King-Ting Lim¹, Rohani Md Yasin², Chew-Chieng Yeo³, Savithri-Devi Puthucheary⁴, Ganeswrie Balan⁵, Nurahan Maning⁶, Zubaidah Abdul Wahab⁷, Noraini Ismail⁸, Eng-Am Tan⁹, Azizah Mustaffa¹⁰, Kwai-Lin Thong^1
1Microbiology Division, Institute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur; ²Specialized Diagnostic Centre, Institute of Medical Research, Kuala Lumpur; ³Department of Biotechnology, Malaysia University of Science and Technology, Petaling Jaya; ⁴Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur; ⁵Sultanah Aminah Hospital, Johor Bharu; ⁶Kota Bharu Hospital, Kelantan; ⁷Kuala Lumpur Hospital, Kuala Lumpur; ⁸Queen Elizabeth Hospital, Kota Kinabalu; ⁹Ipoh Hospital, Ipoh; and ¹⁰Tengku Ampuan Rahimah Hospital, Kelang, Malaysia

Received: May 20, 2008     Revised: July 1, 2008     Accepted: July 23, 2008

Corresponding author: Dr. Kwai-Lin Thong, Microbiology Division, Institute of Biological Sciences, Faculty of Science, University of Malaya, 50603 Kuala Lumpur, Malaysia. E-mail: This e-mail address is being protected from spam bots, you need JavaScript enabled to view it

Background and purpose: Pseudomonas aeruginosa is the third most common pathogen causing nosocomial infections. The objective of this study was to investigate the antimicrobial resistance profiles and genetic diversity of hospital isolates of P. aeruginosa and to investigate the presence of several resistance genes and integrons.

Methods: In this retrospective study, 48 clinical isolates of P. aeruginosa from 6 public hospitals in Malaysia were analyzed by antimicrobial susceptibility test and DNA fingerprinting techniques.

Results: Most of the P. aeruginosa isolates were resistant to tetracycline (73%) and chloramphenicol (60%) and, to a lesser extent, cefotaxime (40%), ceftriaxone (31%), cefoperazone (29%), ticarcillin (25%), piperacillin (23%), and imipenem (21%). Less than 20% of the isolates were resistant to ceftazidime, gentamicin, cefepime, ciprofloxacin, amikacin, piperacillin-tazobactam, and aztreonam (10%). Of the 48 isolates, 33 were multidrug resistant. Two isolates were extended-spectrum β-lactamase (ESBL) producers using the double-disk synergy test. However, polymerase chain reaction (PCR) failed to detect any common ESBL-encoding genes in all isolates, except for bla_OXA-10 in PA7 that was found to be part of a class 1 integron-encoded aacA4-bla_IMP-9-catB8-bla_OXA-10 gene cassette. Using PCR, class 1 integron-encoded integrases were detected in 19% of the P. aeruginosa isolates. Repetitive extragenic palindrome-PCR generated 40 different profiles (F = 0.50-1.0) and enterobacterial repetitive intergenic consensus-PCR produced 46 profiles (F = 0.51-1.0). Pulsed-field gel electrophoresis with SpeI-digested genomic DNA resulted in 45 different profiles (F = 0.50-1.00).

Conclusion: Aztreonam appeared to be the most effective agent against multidrug-resistant P. aeruginosa isolates. Sixty nine percent of the P. aeruginosa isolates analyzed were multidrug resistant and the isolates were genetically diverse.

Key words: DNA fingerprinting; Drug resistance, microbial; Drug resistance, multiple; Pseudomonas aeruginosa

J Microbiol Immunol Infect. 2009;42:197-209.