G. Bonfiglio et al., Mechanisms of beta-lactam resistance amongst Pseudomonas aeruginosa isolated in an Italian survey, J ANTIMICRO, 42(6), 1998, pp. 697-702
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), carben
icillin (>128 mg/L), ceftazidime (>8 mg/L), piperacillin and ticarcillin/cl
avulanate (>64 mg/L). The most frequent mechanism of resistance was beta-la
ctamase-independent, so called 'intrinsic resistance', which was found in 1
83 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 i
n 64 isolates, most of which were resistant to ceftazidime and piperacillin
but susceptible to meropenem, whereas secondary plasmid-encoded beta-lacta
mases were round in 34 isolates, all of them resistant to carboxypenicillin
s and ureidopenicillins and susceptible to carbapenerms. Twelve strains sho
wed more than one plasmid-encoded beta-lactamase plus derepression of chrom
osomal Class C enzyme. Resistance to carbapenems was independent of resista
nce to other beta-lactam antibiotics, indicating a different mechanism of r
esistance, probably due to the loss of the D2 porin. In total, 32 strains w
ere resistant to carbapenems: 24 only to imipenem;and eight to both imipene
m and meropenem.