Insertion sequence ISAba11 is involved in colistin resistance and loss of lipopolysaccharide in Acinetobacter baumannii

Abstract

Infections caused by Acinetobacter baumannii are of increasing concern, largely due to the multidrug resistance of many strains. Here we show that insertion sequence ISAba11 movement can result in inactivation of the A. baumannii lipid A biosynthesis genes lpxA and lpxC, resulting in the complete loss of lipopolysaccharide production and high-level colistin resistance.

Fig. 1.

Colistin-resistant derivatives of ATCC 19606 do not produce LPS. SDS-PAGE separation and carbohydrate-specific silver staining of proteinase K-treated whole-cell lysates of the colistin-sensitive strain ATCC 19606 and eight colistin-resistant derivatives. The positions of standard molecular mass markers are shown on the left.

Fig. 2.

The insertion sequence ISAba11 is mobile and replicative in ATCC 19606. Southern hybridization using a probe specific for the ISAba11 transposase gene against DraI-digested genomic DNA isolated from ATCC 19606, AL1835 to AL1841 (lpxC::ISAba11 mutants), and AL1850 (lpxA::ISAba11 mutant). The positions of DNA size markers are shown on the left. Arrows shown on the right indicate the positions and sizes of the novel hybridizing fragments present in the LPS-deficient, colistin-resistant strains.