Antimicrobial treatment of Klebsiella pneumoniae infections can be complicated by the existence of multiply-antibiotic resistant (multiresistant) strains carrying plasmids coding for extended-spectrum β-lactamases (ESBLs), AmpC-type β-lactamases (ACTBLs), or aminoglycoside-modifying enzymes. This situation has become an increasingly serious problem worldwide with incidences ranging from 5% in the United States (1) to 16% in Europe (2), and higher incidences have been reported for particular hospitals or areas due to nosocomial outbreaks (3). Additionally, it should be noted that a large proportion of ESBL-producing strains are also resistant to fluoroquinolones, probably because of mutations in the genes coding for the A subunits of topoisomerases II (DNA-gyrase) and IV. When ESBLs or ACTBLs expression is accompanied by a decreased permeability of the bacterial outer membrane (OM), a major increase in the MICs of β-lactams (including carbapenems in strains expressing ACTBLs) has been observed (4, 5). Similarly, a reduction in permeability also causes moderate increases in the MICs of fluoroquinolones (3, 5, 6). This decreased permeability is caused by the loss or reduced expression of porins, the nonspecific pore outer membrane proteins (OMPs), with the subsequent reductions of antibiotic influx and of access to the antibiotic target. Reduction of porin expression during antimicrobial treatment are caused by different mutations in the porin genes, including point mutations, small and large deletions, and interruption of porin genes by insertion sequences (7).