Objectives: Little is known about the molecular epidemiology of KPC-producing E. coli (KPEC). We aimed to describe the clonal structure and resistance mechanisms of KPEC in a multicenter study.
Methods: The study included patient-unique KPEC isolates collected from January 2009 until June 2012 at the Tel-Aviv Medical Center (TASMC), Laniado Hospital (LH), Sha'are-Zedek Medical Center (SZMC) and Rambam Medical Center (RMC). The clonal structure was studied by PFGE and MLST. The blaKPC and blaESBL genes were studied by sequencing.
Results: The study included 88 KPEC isolates, 38 from SZMC, 21 from RMC, 17 from TASMC and 12 from LH. Twelve KPEC were from clinical sites and the rest from surveillance cultures. The clonal structure was highly diverse, with 79 and 45 different PFGE types and sequence types (ST), respectively. The most common clones were clonal complexes (CC's) 131 (n=16), CC-410 (n=14) and CC-10 (n=17). blaKPC-2 and blaKPC-3 were identified in 68 and 20 isolates, respectively. blaESBL genes were found in 28 isolates, most commonly blaCTX-M-15 and blaCTX-M-27. All isolates were non-susceptible to ertapenem; 16 (18%) and 35 (40%) isolates were susceptible (MIC≤1 mg/L) to imipenem and meropenem, respectively. Isolates were susceptible to colistin, amikacin, ciprofloxacin, gentamicin and trimethoprim-sulfamethoxazole in 100, 87, 28, 27 and 21% of the cases, respectively.
Conclusion: The clonal structure of KPEC in Israel is characterized by the predominance of known international ESBL-producing clones and by high intra- and inter-institutional diversity. This suggests that clonal spread does not play a major role in the dissemination of KPEC.
