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Species of the Enterobacter cloacae complex are widely encountered in nature, but they can act as pathogens. The biochemical and molecular studies on E. cloacae have shown genomic heterogeneity, comprising six species: Enterobacter cloacae, Enterobacter asburiae, Enterobacter hormaechei, Enterobacter kobei, Enterobacter ludwigii and Enterobacter nimipressuralis, E. cloacae and E. hormaechei are the most frequently isolated in human clinical specimens. Phenotypic identification of all species belonging to this taxon is usually difficult and not always reliable; therefore, molecular methods are often used. Although the E. cloacae complex strains are among the most common Enterobacter spp. causing nosocomial bloodstream infections in the last decade, little is known about their virulence-associated properties. By contrast, much has been published on the antibiotic-resistance features of these microorganisms. In fact, they are capable of overproducing AmpC β-lactamases by derepression of a chromosomal gene or by the acquisition of a transferable ampC gene on plasmids conferring the antibiotic resistance. Many other resistance determinants that are able to render ineffective almost all antibiotic families have been recently acquired. Most studies on antimicrobial susceptibility are focused on E. cloacae, E. hormaechei and E. asburiae; these studies reported small variations between the species, and the only significant differences had no discriminating features.

The intestinal microbiota is an important contributor to the health of preterm infants, and may be destabilized by a number of environmental factors and treatment modalities. How to promote the development of a healthy microbiota in preterm infants is largely unknown. We collected fecal samples from 45 breastfed preterm very low birth weight (birth weight < 1500 g) infants from birth until 60 days postnatal age to characterize the intestinal microbiota development during the first weeks of life in preterm infants. Fecal microbiota composition was determined by 16S rRNA amplicon sequencing. The main driver of microbiota development was gestational age; antibiotic use had strong but temporary effects and birth mode had little influence. Microbiota development proceeded in four phases indicated by the dominance of Staphylococcus, Enterococcus, Enterobacter , and finally Bifidobacterium . The Enterococcus phase was only observed among the extremely premature infants and appeared to delay the microbiota succession. The results indicate that hospitalized preterm infants receiving breast milk may develop a normal microbiota resembling that of term infants.

Background Enterobacter cloacae complex (ECC) including different species are isolated from different human clinical samples. ECC is armed by many different virulence genes (VGs) and they were also classified among ESKAPE group by WHO recently. The present study was designed to find probable association between VGs and antibiotic susceptibility in different ECC species. Methods Forty-five Enterobacter isolates that were harvested from different clinical samples were classified in four different species. Seven VGs were screened by PCR technique and antibiotic susceptibility assessment was performed by disk-diffusion assay. Result Four Enterobacter species; Enterobacter cloacae (33.3%), Enterobacter hormaechei (55.6%), Enterobacter kobei (6.7%) and Enterobacter roggenkampii (4.4%) were detected. Minimum antibiotic resistance was against carbapenem agents and amikacin even in MDR isolates. 33.3% and 13.3% of isolates were MDR and XDR respectively. The rpoS (97.8%) and csgD (11.1%) showed maximum and minimum frequency respectively. Blood sample isolated were highly virulent but less resistant in comparison to the other sample isolates. The csgA , csgD and iutA genes were associated with cefepime sensitivity. Conclusion The fepA showed a predictory role for differentiating of E. hormaechei from other species. More evolved iron acquisition system in E. hormaechei was hypothesized. The fepA gene introduced as a suitable target for designing novel anti-virulence/antibiotic agents against E. hormaechei . Complementary studies on other VGs and ARGs and with bigger study population is recommended.

Colistin has emerged as the last resort for treating multidrug-resistant complex (ECC) infections. The primary purposes of this study were to demonstrate the presence of colistin heteroresistance in ECC and to further investigate their clinical characteristics, molecular epidemiology and mechanisms. Population analysis profiles (PAP) were performed to confirm the heteroresistance phenotype. Average nucleotide identity (ANI) was determined to classify ECC species. Phylogenetic analysis based on core genome single nucleotide polymorphisms (cg-SNPs), multilocus sequence typing (MLST) and core genome MLST (cg-MLST). Risk factors and clinical outcomes of infections were analyzed through a retrospective case-control study. Potential mechanisms of colistin heteroresistance were evaluated using polymerase chain reaction (PCR), efflux pump inhibition assays and reverse transcription quantitative PCR (RT-qPCR). A high proportion (24.4%) of the non-resistant strains were colistin-heteroresistant isolates. Among the several ECC species, had the largest percentage (29.4%) of colistin-heteroresistant isolates, followed by (20.5%) and (20.0%). Notably, only one strain (0.8%; 1/132) of was fully resistant to colistin. Different ECC species showed varying heteroresistance levels: , , and displayed high heteroresistance levels  (MIC ≥ 128 mg/L). 75% of all ST116 and ST56 strains were heteroresistant to colistin. The infection of ST116 and ST56 strains as well as exposure to cephalosporin antibiotics were independent risk factors for colistin-heteroresistant ECC infections. Mechanistic analysis revealed that heteroresistance strongly correlated with the overexpression of , regulated by the PhoPQ two-component system (TCS). Notably, had minimal impact. AcrAB-TolC efflux pump genes showed unsynchronized expression; High expression was strongly associated with colistin heteroresistance, while and were not. Colistin heteroresistance showed species-dependent variations in levels and prevalence rates. The colistin-heteroresistant mechanisms were complex, involving coordinated regulation of multiple genes. These results highlighted the need for tailored antimicrobial stewardship. In addition, the development of direct, reliable and rapid clinical methods for detecting heteroresistance is essential for improving infection management and prevention.

