[Susceptibility of 570 Pseudomonas aeruginosa strains to 11 antimicrobial agents and the mechanism of its resistance to fluoroquinolones].
OBJECTIVE
To investigate the resistance of Pseudomonas aeruginosa (P. aeruginosa) to 11 antimicrobial agents and the mechanism of its resistance to fluoroquinolones (FQs).


METHODS
The susceptibility of 570 strains of P. aeruginosa isolated clinically to 11 antimicrobial agents were detected by Kirby-Bauer disc diffusion method. The minimal inhibitory concentration (MIC) of 111 strains thereof to two FQs was determined by agar dilution method. 80 strains resistant to ciprofloxacin (MIC >or= 4 mg/L) were studied for the presence of point mutations in the gyrA and parC gene by direct sequencing and polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) method.


RESULTS
The resistance rates of P. aeruginosa to cefepine, imipenem, amikacin, and ceftazidine, and aztreonam were 10.9%, 11.1%, 11.8%, 12.5%, and 16.6% respectively. The resistance rates to ciprofloxacin, levofloxacin, cefoperazone/sulbactam, and piperacillin were 29.2%, 32.9%, 23.5% and 33.7% respectively. The resistance rates to gentamycin and cefotaxime were 35.7% and 41.1% respectively. More than 60% of the ciprofloxacin resistant strains and the intensive care units (ICU) isolates were multidrug resistant. Among the 80 ciprofloxacin resistant strains, 66 (75%) had a mutation in gyrA codon: Thr83 (ACC)-->Ile (ATC), 52 strains (65%) had a mutation at parC codon: Ser87 (TCG)-->Leu (TTG), and 52 strains (65%) had both the above mentioned gyrA and parC mutations; while gyrA or parC mutation was not observed in the 31 ciprofloxacin susceptible strains. The MIC of ciprofloxacin for the 52 strains with mutations in both gyrA and parC genes was 19.80 mg/L +/- 2.11 mg/L, significantly higher than those for the 14 strains with mutation only in gyrA gene (11.88 mg/L +/- 2.73 mg/L, P < 0.05) and the 143 strains without gyrA and parC gene mutants (11.89 mg/L +/- 2.12 mg/L, P < 0.05).


CONCLUSIONS
Resistance to antimicrobial agents of P. aeruginosa strains remains a problem. In particular, those ciprofloxacin resistant strains and ICU isolates are resistant to most of the antimicrobial agents. The resistance to fluoroquinolones of the clinical isolates of P. aeruginosa is mainly due to the mutations in gyrA and parC genes encoding the target enzyme of fluoroquinolones.
Lei
Yan-Chang
YC
Department of Nosocomial Infection Control, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Wang
Hong-Bo
HB
Sun
Zi-Yong
ZY
Shen
Zheng-Yi
ZY
D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002939:Ciprofloxacin / Q000494:pharmacology; D027101:DNA Topoisomerase IV / Q000235:genetics; D004250:DNA Topoisomerases, Type II / Q000235:genetics; D024881:Drug Resistance, Bacterial / Q000235:genetics*; D005260:Female; D024841:Fluoroquinolones / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008826:Microbial Sensitivity Tests; D017354:Point Mutation; D016133:Polymerase Chain Reaction; D012150:Polymorphism, Restriction Fragment Length; D011550:Pseudomonas aeruginosa / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics
D000900:Anti-Bacterial Agents; D024841:Fluoroquinolones; D002939:Ciprofloxacin; D027101:DNA Topoisomerase IV; D004250:DNA Topoisomerases, Type II