Review article
Antimicrobial resistance in Pseudomonas aeruginosa
Marija Gužvinec
; Klinika za infektivne bolesti "Dr. Fran Mihaljević", Zagreb, Hrvatska
Iva Butić
; Klinika za infektivne bolesti "Dr. Fran Mihaljević", Zagreb, Hrvatska
Marko Jelić
; Klinika za infektivne bolesti "Dr. Fran Mihaljević", Zagreb, Hrvatska
Suzana Bukovski
; Klinika za infektivne bolesti "Dr. Fran Mihaljević", Zagreb, Hrvatska
Sandra Lucić
; Klinika za infektivne bolesti "Dr. Fran Mihaljević", Zagreb, Hrvatska
Arjana Tambić Andrašević
; Klinika za infektivne bolesti "Dr. Fran Mihaljević", Zagreb, Hrvatska
Abstract
Pseudomonas aeruginosa is one of the leading causes of nosocomial infections, mostly in intensive care unit patients. In addition to being intrinsically resistant to many antibiotics, in hospital setting it often develops resistance also to antipseudomonal drugs. Mechanisms of resistance in P. aeruginosa include efflux, decreased permeability, target site alterations and production of antibiotic-hydrolyzing enzymes. Some strains accumulate different resistance mechanisms, thus becoming multiresistant or even panresistant, and growing prevalence of such strains is severely compromising the choice of effective therapy. Studies suggest that multiresistance most often results from accumulation of mutations affecting efflux, cell permeability and expression of chromosomally encoded β-lactamase AmpC, while acquired β-lactamases are only sporadically found. Recent epidemiological studies also show that most of multiresistant clinical strains belong to only a few widely spread nosocomial P. aeruginosa clones.
Keywords
Pseudomonas aeruginosa; resistance; β-lactamases; clonal spread
Hrčak ID:
98104
URI
Publication date:
30.9.2012.
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