Research Article Diversity of Molecular Mechanisms Conferring Carbapenem Resistance to Pseudomonas aeruginosa Isolates from Saudi Arabia Mohamed H. Al-Agamy, 1,2 Katy Jeannot, 3,4 Taghrid S. El-Mahdy, 5 Hassan A. Samaha, 2,6 Atef M. Shibl, 1,7 Patrick Plésiat, 3 and Patrice Courvalin 4 1 Pharmaceutics Department, College of Pharmacy, King Saud University, Riyadh, Saudi Arabia 2 Microbiology and Immunology Department, Faculty of Pharmacy, Al-Azhar University, Cairo, Egypt 3 Laboratoire de Bact´ eriologie, Centre National de R´ ef´ erence de la R´ esistance aux Antibiotiques, Besanc ¸on, France 4 Unit´ e des Agents Antimicrobiens, Institut Pasteur, Paris, France 5 Microbiology and Immunology Department, Faculty of Pharmacy, Helwan University, Cairo, Egypt 6 College of Pharmacy, Al Baha University, Al Baha, Saudi Arabia 7 College of Medicine, Alfaisal University, Riyadh, Saudi Arabia Correspondence should be addressed to Mohamed H. Al-Agamy; elagamy71@yahoo.com Received 17 May 2016; Accepted 19 July 2016 Academic Editor: Maria De Francesco Copyright © 2016 Mohamed H. Al-Agamy et al. Tis 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. Background. Tis study described various molecular and epidemiological characters determining antibiotic resistance patterns in Pseudomonas aeruginosa isolates. Methods. A total of 34 carbapenem-resistant P. aeruginosa clinical isolates were isolated from samples collected at a tertiary hospital in Riyadh, Saudi Arabia, from January to December 2011. Susceptibility testing, serotyping, molecular characterization of carbapenem resistance, and pulsed-feld gel electrophoresis (PFGE) were performed. Results. All isolates were resistant to cefazidime, and more than half were highly resistant (minimum inhibitory concentration (MIC) > 256 mg/L). Fifeen isolates had MIC values ≥64 mg/L for any of the carbapenems examined. Vietnamese extended-spectrum - lactamase (VEB-1) ( = 16/34) and oxacillinase (OXA-10) ( = 14/34) were the most prevalent extended-spectrum -lactamase and penicillinase, respectively. Verona imipenemase (VIM-1, VIM-2, VIM-4, VIM-11, and VIM-28) and imipenemase (IMP-7) variants were found in metallo--lactamase producers. A decrease in outer membrane porin gene (oprD) expression was seen in nine isolates, and an increase in efux pump gene (MexAB) expression was detected in fve isolates. Six serotypes (O:1, O:4, O:7, O:10, O:11, and O:15) were found among the 34 isolates. Te predominant serotype was O:11 (16 isolates), followed by O:15 (nine isolates). PFGE analysis of the 34 carbapenem-resistant P. aeruginosa isolates revealed 14 diferent pulsotypes. Conclusions. Tese results revealed diverse mechanisms conferring carbapenem resistance to P. aeruginosa isolates from Saudi Arabia. 1. Background Pseudomonas aeruginosa is a pathogen emerging as a frequent cause of nosocomial infections, especially pneumonia and sepsis, with mortality rates of 27–48% in critically ill patients [1, 2]. Te increasing prevalence of infections caused by multidrug-resistant (MDR) P. aeruginosa strains is associated with signifcant morbidity and mortality [3]. Management of the infections is difcult since strains ofen display intrinsic and acquired resistance to multiple classes of antibiotics, severely limiting therapeutic options [4]. One feature of P. aeruginosa isolates is their high level of intrinsic resistance to a number of antimicrobial agents. Te broad-spectrum resistance of these organisms is largely due to low outer membrane permeability [5] and to efux systems [6]. More- over, they possess inducible, chromosomally encoded AmpC cephalosporinase belonging to Ambler class C enzymes [7]. Extended-spectrum -lactamases (ESBLs), including TEM, SHV, PER, VEB, GES, OXA-2, and OXA-10 enzymes, are increasingly reported in P. aeruginosa [8, 9]. Tis situation has Hindawi Publishing Corporation Canadian Journal of Infectious Diseases and Medical Microbiology Volume 2016, Article ID 4379686, 7 pages http://dx.doi.org/10.1155/2016/4379686