Abstract
The Enterobacter cloacae complex (ECC) includes common nosocomial pathogens capable of producing a wide variety of infections. Broad-spectrum antibiotic resistance, including the recent emergence of resistance to last-resort carbapenems, has led to increased interest in this group of organisms and carbapenem-resistant E. cloacae complex (CREC) in particular. Molecular typing methods based on heat-shock protein sequence, pulsed-field gel electrophoresis, comparative genomic hybridization, and, most recently, multilocus sequence typing have led to the identification of over 1069 ECC sequence types in 18 phylogenetic clusters across the globe. Whole-genome sequencing and comparative genomics, moreover, have facilitated global analyses of clonal composition of ECC and specifically of CREC. Epidemiological and genomic studies have revealed diverse multidrug-resistant ECC clones including several potential epidemic lineages. Together with intrinsic β-lactam resistance, members of the ECC exhibit a unique ability to acquire genes encoding resistance to multiple classes of antibiotics, including a variety of carbapenemase genes. In this review, we address recent advances in the molecular epidemiology of multidrug-resistant E. cloacae complex, focusing on the global expansion of CREC.
Highlights
Enterobacter spp., the second most common carbapenem-resistant Enterobacteriaceae (CRE) in the United States, increasingly contribute to the spread of carbapenem-resistant infections (Wilson et al, 2017)
We found 61 publicly available English-language publications identifying carbapenemase alleles in Enterobacter cloacae complex (ECC) with a corresponding geographic location (Supplementary Table S2)
ST171 was rare in global surveys of both primarily carbapenem-susceptible (Girlich et al, 2015; Izdebski et al, 2015) and carbapenemase-producing ECC (Peirano et al, 2018), harboring three different carbapenemase genes presumably on different plasmid backbones
Summary
Enterobacter spp., the second most common carbapenem-resistant Enterobacteriaceae (CRE) in the United States, increasingly contribute to the spread of carbapenem-resistant infections (Wilson et al, 2017). Specific substitutions in chromosomal fluoroquinolone resistance-determining regions (QRDRs), such as the previously characterized double-serine/threonine substitutions in gyrA and parC (Hiramatsu et al, 2012), have been associated with improved fitness in major STs of other Enterobacteriaceae, including ESBL-producing Escherichia coli (Johnson et al, 2015) and K. pneumoniae (Tóth et al, 2014). This fitness advantage has been hypothesized to contribute to the spread of high-risk international STs while selecting against minor STs (Fuzi et al, 2017). Their contribution to the spread of specific ECC and CREC clones has yet to be determined
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