Colistin-Resistant Acinetobacter baumannii Clinical Strains with Deficient Biofilm Formation

Abstract

In two pairs of clinical colistin-susceptible/colistin-resistant (Cst(s)/Cst(r)) Acinetobacter baumannii strains, the Cst(r) strains showed significantly decreased biofilm formation in static and dynamic assays (P < 0.001) and lower relative fitness (P < 0.05) compared with those of the Cst(s) counterparts. The whole-genome sequencing comparison of strain pairs identified a mutation converting a stop codon to lysine (*241K) in LpsB (involved in lipopolysaccharide [LPS] synthesis) in one Cst(r) strain and a frameshift mutation in CarO and the loss of a 47,969-bp element containing multiple genes associated with biofilm production in the other.

FIG 1

Relative fitness of Cst^s/Cst^r A. baumannii strains. Values represent the means ± SD from three independent experiments performed at 5 and 20 h. Fitness values below 1 denote fitness cost, while those above 1 denote a fitness benefit. Asterisks indicate statistically significant differences between strains (*, P < 0.05; **, P = 0.001; ***, P < 0.001).

FIG 2

Adhesion and biofilm formation by Cst^s/Cst^r A. baumannii strains at 6 h (A) and 24 h (B) in a static model. Results represent the mean values ± SD from three independent experiments (OD, optical density). Asterisks indicate statistically significant differences between strains (*, P < 0.001). (C) Biofilm formation in a dynamic model; results represent the mean values ± SD from three independent experiments (IntDen, integrated density). Asterisks indicate statistically significant differences between strains (*, P < 0.001). (D) Fluorescence microscopy images of BioFlux channels.