Journal of Antimicrobial Chemotherapy, Vol 42, 697-702, Copyright © 1998 by The British Society for Antimicrobial Chemotherapy
G Bonfiglio, Y Laksai, L Franchino, G Amicosante and G Nicoletti
The mechanisms of resistance to beta-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 beta-lactamase-independent, so called 'intrinsic
resistance', which was found in 183 isolates and was probably due to
impermeability and/or efflux mechanisms. beta-Lactamase-mediated resistance
was demonstrated in 111 strains (11.1%). Derepression of Ambler Class C
chromosomal beta-lactamase was detected in 64 isolates, most of which were
resistant to ceftazidime and piperacillin but susceptible to meropenem,
whereas secondary plasmid-encoded beta- 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 beta- lactamase plus derepression of chromosomal Class C
enzyme. Resistance to carbapenems was independent of resistance to other
beta-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.
Mechanisms of beta-lactam resistance amongst Pseudomonas aeruginosa isolated in an Italian survey [In Process Citation]
Instituto di Microbiologia, Universita di Catania, Italy. bonfigio@mbox.unict.it
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