Gammarus fossarum. Organisms were exposed for 21 days to the antibiotic ciprofloxacin (307 µg L-1) or the insecticide thiacloprid (0.625, 1.25, 2.5 µg L-1), while accounting for short- and long-term acclimatization prior to exposure. Feeding behavior, growth, gut microbiome composition, fatty acid profiles, and proteomic responses were assessed. Both chemicals induced a tightly coupled, energy-centered stress response integrating reduced feeding, lipid mobilization, altered protein expression, and microbiome shifts, but proposedly via distinct pathways. We suggest that ciprofloxacin primarily impaired nutrient assimilation through abundance shifts in multiple bacterial classes of the gut microbiome. In contrast, thiacloprid reduced feeding potentially through neurophysiological mechanisms, with secondary effects on the microbiome. These pathways converged on an energetic bottleneck characterized by fatty acid depletion and downregulation of energetically costly proteins, constraining molting and growth. Long-term acclimatization markedly amplified these effects, identifying energetic state as a critical modulator of chemical sensitivity.