Background
The bloodstream infections (BSI) caused by Escherichia coli pose a serious threat to human health. To explore molecular characteristics of E. coli causing BSI, we collected E. coli isolates causing BSI in Huashan Hospital, Shanghai, China during 2010-2015.
Conclusion
E. coli strains isolated from BSI were still highly susceptible to carbapenems and β-lactamase inhibitor combinations, and bla CTX-M was the dominant genotype of ESBLs. The low expression of bla KPC may be the reason for the low resistance to carbapenems.
Methods
In all E. coli isolates causing BSI collected from this study, polymerase chain reaction (PCR) was used to detect ESBLs and carbapenemase genes, and minimum inhibitory concentrations (MICs) were determined with agar dilution method. Outer membrane proteins were examined by SDS-PAGE in carbapenem-resistant strains. The genetic background of bla KPC gene was investigated by combining next-generation sequencing with a PCR mapping approach. Conjugation and transformation experiments were performed to verify the mobilization of bla KPC. The transcription levels of the bla KPC gene were measured by RT-PCR.
Results
During 2010-2015, a total of 207 E. coli BSI strains were isolated. The positive rates of β-lactamase resistant genes were 0.48% (bla KPC), 57% (bla TEM), 23.67% (bla CTX-M-1), 18.84% (bla CTX-M-9), and 1.93% (bla SHV). High rates of bla TEM, bla CTX-M-1, and bla CTX-M-9 were consistent with the poor activity of third-generation cephalosporins and aztreonam in vitro, except for carbapenem and β-lactamase inhibitor combinations. Low susceptibility rates were observed for piperacillin (25.1%) in contrast to the increased susceptibility when combined with β-lactamase inhibitors, namely piperacillin-tazobactam (90.8%). Only one KPC-producing E. coli strain was detected. Despite the combination of OmpC loss, the low expression level of KPC may be responsible for its lower resistance to carbapenems compared to E. coli DH5α (pKP12-100).