| Abstract: | Objective To investigate molecular typing and drug resistance analysis of carbapenem-resistant Escherichia coli (CREC) in our hospital in order to provide evidence for clinical prevention and treatment. Methods From September 2017 to December 2018, 14 CREC strains obtained from different routes of infections in our hospital were collected. The strain identification and drug sensitivity were tested by VITEK 2-compact automatic bacterial identification/drug sensitivity system, combined with the disk diffusion method (K-B method) and the E-test method. Carbapenem resistance gene (blaKPC, blaNDM, blaIMP, blaVIM, and blaOXA-48), extended spectrum β-lactamase gene(blaSHV, blaTEM, blaCTX, blaOXA-1), AmpC enzyme gene (blaFOX, blaMOX and blaDHA), and membrane pore protein gene (ompk35 and ompk36) were detected by PCR. At the same time, they were tested by plasmid conjugation experiments, in order to understand the distribution and prevalence of drug-resistant genes of CREC in our hospital. The homology analysis of 14 different infection pathways of CREC was carried out by PFGE, and the epidemiological characteristics of CREC in our hospital were analyzed. Results Clinical data: 14 CREC were mainly from the intensive care unit, accounting for 57.14% (8/14). 5 of 14 strain were detected in sputum, 4 in urine, 2 in blood, 1 in lavage fluid, cerebrospinal fluid, and catheter tip respectively. Detection of drug resistance genes: 12 strains of 14 CREC carry blaNDM-5, 1 strain carries blaKPC-2, and 1 strain carries blaNDM-1. The CREC resistance mechanism in our hospital is that these CREC usually carried blaNDM-5 and ESBLs resistance gene, accompanied by ompk36 gene deletion. The results of conjugation experiment: only one CREC was successful. The results of PFGE typing showed that 14 CREC were divided into 4 PFGE types, among which PT03 was the dominant type, including 11 strains. Drug resistance: CREC resistance was very serious. All strains were resistant to monocyclic β-lactams, cephalosporins, levofloxacin, and carbapenems. The resistance rate of the strains to aminoglycosides and sulfonamides reached 92.86%. These strains were sensitive to both tigecycline and polymyxin. Conclusion The CREC in our hospital was mainly from respiratory specimens, and there was a clonal epidemic. The dominant strains carried blaNDM-5 and ESBLs resistance genes, accompanied by the deletion of ompk36 gene, and they were highly resistant to various antibiotics. It is suggested that we should increase the control of CREC, close monitoring and control measures should be taken to block the spread and outbreak of CREC in the |
