A total of 1102 consecutive clinical blood isolates, including 897 Enterobacteriaceae and 205 non-fermenting bacilli, were obtained from 13 university and university-affiliated hospitals, which were divided into a Northern and a Southern group. Resistance to gentamicin, tobramycin, netilmicin, amikacin and isepamicin was determined using a microdilution technique according to NCCLS procedures. The overall mean resistance level was 5.9% for gentamicin, 7.7% for tobramycin, 7.5% for netilmicin, 2.8% for amikacin and 1.2% for isepamicin. Resistance to amikacin and isepamicin was significantly higher in the Northern hospitals than in the Southern hospitals. In total, 157 isolates were found not to be susceptible to aminoglycosides. By PCR, 179 aminoglycoside resistance mechanisms, i.e. 150 genes encoding modifying enzymes and 29 permeability mechanisms, were detected in 148 isolates. A resistance mechanism could not be detected in nine isolates. Moreover, in a further 14 isolates the resistance profile was not fully explained by the detected genes. The aac(6 ′ )-I genes were found to be the most predominant resistance mechanism in both the Northern and Southern isolates, followed by aac(3) genes and permeability resistance. A total of 29 non-susceptible isolates harboured a combination of genes, 72.4% of which were a combination with the aac(6 ′ )-Ib gene. The majority of these combinations were broad-spectrum combinations which represented 9.0% of the resistance mechanisms in non-susceptible Enterobacteriaceae and 19.3% in the non-fermenting bacilli.