We investigated the colistin resistance rate among 356 Enterobacter spp. clinical isolates from eight hospitals in Korea. Antibiotic susceptibility testing was performed by broth microdilution. While 51 of 213 (23.9%) Enterobacter cloacae isolates were colistin-resistant, only six of 143 (4.2%) E. aerogenes isolates showed resistance. We also identified the skip well phenotype in eight E. cloacae and three E. aerogenes isolates. Multilocus sequence typing for E. cloacae and randomly amplified polymorphic DNA analysis and enterobacterial repetitive intergenic consensus PCR for E. aerogenes revealed that clonal spreading of colistin-resistant and skip well Enterobacter spp. isolates had not occurred. In vitro time-kill assays were performed with three colistin-resistant, three skip well, and two colistin-susceptible isolates of E. cloacae and E. aerogenes . Inconsistent results were observed among isolates with skip well phenotypes; while some were eradicated by 2 mg/L colistin, others were not. This suggests that skip well isolates have differentiated into different categories. As the high rates of colistin resistance in E. cloacae detected are of clinical concern, continuous monitoring is warranted. In addition, the clinical implications and mechanisms of the skip well phenotype should be investigated to ensure the appropriate use of colistin against Enterobacter infections.

Enterobacter cloacae and E. aerogenes have been increasingly reported as important opportunistic pathogens. In this study, a high prevalence of multi-drug resistant isolates from Brazil, harboring several β-lactamase encoding genes was found. Several virulence genes were observed in E. aerogenes, contrasting with the E. cloacae isolates which presented none.

BackgroundThe majority of preterm infants at NICUs receives a central venous, or umbilical vein catheter (UVC) and is therefore at risk for catheter associated sepsis. Silver-impregnated UVCs with the AgIONTM antimicrobial system may prevent sepsis and may have longer insertion time.ObjectiveTo assess sepsis and additional CVC insertion with the use of silver-impregnated UVCs compared with conventional ones.MethodsCatheter-duration, sepsis and additional CVC use was compared between infants with silver-impregnated UVCs (silvergroup) during 1 year (2012-2013) and infants with conventional UVCs (controls) during 2011, when inserted >3 days.ResultsIn 156/249 (2012-2013) infants a silver-impregnated and all 273 with an UVC in 2011 a conventional UVC was inserted. Mean catheter-duration was 5.8 (3-15) days in the silvergroup vs 5.7 (3-12) days in the controls (NS). 11/156 (7%) infants from the silvergroup developed sepsis during catheterisation vs 17/267 (6.4%) controls [NS]. Main causative microorganisms: CoNS (62.5%), S. aureus (15.6%), Enterobacter (9.3%). In 22/156 infants of the silvergroup, UVC use was longer than 8 days, vs in 20/273 controls (NS). 3/22 of the silvergroup with UVC use > 8 days developed sepsis vs 1/273 controls (p = 0.015). Significant more infants in the silvergroup needed additional CVC insertion 18/156 (11.5%) vs in 28/273 (10.3%) controls (p = 0.00).ConclusionsDuration of > 8 days of silver-impregnated UVC significantly increased the risk for sepsis as compared with conventional UVC use.Silver-impregnated UVCs were not inserted for longer periods than conventional UVCs.Anti-infectious advantage of the silver-impregnated UVCs could not be proven.

