Fereshteh Eftekhar1, Parvaneh Nouri1. 1. Associate Professor, Department of Microbiology, Faculty of Biological Sciences, Shahid Beheshti University , G.C., Chamran Highway, Tehran, Iran .
Abstract
BACKGROUND: Multidrug resistant K. pneumoniae, particularly the extended-spectrum β-lactamase (ESBL) producing strains, are often responsible for the failure of antibiotic treatment in nosocomial infections. Employing molecular methods to distinguish between ESBL and non-ESBL producing isolates can help quick identification of these multidrug resistant pathogens and thereby initiating appropriate antibiotic therapy. The aim of this study was to employ RAPD-PCR to distinguish the genetic fingerprints of ESBL producing clinical isolates of K. pneumoniae from ESBL negative strains. MATERIALS AND METHODS: Antibacterial susceptibility of 104 K. pneumoniae clinical isolates was determined to 13 antibacterial agents by disc diffusion. ESBL production was measured by the double disc synergy test followed by phenotypic confirmatory tests. Genetic fingerprinting was carried out by RAPD-PCR. RESULTS: All isolates were susceptible to imipenem. Antibiotic resistance rates were: piperacillin (100%), ceftazidime (62.5%), cefotaxime (57.6%), aztreonam (52.8%), cefepime (51.9%), kanamycin (50.9%), gentamicin (41.3%), ciprofloxacin (37.5%), nitrofurantoin (30.6%), nalidixic acid (22.1%), piperacillin/tazobactam (21.1%) and amikacin (9.6%). ESBL production was observed in 14 isolates (13.4%). Genetic fingerprinting performed on 43 isolates (14 ESBL positive and 29 ESBL negative) by RAPD-PCR, showed that 46.5% of the isolates belonged to a single profile (genotype 1), of which, the majority (62.1%) were non-ESBL producers. CONCLUSION: RAPD-PCR results showed heterogeneity among the isolates. There was no association between ESBL production with any specific genetic fingerprint.
BACKGROUND: Multidrug resistant K. pneumoniae, particularly the extended-spectrum β-lactamase (ESBL) producing strains, are often responsible for the failure of antibiotic treatment in nosocomial infections. Employing molecular methods to distinguish between ESBL and non-ESBL producing isolates can help quick identification of these multidrug resistant pathogens and thereby initiating appropriate antibiotic therapy. The aim of this study was to employ RAPD-PCR to distinguish the genetic fingerprints of ESBL producing clinical isolates of K. pneumoniae from ESBL negative strains. MATERIALS AND METHODS: Antibacterial susceptibility of 104 K. pneumoniae clinical isolates was determined to 13 antibacterial agents by disc diffusion. ESBL production was measured by the double disc synergy test followed by phenotypic confirmatory tests. Genetic fingerprinting was carried out by RAPD-PCR. RESULTS: All isolates were susceptible to imipenem. Antibiotic resistance rates were: piperacillin (100%), ceftazidime (62.5%), cefotaxime (57.6%), aztreonam (52.8%), cefepime (51.9%), kanamycin (50.9%), gentamicin (41.3%), ciprofloxacin (37.5%), nitrofurantoin (30.6%), nalidixic acid (22.1%), piperacillin/tazobactam (21.1%) and amikacin (9.6%). ESBL production was observed in 14 isolates (13.4%). Genetic fingerprinting performed on 43 isolates (14 ESBL positive and 29 ESBL negative) by RAPD-PCR, showed that 46.5% of the isolates belonged to a single profile (genotype 1), of which, the majority (62.1%) were non-ESBL producers. CONCLUSION: RAPD-PCR results showed heterogeneity among the isolates. There was no association between ESBL production with any specific genetic fingerprint.
Authors: Sobhan Ghafourian; Zamberi Bin Sekawi; Nourkhoda Sadeghifard; Reza Mohebi; Vasantah Kumari Neela; Abbas Maleki; Ali Hematian; Mohammad Rhabar; Mohammad Raftari; Reza Ranjbar Journal: Open Microbiol J Date: 2011-08-16