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.
Highlights
AmpC β-lactamase, altered porins, or both are usually responsible for cefoxitin resistance in Escherichia coli
We created cephamycin-resistant strains of E. coli by serial passage on cefoxitin-containing medium to determine which of these two resistance mechanisms was predominant and if our findings were representative of those seen in clinical isolates
The emergence of E. coli strains resistant to extendedspectrum cephalosporins and cephamycins should be a cause of concern to clinicians managing infections in both the community and institutional setting
Summary
AmpC β-lactamase, altered porins, or both are usually responsible for cefoxitin resistance in Escherichia coli. 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. Surveys of resistance mechanisms in cephamycin-resistant strains have most often identified promoter or attenuator mutations, which results in an up-regulation of AmpC β-lactamase production [5,6,7]. Mutation or altered expression of outer membrane proteins constituting porins can contribute to cephamycin resistance. We created cephamycin-resistant strains of E. coli by serial passage on cefoxitin-containing medium to determine which of these two resistance mechanisms was predominant and if our findings were representative of those seen in clinical isolates
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