Resistance Island: What is new in an Extensive-Drug Resistant Clinical Strain of Acinetobacter baumannii?

Chieng, Yeo Chew (2014) Resistance Island: What is new in an Extensive-Drug Resistant Clinical Strain of Acinetobacter baumannii? In: 21st Malaysian Society for Molecular Biology & Biotechnology (MSMBB) Annual Scientific Meeting, 01-03 October 2014, Monash University Malaysia.

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Abstract

Acinetobacter baumannii is an important nosocomial Gram-negative pathogen that is difficult to treat due to its increasing resistance towards almost all antimicrobials. Clusters of antibiotic resistance determinants in A. baumannii are often found in structures known as resistance islands (RIs). These RIs are usually transposable elements which can be transferred from one organism to another and thus play an essential role in the development of antimicrobial resistance. The objective of this study was to identify any RI that may contribute to the extensive drug-resistance (XDR) phenotype in A. baumannii strain AC12 which was isolated from a tertiary hospital in Terengganu, Malaysia. Whole genome sequences of A. baumannii AC12 (GenBank accession no. AC007549) were mapped to the reference RI using CLCBio Genomics Workbench 5.0. Visualisation of RI and gene orientations was carried out using Artemis. Whole genome analyses of A. baumannii AC12 revealed the presence of a 10.3 kb antibiotic resistance island, ACRI12-2, which interrupts the D-serine/D-alanine/glycine transporter gene and a flavin monooxygenase at the 3’-end. This RI was flanked by two copies of IS26 but lack the class 1 integron containing the aacC1-orfP-orfP-orfQ-aadA1 array and an incomplete Tn21 at the 3’-end when compared to AbGRI2-1. Drug resistance genes such as aphA1b (conferring kanamycin and neomycin resistance) and blaTEM (conferring β-lactam resistance) were found present in ACRI12-2. Different variants of AbGRI2-1 have been reported in other strains. The aphA1b and blaTEM genes in AC12-RI2 were flanked by IS elements which may provide an external promoter to increase the expression levels of these genes, thereby conferring resistance to the respective antimicrobials. The genetic structure of ACRI12-2 explained the resistance phenotype of A. baumannii AC12 shown towards β-lactams and aminoglycosides.

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