[Occurrence and mechanisms of resistance to beta-lactam antibiotics in clinically important species of Enterobacter]. / Výskyt a mechanizmy rezistencie proti beta-laktámovým antibiotikám u klinicky významných druhov rodu Enterobacter.

Extended-spectrum beta-lactam antibiotics have found great medical importance, but their wide use in clinical practice leads to increasing resistance to them. The more frequent occurrence of infections caused by Bush group 1 beta-lactamase producing organisms, including species of the genus Enterobacter, is a serious problem in this field. Resistance to beta-lactams in this important nosocomial pathogens can be due to 1) reduction in outer membrane permeability to antibiotics caused by alterations in outer membrane lipopolysacharides or proteins (porins); 2) production of beta-lactamases, which inactivate beta-lactams and can also lead to resistance by non-hydrolytic mechanism called trapping. Production of plasmid-mediated extended-spectrum beta-lactamases, but especially chromosomally-mediated inducible cephalosporinase AmpC, which can be synthesized constitutively in large amounts as consequence of spontaneous chromosomal mutations, are of great clinical importance. Fourth-generation cephalosporins and carbapenems are the most effective in the treatment of infections caused by species belonging to the genus Enterobacter, but combination of high level beta-lactamase production and decreased outer membrane permeability, which is not rare in Enterobacter spp., leads to resistance even to these drugs.

Occurrence and transferability of beta-lactam resistance in Enterobacteriaceae isolated in Children's University Hospital in Bratislava.

Occurrence and transferability of beta-lactam resistance in 30 multi-resistant Escherichia coli, Klebsiella spp., Enterobacter spp., Pantoea agglomerans, Citrobacter freundii and Serratia marcescens strains isolated from children between 0 and 3 years of age is presented. The strains were resistant to ampicillin (30), cefoxitin (22), cefotaxime (30), ceftriaxone (30), ceftazidime (30) and aztreonam (28), but susceptible to cefepime (30) and imipenem (26). Twenty-eight of 30 isolates possessed a transferable resistance confirmed by conjugation and isolation of 79-89-kb plasmids. The beta-lactam resistance was due to production of beta-lactamases and ceftazidime proved to be stronger beta-lactamase inductor than ceftriaxone. Twenty-five clinical isolates expressed transferable extended spectrum beta-lactamases, and chromosomally encoded AmpC beta-lactamase.