Antimicrobial resistance and prevailing resistance mechanisms among problematic clinical isolates of Pseudomonas aeruginosa from the university hospitals in Sofia, Bulgaria
Abstract number: 1733_166
Strateva T., Ouzounova-Raykova V., Markova B., Marteva-Proevska Y., Mitov I.
Objectives: To assess the current levels of antimicrobial susceptibility and to evaluate the resistance mechanisms to antipseudomonal antimicrobial agents among Bulgarian nosocomial isolates of Pseudomonas aeruginosa.
Methods: A total of 203 clinical isolates of P. aeruginosa, resistant to one or more of the following groups of antimicrobials extended-spectrum cephalosporins, carbapenems, aminoglycosides, fluoroquinolones, were collected from 5 University hospitals in Sofia during 20012006. Antimicrobial susceptibilities were detected by the disk diffusion method and Etest (AB Biodisk, Solna, Sweden). The resistance mechanisms were studied with phenotypic methods as previously described by Jarlier V. et al., Lee K. et al. and Miller G. et al. Polymerase chain reaction and sequencing of genes, encoding Ambler class A, B and D b-lactamases, were performed.
Results: The antibiotic resistance rates were: to carbenicillin 93.1%, azlocillin 91.6%, piperacillin 86.2%, piperacillin/tazobactam 56.8%, ceftazidime 45.8%, cefoperazone 86.2%, cefepime 48.9%, cefpirome 58.2%, aztreonam 49.8%, imipenem 42.3%, meropenem 45.5%, amikacin 59.1%, gentamicin 79.7%, tobramycin 89.6%, netilmicin 69.6%, and ciprofloxacin 80.3%. 101 of the studied P. aeruginosa isolates (49.8%) were multidrug-resistant. Structural genes encoding Ambler class A and class D b-lactamases showed the following frequency: blaVEB-1 33.1%, blaPSE-1 22.5%, blaPER-1 0%, blaOXA-groupI 41.3%, and blaOXA-groupII 8.8%. IMP- and VIM-type carbapenemases from molecular class B were not detected.
Conclusions: The studied clinical stains of P. aeruginosa were problematic nosocomial pathogens. VEB-1 ESBLs appear to have a significant presence among the clinical P. aeruginosa isolates from Sofia. The carbapenem resistance was related to non-enzymatic mechanisms such as OprD deficiency and active efflux.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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