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. 2013 Sep;57(9):4381–4386. doi: 10.1128/AAC.00660-13

Table 1.

Trimethoprim, sulfamethoxazole, and trimethoprim-sulfamethoxazole susceptibilities of selected clinical and environmental isolates with and without the BpeEF-OprC efflux pumpa

Strain MIC (μg/ml)
SXT (bpeE+F+-oprC+) SMX (bpeE+F+-oprC+) TMP
bpeE+F+-oprC+ Δ(bpeEF-oprC) Δ(bpeEF-oprC), complemented,b uninduced Δ(bpeEF-oprC), complemented,b +1 mM IPTG
1026b 0.094/1.79 4 0.75 0.5 0.5 6
Thailand Clinical
    2650a 1/19 8 ≥32 1.5 1.5 ≥32
    2665a 1/19 16 ≥32 1.5 1.5 16
    2677a 1.5/28.5 24 ≥32 2 2 ≥32
    2719a 1/19 12 ≥32 1 1 16
    2769a 0.75/14.25 12 16 1.5 2 ≥32
Thailand environmental
    E0016 0.75/14.25 12 ≥32 1 1.5 16
    E0235 1.5/28.5 24 ≥32 1.5 3 ≥32
    E0237 0.5/9.5 8 4 1 2 16
    E0342 0.75/14.25 24 ≥32 1 1.5 16
Australia clinical
    MSHR305 0.5/9.5 32 ≥32 2 2 16
    MSHR668 0.38/7.22 16 ≥32 2 2 32
    MSHR465a 1/19 32 ≥32 3 2 ≥32
a

Abbreviations: TMP, trimethoprim; SMX, sulfamethoxazole; SXT, trimethoprim-sulfamethoxazole.

b

The respective strains containing the Δ(bpeEF-oprC) mutation have a mini-Tn7T-Ptac-bpeE+F+-oprC+ element integrated at the chromosomal glmS2 locus, except for the MSHR668 derivative, which has the same element integrated at glmS3. The bpeE+F+-oprC+ operon contained on this mini-Tn7 element is derived from prototype strain 1026b (18).