Abstract

Enterobacter spp. are important nosocomial pathogens responsible of a wide variety of infections, mainly due to Extended Spectrum β-Lactamase (ESBL) producing isolates, constituting a global public health issue in terms of clinical treatment and infection control, especially in low-income countries, where last-line treatment is often unavailable and there is weak nosocomial surveillance. In this study, we conducted a phenotypic and molecular characterization of 8 clinical Enterobacter spp. strains, isolated from patient’s blood in three hospitals in Mozambique. Isolates were identified by MALDI-TOF and antimicrobial Susceptibility Testing was performed by VITEK 2 system. Half of isolates were analyzed by PCR for β-lactamases genes, other isolates by Whole Genome Sequencing. We identified all isolates as Enterobacter cloacae complex (ECC), those from Maputo Central Hospital were polyclonal, multidrug resistant (5/8), and ESBL producers (50%), carrying blaCTX-M-15 and different assortment of blaSHV-12, blaTEM-1B and blaOXA-1, and AmpCs blaCMH-3, blaACT-7 and blaACT-9 genes. Resistance determinants linked to fluoroquinolone (aac(6')Ib-cr and qnrB1) and others antimicrobials were also found. Notably, one isolate showed phenotypically resistance to colistin, while another colistin susceptible isolate carried a silent mcr-9 gene. ECC nosocomial surveillance is urgently needed to contain and prevent the dissemination of ESBLs producing clones, and mcr-9 spread to other Enterobacteriaceae.

Highlights

  • Enterobacter is a member of the ESKAPE group (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species), which includes the 6 most important nosocomial pathogens (Santajit and Indrawattana 2016; Davin-Regli et al 2019).Enterobacter spp., are mainly cause of nosocomial infections, including urinary tract infections (UTI), pneumonia, soft tissue infections, endocarditis and septicemia, while they are less commonly found in community-acquired infections (Ramirez and Giron 2020)

  • ExpandedSpectrum Beta-Lactamases (ESBLs) are often associated with other resistance genes, mainly found within conjugative plasmids or other mobile genetic elements, which can be transmitted intra and interspecies, conferring resistance to antimicrobials extensively used in human and animals (Jiang et al 2008; Rozwandowicz et al 2018)

  • We reported the presence of a polyclonal multidrug resistance (MDR) Enterobacter cloacae complex circulating in the Maputo Central Hospital, Mozambique

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Summary

Introduction

Enterobacter is a member of the ESKAPE group (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species), which includes the 6 most important nosocomial pathogens (Santajit and Indrawattana 2016; Davin-Regli et al 2019).Enterobacter spp., are mainly cause of nosocomial infections, including urinary tract infections (UTI), pneumonia, soft tissue infections, endocarditis and septicemia, while they are less commonly found in community-acquired infections (Ramirez and Giron 2020). Enterobacter spp. are associated to multidrug resistance (MDR) phenotypes thanks to their adaptation capability to the hospital environment and their ability to acquire resistance and virulence determinants through genetic mobile elements (Uhlemann 2019; Davin-Regli et al 2019). Enterobacter spp. and in general all Enterobacteriaceae, are resistant to beta-lactams, such as natural and synthetic penicillins and cephalosporins of 2nd and 3rd generation, due to the production of ExpandedSpectrum Beta-Lactamases (ESBLs) (Davin-Regli 2015). Enterobacter spp. isolates harboring blaCTX-M-15 and other antimicrobial resistance, including quinolone, aminoglycoside and more recently carbapenem and colistin determinants (Huang et al 2012; Kananizadeh 2020), constitute a serious health problem due to the lack of treatments (Lim et al 2010; Osei Sekyere 2016), and increased mortality worldwide (Fernández et al 2015; Bonomo et al 2018; Etemadi et al 2020; Shawa et al 2021)

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