In vivo reversion to the wild-type beta-lactam resistance phenotype mediated by a plasmid carrying ampR and qnrA1 in Enterobacter cloacae.

Resistance to beta-lactams and quinolones in two isogenic Enterobacter cloacae isolates was studied. One was susceptible to cefoxitin and amoxicillin-clavulanate. The other one showed its natural beta-lactam resistance pattern. Both isolates had a nonfunctional AmpR regulator. However, within the second one, the presence of a plasmid carrying ampR and qnrA1 allowed reversion to the wild-type beta-lactam resistance phenotype and decreased susceptibility to fluoroquinolones.