TABLE 3.
Influence of ompF, rseA, and ompR mutations on late-generation cephalosporin and carbapenem MICs against E. coli producing CTX-M variantsa
| Strain name (CTX-M variant) | MIC (μg·ml−1) of: |
||||
|---|---|---|---|---|---|
| Cefepime | Cefquinome | Ceftazidime | Ceftiofur | Ertapenem | |
| ATCC 25922(pK18) | 0.25 | 0.125 | 0.25 | 0.25 | 0.016 |
| ATCC 25922(pK18) (CTX-M-1) | >128 | >128 | 16 | >128 | 0.0625 |
| ATCC 25922(pK18) (CTX-M-15) | >128 | >128 | 32 | >128 | 0.125 |
| ATCC 25922(pK18) (CTX-M-14) | 64 | >128 | 2 | >128 | 0.0313 |
| ATCC 25922(pK18) ompF | 0.25 | 0.125 | 0.5 | 0.5 | 0.016 |
| ATCC 25922(pK18) ompF (CTX-M-1) | >128 | >128 | 32 | >128 | 0.25 |
| ATCC 25922(pK18) ompF (CTX-M-15) | >128 | >128 | 64 | >128 | 0.5 |
| ATCC 25922(pK18) ompF (CTX-M-14) | >128 | >128 | 4 | >128 | 0.0313 |
| ATCC 25922(pK18) rseA | 0.25 | 0.25 | 0.5 | 0.5 | 0.0313 |
| ATCC 25922(pK18) rseA (CTX-M-1) | >128 | >128 | 16 | >128 | 0.5 |
| ATCC 25922(pK18) rseA (CTX-M-15) | >128 | >128 | 32 | >128 | 0.5 |
| ATCC 25922(pK18) rseA (CTX-M-14) | >128 | >128 | 4 | >128 | 0.125 |
| PSA | 0.125 | 0.125 | 0.5 | 0.25 | 0.016 |
| PSA CTX-M-1 | >128 | >128 | 32 | >128 | 0.125 |
| PSA CTX-M-15 | >128 | >128 | 32 | >128 | 0.25 |
| PSA CTX-M-14 | 128 | >128 | 8 | >128 | 0.0313 |
| PSA (M) (ompR) | 0.125 | 0.25 | 0.5 | 0.5 | 0.0625 |
| PSA (M) (ompR) (CTX-M-1) | >128 | >128 | 16 | >128 | 1 |
| PSA (M) (ompR) (CTX-M-15) | >128 | >128 | 16 | >128 | 1 |
| PSA (M) (ompR) (CTX-M-14) | >128 | >128 | 4 | >128 | 0.5 |
a
CTM-M variants were delivered on natural plasmids by conjugation. Plasmid pK18 (33) was added to provide a marker (kanamycin resistance) to allow selection for recipients in conjugation. Isolate PSA is fluoroquinolone resistant, so this was not necessary. Shading is “nonsusceptible” (resistant or intermediate) according to CLSI breakpoints (24).