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Two different mechanisms of resistance to colistin in  Acinetobacter baumannii  have been described. The first involves the total loss of lipopolysaccharide (LPS) due to mutations in the  lpxACD  operon, which is involved in the lipid A biosynthesis pathway. The second entails the addition of ethanolamine to the lipid A of the LPS resulting from mutations in the  PmrAB  two-component system. To evaluate the impact of colistin resistance-associated mutations on antimicrobial resistance and virulence properties, four pairs of clinical and laboratory-evolved colistin-susceptible/colistin-resistant (Col S /Col R )  A. baumannii  isolates were used. Antimicrobial susceptibility, surface motility,  in vitro  and  in vivo  biofilm-forming capacity,  in vitro  and  in vivo  expression levels of biofilm-associated genes, and  in vitro  growth rate were analyzed in these strains. Growth rate,  in vitro  and  in vivo  biofilm formation ability, as well as expression levels of biofilm-associated gene were reduced in Col R  LPS-deficient isolate (the  lpxD  mutant) when compared with its Col S  partner, whereas there were not such differences between LPS-modified isolates (the  pmrB  mutants) and their parental isolates. Mutation in  lpxD  was accompanied by a greater reduction in minimum inhibitory concentrations of azithromycin, vancomycin, and rifampin than mutation in  pmr B. Besides, loss of LPS was associated with a significant reduction in surface motility without any change in expression of type IV pili. Collectively, colistin resistance through loss of LPS causes a more considerable cost in biological features such as growth rate, motility, and biofilm formation capacity relative to LPS modification. Therefore, Col R  LPS-modified strains are more likely to spread and transmit from one patient to another in hospital settings, which results in more complex treatment and control.

Growth Rate and Biofilm Formation Ability of Clinical and Laboratory-Evolved Colistin-Resistant Strains of Acinetobacter baumannii