Objectives: Carbapenem resistance in Klebsiella pneumoniae (CRKp) may be caused by the presence of carbapenemase enzymes or by combined mechanisms. Our objectives were to examine the effects of resistance mechanisms on several resistance phenotypes in CRKp with carbapenem MICs that are close to the breakpoints.
Methods: The study compared isolates from two populations: 1) carbapenemase-producing CRKP (C-CRKp) and 2) non carbapenemase-producing CRKp (NC-CRKp). Both groups included ertapenem-resistant isolates that were not highly resistant to imipenem and/or meropenem (MIC`s range 0.5-4 mg/L). Inoculum effect was tested by comparing standard AD MIC measurement (104) with higher inoculums. We defined a resistance index as the relative expression of the β-lactamase genes divided by the ompK36 expression.
Results: The C-CRKp group included 24 isolates, with various carbapenemase enzymes (KPC: 6, OXA-48: 15, VIM: 2 and NDM: 1). The NC-CRKp group included 9 isolates, of various CTX-M enzymes. At least one truncated ompK gene was found in 6 of the 9 (66%) NC-CRKp isolates but in only 5 of the 24 (20.8%) C-CRKp isolates. The resistance index was highest in the NC-CRKp isolates (mean-58.2%) compared with 30.3% in the KPC-producers and less than 5% in the other C-CRKp isolates. Inoculum effect was found in 22 of the 24 (91.6%) C-CRKp isolates but in only 3 of the 9 (33.3%) NC-CRKp isolates.
Conclusions: This study suggests that MIC measurements alone without carbapenemase testing may not be sufficient in predicting therapeutic efficiency in infections caused by CRKP isolates with borderline resistance to carbapenems.
