Abstract
AmpC β-lactamase, altered porins, or both are usually responsible for cefoxitin resistance in Escherichia coli. We examined the relative importance of each. We studied 18 strains of clinical isolates with reduced cefoxitin susceptibility and 10 initially-susceptible strains passaged through cefoxitin-gradient plates. Of 18 wild-resistant strains, 9 had identical promoter mutations (including creation of a consensus 17-bp spacer) and related pulsed-field gel electrophoresis patterns; the other 9 strains were unrelated. Nine strains had attenuator mutations; two strains did not express OmpC or OmpF. After serial passage, 8 of 10 strains developed cefoxitin resistance, none developed promoter or attenuator mutations, 6 lost both the OmpC and OmpF porin proteins, and 1 showed decreased production of both. One strain had neither porin alteration or increased AmpC production. Porin mutants may occur more commonly and be less fit and less inclined to spread or cause disease than strains with increased β-lactamase expression.