Colistin Resistance in Environmental Isolates ofAcinetobacter baumannii

Although the molecular mechanisms of carbapenem resistance of environmental isolates ofAcinetobacter baumanniiare well described, data on the mechanisms of colistin resistance are scarce. In this study, we report the molecular mechanisms of colistin resistance in environmental isolates ofA. baumannii. Seven clinically relevant isolates ofA. baumanniibelonging to ST-2(Pasteur)were recovered from hospital wastewater and wastewater treatment plant. The phenotypic resistance to colistin was confirmed by broth microdilution with minimum inhibitory concentration values ranging from 20 to 160 mg/L. Colistin sulfate and colistimethate sodium showed bactericidal activity against two colistin-heteroresistant isolatesin vitro, but substantially recovery of population was observed after prolonged incubation.In silicogenome analysis revealed nucleotide variations resulting in amino acid changes in LpxC (N286D), LpxD (E117K), PmrB (A138T, R263S, L267W, Q309P, and A444V), and EptA (F166L, I228V, R348K, A370S, and K531T). According to reverse transcription quantitative PCR, all isolates had increased levels ofeptAmRNA and decreased levels oflpxAandlpxDmRNA. Isolates expressed low hydrophobicity, biofilm, and pellicle formation, but showed excellent survival in river water during 50 days of monitoring. Colistin- and pandrug-resistantA. baumanniidisseminated in the environment could represent the source for the occurrence of serious community-acquired infections.

Automated summary

The molecular mechanisms of colistin resistance in environmental isolates of A. baumannii were investigated in this study, revealing nucleotide variations resulting in amino acid changes and increased levels of eptA mRNA. Isolates with colistin and pandrug resistance could potentially be a source for serious community-acquired infections, as they showed excellent survival in river water.