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[Beta-lactamases in laboratory and their role in resistance Part I.: Evolution of bacterial resistance mediated by beta-lactamases].

Beta-lactamases are the commonest cause of bacterial resistance to beta-lactam antibiotics. They have been classified phenotypically by their isoelectric point, substrate profile, susceptibility to inhibitors and genetic origin. Chromosomal beta-lactamases are typical for certain bacterial species and plasmid beta-lactamases are transferable between different species and genera. Sequencing of beta-lactamase genes enabled to divide them into four classes: A, B, C and D. The ability of a beta-lactamase to confer resistance depends on its location, kinetics, quantity and physicochemical conditions. First beta-lactamases were described soon after introduction of penicillin. Plasmid-mediated broad-spectrum beta-laktamases appeared in the middle 60-s of the XX century and confer resistance to penicillins and some first generation cephalosporins. They include TEM-1, TEM-2, SHV-1, ROB, BRO, OXA and PSE beta-lactamases and are transferred by conjugation between different species and strains of Gram-negative bacteria. The new beta-lactam agents nowadays are compromised mostly by extended-spectrum beta-lactamases, inhibitor-resistant beta-lactamases and carbapenemases. Extended-spectrum beta-lactamases (ESBLs) were described for the first time 20 years ago and are derived from the parental TEM and SHV-1 beta-lactamases by mutations that alter the configuration of the active site to expand their spectrum of activity. They hydrolyse oxymino-cephalosporins and aztreonam. The rapid and accurate laboratory detection of ESBLs is important for choosing appropriate antibiotic therapy. Infections caused by Enterobacteriaceae producing ESBLs pose a therapeutic problem due to multiple antibiotic resistance which includes non-beta-lactam antibiotics as well. Carbapenems are the first-line antibiotics for treatment of such infections.