Mechanisms of β-lactam resistance amongst Pseudomonas aeruginosa isolated in an Italian survey

Abstract

The mechanisms of resistance to β-lactam antibiotics in 325 isolates of Pseudomonas aeruginosa were examined. These isolates were selected because of their resistance to meropenem and imipenem (breakpoint, > 4 mg/L), carbenicillin (> 128 mg/L), ceftazidime (> 8 mg/L), piperacillin and ticarcillin/clavulanate (> 64 mg/L). The most frequent mechanism of resistance was β-lactamase-independent, so called 'intrinsic resistance', which was found in 183 isolates and was probably due to impermeability and/or efflux mechanisms. β-Lactamase-mediated resistance was demonstrated in 111 strains (11.1%). Derepression of Ambler Class C chromosomal β-lactamase was detected in 64 isolates, most of which were resistant to ceftazidime and piperacillin but susceptible to meropenem, whereas secondary plasmid-encoded β-lactamases were found in 34 isolates, all of them resistant to carboxypenicillins and ureidopenicillins and susceptible to carbapenems. Twelve strains showed more than one plasmid-encoded β-lactamase plus derepression of chromosomal Class C enzyme. Resistance to carbapenems was independent of resistance to other β-lactam antibiotics, indicating a different mechanism of resistance, probably due to the loss of the D2 porin. In total, 32 strains were resistant to carbapenems: 24 only to imipenem and eight to both imipenem and meropenem.