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

Two different mechanisms of resistance to colistin in have been described. The first involves the total loss of lipopolysaccharide (LPS) due to mutations in the 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 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/Col) isolates were used. Antimicrobial susceptibility, surface motility, and biofilm-forming capacity, and expression levels of biofilm-associated genes, and growth rate were analyzed in these strains. Growth rate, and biofilm formation ability, as well as expression levels of biofilm-associated gene were reduced in Col LPS-deficient isolate (the mutant) when compared with its Col partner, whereas there were not such differences between LPS-modified isolates (the mutants) and their parental isolates. Mutation in was accompanied by a greater reduction in minimum inhibitory concentrations of azithromycin, vancomycin, and rifampin than mutation in 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 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.