[Present status of the sensitivity of Pseudomonas aeruginosa to aminoglycosides in France].

9,119 strains of P. aeruginosa were collected from 10 French hospitals from 1981 to 1984. The MIC of gentamicin (GM), sisomicin (SIS), tobramycin (TOB), dibekacin (DBK), netilmicin (NET), amikacin (AMK), and habekacin (HBK) was determined by the two fold microdilution method. 81% of the strains were susceptible to the 4 aminoglycosides. The MICs (geometric mean, mg/l) for these susceptible strains were: GM: 1.69, SIS: 1.58, TOB: 1.06, DBK: 1.12, NET: 2.73, AMK: 4.16, HBK: 2.70. 19% of the 9 119 strains were resistant to SIS, 18% to GM, 16% to TOB and DBK, 11% to NET, 3% to AMK and HBK. Among the 1 758 strains resistant to one or several aminoglycosides, the frequency of the resistance phenotypes was GM-SIS: 11%, GM-SIS-NET: 4.95%, GM-SIS-TOB-DBK: 32.7%, GM-SIS-TOB-DBK-NET: 34.45%, SIS-TOB-DBK-NET: 2.5%, SIS-TOB-DBK-NET-AMK-HBK: 2.39%, GM-SIS-TOB-DBK-NET-AMK-HBK: 11.61%. The mechanism of resistance of the phenotypes 1 to 6 is enzymatic. The mechanism of resistance of the phenotype 7 (resistance to the six aminoglycosides) is either enzymatic or due to decreased uptake or penetration of antibiotic. HBK and AMK are the aminoglycosides most frequently active against P. aeruginosa. The patterns of resistance to both antibiotics are the same. On a weight-for-weight basis, HBK is more active than AMK.