[Surveillance of Pseudomonas aeruginosa sensitivity to antibiotics in France and distribution of beta-lactam resistance mechanisms: 1998 GERPB study].

In a prospective study carried out during a three-week period in October 1998 in 13 teaching hospitals, 735 non-repetitive isolates of Pseudomonas aeruginosa were collected. In patients presenting cystic fibrosis (70 strains), the main serotypes isolated were O:6 (14.3%) and O:1 (14.3%). Serotypes O:11 and O:12 were exceptional. In other patients (665 strains), the most frequent serotypes were O:6 (15.9%), O:11 (15.6%), O:1 (10.7%) and O:12 (9.2%). The antibiotic susceptibility rates were as follows (respectively, non-cystic fibrosis and cystic fibrosis strains): ticarcillin, 55 and 59%, piperacillin, 71 and 67%, ceftazidime, 75 and 67%, cefepime, 56 and 43%, cefpirome, 37 and 21%, aztreonam, 57 and 56%, imipenem, 83 and 70%, amikacin, 69 and 33%, ciprofloxacin, 56 and 61% and fosfomycin, 33 and 43%. Serotype O:12 was the least susceptible to antibiotics. Forty-five percent of the non-cystic fibrosis strains presented intermediate susceptibility or resistance to ticarcillin. The most frequent mechanisms of resistance were: non-enzymatic resistance (14.3%), overproduction of the constitutive cephalosporinase (13.8%), production of transferable beta-lactamase (8.6%) and a combination of these mechanisms (4.2%). Among cystic fibrosis strains, resistance to beta-lactam antibiotics was mainly due to overproduction of the constitutive cephalosporinase (18.6%), whereas production of a transferable beta-lactamase was rare (1.4%). Susceptibility to aminoglycosides and fluoroquinolones was less frequent in isolates producing transferable beta-lactamases and/or overproducing cephalosporinase. Decreased susceptibility to imipenem was more frequent in strains presenting a high level of cephalosporinase production. Among the cephalosporins, cefepime was the least affected by the overproduction of constitutive cephalosporinase. Ceftazidime remained the most efficient antibiotic against both susceptible isolates and strains presenting a non-enzymatic or PSE-1 penicillinase-producing mechanism.