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 2001–2006. 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.