Genomic and clinical characteristics of carbapenem-resistant Enterobacter cloacae complex isolates collected in a Chinese tertiary hospital during 2013–2021

Abstract

ObjectiveTo analyze the molecular epidemiology of carbapenem-resistant Enterobacter cloacae complex (CREC) by whole-genome sequencing and to explore its clinical characteristics.MethodsEnterobacter cloacae complex isolates collected in a tertiary hospital during 2013–2021 were subjected to whole-genome sequencing to determine the distribution of antimicrobial resistance genes (ARGs), sequence types (STs), and plasmid replicons. A phylogenetic tree of the CREC strains was constructed based on the whole-genome sequences to analyze their relationships. Clinical patient information was collected for risk factor analysis.ResultsAmong the 51 CREC strains collected, blaNDM-1 (n = 42, 82.4%) was the main carbapenem-hydrolyzing β-lactamase (CHβL), followed by blaIMP-4 (n = 11, 21.6%). Several other extended-spectrum β-lactamase-encoding genes were also identified, with blaSHV-12 (n = 30, 58.8%) and blaTEM-1B (n = 24, 47.1%) being the predominant ones. Multi-locus sequence typing revealed 25 distinct STs, and ST418 (n = 12, 23.5%) was the predominant clone. Plasmid analysis identified 15 types of plasmid replicons, among which IncHI2 (n = 33, 64.7%) and IncHI2A (n = 33, 64.7%) were the main ones. Risk factor analysis showed that intensive care unit (ICU) admission, autoimmune disease, pulmonary infection, and previous corticosteroid use within 1 month were major risk factors for acquiring CREC. Logistic regression analysis showed that ICU admission was an independent risk factor for CREC acquisition and was closely related with acquiring infection by CREC with ST418.ConclusionBlaNDM-1 and blaIMP-4 were the predominant carbapenem resistance genes. ST418 carrying BlaNDM-1 not only was the main clone, but also circulated in the ICU of our hospital during 2019–2021, which highlights the necessity for surveillance of this strain in the ICU. Furthermore, patients with risk factors for CREC acquisition, including ICU admission, autoimmune disease, pulmonary infection, and previous corticosteroid use within 1 month, need to be closely monitored for CREC infection.

Plasmid genomic epidemiology of bla KPC carbapenemase-producing Enterobacterales in Canada, 2010–2021

“…There have been limited reports on the E. cloacae complex ST316 lineage elsewhere; one study identified nine E. hormaechei ST316 isolates encoding bla KPC-2 in the United Kingdom between 2014 and 2016 as part of a larger reference study, however, the plasmid content was not reported ( 33 ). Otherwise, eight isolates [one each from references ( 34 – 36 ), and five from reference ( 37 )] of E. hormaechei ST316 have been recently been reported to carry bla NDM-1 in Asia. Although conjugation genes were present, the narrow host range of the plasmid suggests that bla KPC persistence is likely due to the ST316 clone and not driven by the plasmid.…”

Complete genome sequence of multidrug-resistant Enterobacter roggenkampii 0-E

“…( 1 ) cause a variety of foodborne infections in humans and livestock ( 2 ). In particular, resistance to carbapenems, a critical class of broad-spectrum antibiotics ( 3 ), appears widespread among Enterobacter cloacae complex strains ( 4 ). Furthermore, a multidrug-resistant Enterobacter roggenkampii isolated from Japan (OIPH-N260), also a member of the E. cloacae complex ( 5 ), possesses carbapenemase genes bla IMP-1 and bla GES-5 encoded on one IncP6 plasmid, thus placing E. roggenkampii as an emerging threat potentially capable of transferring carbapenem resistance to other pathogens ( 6 ).…”

Hypervirulent Capsular Serotypes K1 and K2 Klebsiella pneumoniae Strains Demonstrate Resistance to Serum Bactericidal Activity and Galleria mellonella Lethality

“…Moreover, hvKps can cause other invasive infections, particularly serotypes K2 and ST-65 [4,8]. However, it is well established that the hypermucoviscosity and hypervirulence are two distinct phenotypes and do not necessarily co-exist in virulent strains [9,10].…”