Abstract
Objectives: Unraveling mechanisms whereby Pseudomonas aeruginosa becomes resistant to carbapenems through testing 114 non-duplicate P. aeruginosa clinical isolates for their susceptibility to various classes of antibiotics and scrutinizing the production of metallo-β-lactamases (MBLs) by tested isolates. Methods: Susceptibility testing of P. aeruginosa to different antibiotics was determined by Kirby-Bauer disk diffusion method and MBLs production by tested isolates was studied phenotypically and genotypically and PCR products were confirmed by sequencing Results: All tested clinical isolates showed eminent resistance to the majority of tested antibiotics and 14 isolates were imipenem (IPM)-resistant. Furthermore, IPM-resistant isolates were verified to be MBLs-producers. MBLs-encoding genes blaSIM and blaSPM genes were detected by PCR where four isolates were found to harbor blaSPM gene while only one isolate harbored blaSIM gene. The correct size of PCR products of blaSIM and blaSPM genes were sequenced and sequences were submitted to the GenBank databases and assigned the accession numbers KX452682 and KX452683 for blaSIM-2 and blaSPM-1, respectively. Conclusion: Here, we report the emanation of P. aeruginosa clinical isolates harboring blaSPM-1 and blaSIM-2 genes. This may reflect the substantial increase in the rate of imipenem resistance due to MBL in P. aeruginosa clinical isolates from Egypt. Early detection and infection-control practices are of the best antimicrobial strategy for combating this organism.
Highlights
Pseudomonas aeruginosa, a notorious primary opportunistic pathogen, is the leading cause of hospitalacquired infections worldwide and commonly associated with high fatality and morbidity rates[1]
Pathogen that causes life threatening respiratory tract infection, urinary tract infections in patients admitted to intensive care units[2,3]
Susceptibility of all tested P. aeruginosa clinical isolates to the 10 tested antibiotics was examined and tested isolates were classified according to their resistance profile into XDR and MDR
Summary
Pseudomonas aeruginosa, a notorious primary opportunistic pathogen, is the leading cause of hospitalacquired infections worldwide and commonly associated with high fatality and morbidity rates[1]. Pathogen that causes life threatening respiratory tract infection, urinary tract infections in patients admitted to intensive care units[2,3]. Infections caused by this pathogen are often difficult to be treated because of both its intrinsic resistance and its remarkable ability to acquire further resistance mechanisms to a plethora of antibiotics[4,5]. The acquired resistance of P. aeruginosa to beta lactam antibiotics has been attributed to several mechanisms including β-lactamase production, upregulation of efflux systems and reduced outer membrane permeability[7,8]. Despite the abundant literature on those mechanisms in P. aeruginosa, there is no data regarding the prevalence of such novel MBLs (especially blaSIM and blaSPM) harbored by P. aeruginosa in Egypt
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