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연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제56권 제4호
발행연도
2015.1
수록면
928 - 934 (7page)

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Purpose: Colistin resistance in Acinetobacter baumannii (A. baumannii) is mediatedby a complete loss of lipopolysaccharide production via mutations in lpxA, lpxC,and lpxD gene or lipid A modifications via mutations in the pmrA and pmrB genes. However, the exact mechanism of therapy-induced colistin resistance in A. baumanniiis not well understood. Materials and Methods: We investigated the genotypicand phenotypic changes that underlie pan-drug resistance mechanisms by determiningdifferences between the alterations in extensively drug-resistant (XDR)A. baumannii (AB001 and AB002) isolates and a pan-drug resistant (PDR) counterpart(AB003) recovered from one patient before and after antibiotic treatment, respectively. Results: All three clinical isolates shared an identical sequence type(ST138), belonging to the global epidemic clone, clonal complex 92, and all producedOXA-23 carbapenemase. The PDR AB003 showed two genetic differences,acquisition of armA gene and an amino acid substitution (Glu229Asp) in pmrB gene,relative to XDR isolates. No mutations were detected in the pmrA, pmrC, lpxA, lpxC,or lpxD genes in all three isolates. In matrix-assisted laser desorption ionization-timeof flight analysis, the three isolates commonly showed two major peaks at 1728 m/zand 1912 m/z, but peaks at 2034 m/z, 2157 m/z, 2261 m/z, and 2384 m/z were detectedonly in the PDR A. baumannii AB003 isolate. Conclusion: Our results showthat changes in lipid A structure via a mutation in the pmrB gene and acquisition ofarmA gene might confer resistance to colistin and aminoglycosides to XDR A. baumanniistrains, resulting in appearance of a PDR A. baumannii strain of ST138.

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