TABLE 1

Bacterial strains used in this studya

StrainDetected porinbEfflux component (AcrAB)Enzyme(s) detectedc
OmpFOmpC
E. coli
    AG100+++AmpC(b)
    ARS100dNDAmpC(b)
    ARS108d+AmpC(b), CTX-M-15
    ARS144d+++AmpC(b), CTX-M-15, DHA-1
    ARS150d+++AmpC(b), CTX-M-15, TEM-1
    ARS237d+++AmpC(b), CTX-M-14, TEM-1
    ARS273d+NDAmpC(b), CTX-M-15
    ARS301d+++CTX-M-15
E. aerogenesOmp35Omp36
    ATCC 15038+++AmpC(b)
    EA2e+++AmpC(d), TEM-24
    EA3e+ (loop 3 mutant)+AmpC(d), TEM-24
    EA5e+AmpC(d), TEM-24
    EA27e+++AmpC(d), TEM-24
    EA117e− (weak signal)+AmpC(d), TEM-24
    EA DFJ85e+++AmpC(d), TEM-24
    EA DFJ46e+ND
K. pneumoniaeOmpK35OmpK36
    ATCC 11296+++/−ND
    KP45e+++ND
    KP55e+ESBL (TEM-3)
    KP63e+ESBL (TEM-3)
    KP74e++ESBL (TEM-3)
    KP80e++ESBL (TEM-3)
    KP89e++ND
  • a Except for AG100, ATCC 15038, and ATCC 11296, these are previously characterized clinical isolates of E. coli, E. aerogenes, and K. pneumoniae.

  • b Porins and efflux components were identified by Western blot-immunodetection (OmpC or OmpF, AcrAB, TolC): −, no signal (whatever the medium used); +, signal detected; +++, AcrAB overproduction. ND, not determined.

  • c AmpC(b), AmpC basal; AmpC(d), derepressed.

  • d Clinical isolates from the laboratory of J. P. Lavigne, CHU Nîmes (32).

  • e Clinical isolates from our laboratory (3336).