Review article

Resistance to antibiotics in Pseudomonas aeruginosa

Sanda Saredlić ; Odjel za mikrobiologiju i parazitologiju, KBC Split, Split, Hrvatska
Branka Bedenić ; Klinički zavod za kliničku i molekularnu mikrobiologiju, KBC Zagreb, Zagreb, Hrvatska

Abstract

Resistance of Pseudomonas aeruginosa to antibiotics is a result of cell wall impermeability, enhanced efflux of antibiotics from bacterial cells, inactivating enzymes and alterations in target molecules. Natural resistance of P. aeruginosa to a number of β-lactam antibiotics is a consequence of inducible ampC β-lactamase (Ambler class C) whose derepression leads to resistance to ureidopenicillines, 3rd (and 4th) generation cephalosporins, and in combination with the loss of porin OprD, to carbapenems. Acquired β-lactamases in pseudomonas can be of serine type from class Aand D, and zinc metallo-hydrolases, so called metallo-β-lactamases (MBLs) from class B. MBLs confer resistance to all β--lactams, including carbapenems. Resistance to aminoglycosides is usually a result of activities of modifying enzymes and efflux. Fluoroquinolone resistance in P. aeruginosa is mediated through alterations in DNA gyrase or topoisomerase, as well as through active efflux. Percentage of resistant pseudomonas isolates in Croatia was not significantly changed in the last 10 years. Among aminoglycosides the resistance rate in 2008 was lowest to amikacin and highest to gentamicin. Resistance to ciprofloxacin was 24%, to ceftazidime 8%, and to carbapenems around 10%.

Keywords

Pseudomonas aeruginosa; resistance; β-lactamases; efflux

Hrčak ID:

50624

URI

https://hrcak.srce.hr/50624

Publication date:

4.12.2009.

Article data in other languages: croatian

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