Research Article Prevalence and Genetic Characterization of Carbapenem- and Polymyxin-Resistant Acinetobacter baumannii Isolated from a Tertiary Hospital in Terengganu, Malaysia Soo-Sum Lean, 1 Zarizal Suhaili, 2 Salwani Ismail, 3 Nor Iza A. Rahman, 3 Norlela Othman, 4 Fatimah Haslina Abdullah, 4 Zakaria Jusoh, 4 Chew Chieng Yeo, 2 and Kwai-Lin Thong 1 1 Institute of Biological Sciences, Faculty of Science, University of Malaya, 50603 Kuala Lumpur, Malaysia 2 Faculty of Agriculture, Biotechnology and Food Sciences, Universiti Sultan Zainal Abidin, 20400 Kuala Terengganu, Malaysia 3 Faculty of Medicine and Health Sciences, Universiti Sultan Zainal Abidin, 20400 Kuala Terengganu, Malaysia 4 Department of Pathology, Hospital Sultanah Nur Zahirah, 20400 Kuala Terengganu, Malaysia Correspondence should be addressed to Kwai-Lin hong; thongkl@um.edu.my Received 5 December 2013; Accepted 9 February 2014; Published 19 March 2014 Academic Editors: B. Ayo, K. Leung, and C. Pazzani Copyright © 2014 Soo-Sum Lean et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Nosocomial infection caused by Acinetobacter baumannii is of great concern due to its increasing resistance to most antimicrobials. In this study, 54 nonrepeat isolates of A. baumannii from the main tertiary hospital in Terengganu, Malaysia, were analyzed for their antibiograms and genotypes. Out of the 54 isolates, 39 (72.2%) were multidrug resistant (MDR) and resistant to carbapenems whereas 14 (25.9%) were categorized as extensive drug resistant (XDR) with additional resistance to polymyxin B, the drug of “last resort.” Pulsed-ield gel electrophoresis analyses showed that the polymyxin-resistant isolates were genetically diverse while the carbapenem-resistant isolates were clonally related. he 14 XDR isolates were further investigated for mutations in genes known to mediate polymyxin resistance, namely, pmrCAB, and the lipopolysaccharide biosynthesis genes, lpxA, lpxC, lpxD, and lpsB. All 14 isolates had a P102H mutation in pmrA with no mutation detected in pmrC and pmrB. No mutation was detected in lpxA but each polymyxin-resistant isolate had 2–4 amino acid substitutions in lpxD and 1-2 substitutions in lpxC. Eight resistant isolates also displayed a unique H181Y mutation in lpsB. he extent of polymyxin resistance is of concern and the novel mutations discovered here warrant further investigations. 1. Introduction Acinetobacter baumannii is a Gram-negative bacterium increas-ing-ly found in the hospital environment due to its ability to survive for long periods on inanimate objects [1, 2]. Nosocomial A. baumannii isolates are mostly multidrug resistant (MDR) (i.e., resistant towards more than three classes of antibiotics) [3]. However, extensive drug resistant (XDR) isolates, which are resistant to all but one or two classes of antibiotics, and even pandrug resistant (PDR) isolates that are resistant to all classes of antibiotics, are developing at an alarming rate [4]. Since A. baumannii has the ability to colonize both viable and damaged tissues and is also resistant towards nearly all antimicrobials, it has become a cause of great concern. Carbapenems are among the very few antibiotics let that can be used for the treatment of A. baumannii infections. Nevertheless, the eicacy of carbapen- ems is increasingly compromised by the rapid emergence of carbapenem-hydrolysing -lactamase enzymes. Several types of class D -lactamases including OXA-23, OXA-24, OXA-58, and intrinsic OXA-51-like enzymes are known to be important contributors to carbapenem resistance [5]. he rapid development of carbapenem-resistant MDR A. baumannii has led to the use of polymyxins (in particular polymyxin B and colistin or polymyxin E) as the drug of “last resort” [6]. Polymyxins are cyclic, positively charged peptide antibiotics capable of posing antimicrobial activities to a broad variety of Gram-negative pathogens, including A. baumannii, due to their interaction with the lipid A moiety of lipopolysaccharide (LPS). his leads to the disorganization Hindawi Publishing Corporation ISRN Microbiology Volume 2014, Article ID 953417, 9 pages http://dx.doi.org/10.1155/2014/953417