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Two mechanisms of resistance to colistin have been described inAcinetobacter baumannii . One involves complete loss of lipopolysaccharide (LPS), resulting from mutations inlpxA ,lpxC , orlpxD , and the second is associated with phosphoethanolamine addition to LPS, mediated through mutations inpmrAB . In order to assess the clinical impacts of both resistance mechanisms,A. baumannii ATCC 19606 and its isogenic derivatives, AL1851 ΔlpxA , AL1852 ΔlpxD , AL1842 ΔlpxC , and ATCC 19606pmrB , were analyzed forin vitro growth rate,in vitro andin vivo competitive growth, infection of A549 respiratory alveolar epithelial cells, virulence in theCaenorhabditis elegans model, and virulence in a systemic mouse infection model. Thein vitro growth rate of thelpx mutants was clearly diminished; furthermore,in vitro andin vivo competitive-growth experiments revealed a reduction in fitness for both mutant types. Infection of A549 cells with ATCC 19606 or thepmrB mutant resulted in greater loss of viability than withlpx mutants. Finally, thelpx mutants were highly attenuated in both theC. elegans and mouse infection models, while thepmrB mutant was attenuated only in theC. elegans model. In summary, while colistin resistance inA. baumannii confers a clear selective advantage in the presence of colistin treatment, it causes a noticeable cost in terms of overall fitness and virulence, with a more striking reduction associated with LPS loss than with phosphoethanolamine addition. Therefore, we hypothesize that colistin resistance mediated by changes inpmrAB will be more likely to arise in clinical settings in patients treated with colistin.

Biological Cost of Different Mechanisms of Colistin Resistance and Their Impact on Virulence in Acinetobacter baumannii