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. 2012 Nov;56(11):5591–5602. doi: 10.1128/AAC.01446-12

Table 5.

Impact of loss of intrinsic aminoglycoside resistance genes on aminoglycoside susceptibility of clinical P. aeruginosa isolates

Strain Relevant property MIC (μg/ml)a
GEN PAR SPC KAN TOB AMI
K2160 Panaminoglycoside resistant 32 1,024 512 256 8 32
K3192 AmgR 8 (4) 512 (2) 256 (2) 64 (4) 1 (8) 4 (8)
K3193 PstB 8 (4) 512 (2) 256 (2) 64 (4) 2 (4) 16 (2)
K3194 FaoA 4 (8) 256 (4) 256 (2) 64 (4) 2 (4) 8 (4)
K3195 PA2798 4 (8) 256 (4) 256 (2) 64 (4) 1 (8) 4 (8)
K3196 PA0392 4 (8) 256 (4) 256 (2) 64 (4) 2 (4) 8 (8)
K3197 LptA 8 (4) 512 (2) 512 (1) 128 (2) 2 (4) 8 (8)
K2168 MexXY 8 (4) 128 (8) 64 (8) 128 (2) 4 (2) 8 (8)
K2162 Panaminoglycoside resistant 256 >4,096 2,048 1,024 32 128
K3198 AmgR 64 (4) 4,096 (2)b 1,024 (2) 512 (2) 8 (4) 32 (4)
K3199 PstB 16 (16) 2,048 (4)b 1,024 (2) 256 (4) 16 (2) 16 (8)
K3200 FaoA 64 (4) 1,024 (8)b 2,048 (1) 512 (2) 16 (2) 32 (4)
K3201 PA2798 8 (32) 1,024 (8)b 1,024 (2) 512 (2) 4 (8) 8 (16)
K3202 PA0392 16 (16) 1,024 (8)b 1,024 (2) 256 (4) 8 (4) 16 (8)
K3203 LptA 64 (4) 4,096 (2)b 2,048 (1) 512 (2) 8 (4) 32 (4)
K2170 MexXY 16 (16) 256 (32)b 128 (16) 256 (4) 8 (4) 16 (8)
a

Fold changes in MIC for the mutants relative to that for the corresponding wild-type clinical parent strain are indicated in parentheses. GEN, gentamicin; PAR, paromomycin; SPC, spectinomycin; KAN, kanamycin; TOB, tobramycin; AMI, amikacin.

b

Because a precise paromomycin MIC was not determined for the K2162 parent of these mutants, the fold change reported in parentheses is a minimum.