Knowledge regarding the genomic structure of Enterobacter spp., the second most prevalent carbapenemase-producing Enterobacteriaceae , remains limited. Here we sequenced 97 clinical Enterobacter species isolates that were both carbapenem susceptible and resistant from various geographic regions to decipher the molecular origins of carbapenem resistance and to understand the changing phylogeny of these emerging and drug-resistant pathogens. Of the carbapenem-resistant isolates, 30 possessed bla KPC-2 , 40 had bla KPC-3 , 2 had bla KPC-4 , and 2 had bla NDM-1 . Twenty-three isolates were carbapenem susceptible. Six genomes were sequenced to completion, and their sizes ranged from 4.6 to 5.1 Mbp. Phylogenomic analysis placed 96 of these genomes, 351 additional Enterobacter genomes downloaded from NCBI GenBank, and six newly sequenced type strains into 19 phylogenomic groups—18 groups (A to R) in the Enterobacter cloacae complex and Enterobacter aerogenes . Diverse mechanisms underlying the molecular evolutionary trajectory of these drug-resistant Enterobacter spp. were revealed, including the acquisition of an antibiotic resistance plasmid, followed by clonal spread, horizontal transfer of bla KPC -harboring plasmids between different phylogenomic groups, and repeated transposition of the bla KPC gene among different plasmid backbones. Group A, which comprises multilocus sequence type 171 (ST171), was the most commonly identified (23% of isolates). Genomic analysis showed that ST171 isolates evolved from a common ancestor and formed two different major clusters; each acquiring unique bla KPC -harboring plasmids, followed by clonal expansion. The data presented here represent the first comprehensive study of phylogenomic interrogation and the relationship between antibiotic resistance and plasmid discrimination among carbapenem-resistant Enterobacter spp., demonstrating the genetic diversity and complexity of the molecular mechanisms driving antibiotic resistance in this genus. IMPORTANCE Enterobacter spp., especially carbapenemase-producing Enterobacter spp., have emerged as a clinically significant cause of nosocomial infections. However, only limited information is available on the distribution of carbapenem resistance across this genus. Augmenting this problem is an erroneous identification of Enterobacter strains because of ambiguous typing methods and imprecise taxonomy. In this study, we used a whole-genome-based comparative phylogenetic approach to (i) revisit and redefine the genus Enterobacter and (ii) unravel the emergence and evolution of the Klebsiella pneumoniae carbapenemase-harboring Enterobacter spp. Using genomic analysis of 447 sequenced strains, we developed an improved understanding of the species designations within this complex genus and identified the diverse mechanisms driving the molecular evolution of carbapenem resistance. The findings in this study provide a solid genomic framework that will serve as an important resource in the future development of molecular diagnostics and in supporting drug discovery programs. Enterobacter spp., especially carbapenemase-producing Enterobacter spp., have emerged as a clinically significant cause of nosocomial infections. However, only limited information is available on the distribution of carbapenem resistance across this genus. Augmenting this problem is an erroneous identification of Enterobacter strains because of ambiguous typing methods and imprecise taxonomy. In this study, we used a whole-genome-based comparative phylogenetic approach to (i) revisit and redefine the genus Enterobacter and (ii) unravel the emergence and evolution of the Klebsiella pneumoniae carbapenemase-harboring Enterobacter spp. Using genomic analysis of 447 sequenced strains, we developed an improved understanding of the species designations within this complex genus and identified the diverse mechanisms driving the molecular evolution of carbapenem resistance. The findings in this study provide a solid genomic framework that will serve as an important resource in the future development of molecular diagnostics and in supporting drug discovery programs.

Understanding the nuances of AmpC β-lactamase–mediated resistance can be challenging, even for the infectious diseases specialist. AmpC resistance can be classified into 3 categories: (1) inducible chromosomal resistance that emerges in the setting of a β-lactam compound, (2) stable derepression due to mutations in ampC regulatory genes, or (3) the presence of plasmid-mediated ampC genes. This review will mainly focus on inducible AmpC resistance in Enterobacteriaceae. Although several observational studies have explored optimal treatment for AmpC producers, few provide reliable insights into effective management approaches. Heterogeneity within the data and inherent selection bias make inferences on effective β-lactam choices problematic. Most experts agree it is prudent to avoid expanded-spectrum (ie, third-generation) cephalosporins for the treatment of organisms posing the greatest risk of ampC induction, which has best been described in the context of Enterobacter cloacae infections. The role of other broad-spectrum β-lactams and the likelihood of ampC induction by other Enterobacteriaceae are less clear. We will review the mechanisms of resistance and triggers resulting in AmpC expression, the species-specific epidemiology of AmpC production, approaches to the detection of AmpC production, and treatment options for AmpC-producing infections.

Carbapenemase-producing (CP-Ent) are the third most prevalent species of CP- worldwide and exhibit greater strain diversity than other CP-species. This study aimed to describe the genomic epidemiology of CP-Ent in south-central Ontario, Canada. CP-Ent isolates collected from colonized/infected patients identified by population-based surveillance in Toronto/Peel Region, Canada (2007-2020), sink/shower drains in 12 regional hospitals (2016-2019), and five municipal wastewater treatment plants (2015, 2017) were analyzed to assess relationships between patient and environmental CP-Ent. Clinical data were collected by chart review/patient interview. CP-Ent isolates were sequenced by Illumina. Genomic analysis included Snippy, IQ-Tree, and ClonalFrameML; ≤ 20 single-nucleotide variant differences defined strains. CP-Ent colonization/infection incidence increased from 2007-2020. Overall, 3.5% of sink/shower drains and 22% of municipal wastewater cultures yielded CP-Ent. Patient and sink/shower drain isolates were similar in species and carbapenemases produced; municipal wastewater isolates were distinct. Forty-one of 116 patients (35%) belonged to 15 transmission clusters: 5/15 (33%) included drain isolates, and 32/41 (78%) patients were linked to others in the same hospital, including 22 (54%) linked by stays in the same ward. Patients were more likely to be linked by ward exposure at different times versus the same time in wards with sink/shower drains yielding CP-Ent versus those without (13/19 vs 2/23,  = <.001). Despite transmission control efforts, a significant proportion of CP-Ent are part of hospital transmission clusters; sink/shower drains may be implicated in transmission. It is likely that undetected patients, drains and/or other reservoirs contribute to CP-Ent transmission in the studied population.