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Intestinal commensal bacteria can inhibit dense colonization of the gut by vancomycin-resistant Enterococcus faecium (VRE), a leading cause of hospital-acquired infections 1 , 2 . A four-strained consortium of commensal bacteria that contains Blautia producta BP SCSK can reverse antibiotic-induced susceptibility to VRE infection 3 . Here we show that BP SCSK reduces growth of VRE by secreting a lantibiotic that is similar to the nisin-A produced by Lactococcus lactis . Although the growth of VRE is inhibited by BP SCSK and L. lactis in vitro, only BP SCSK colonizes the colon and reduces VRE density in vivo. In comparison to nisin-A, the BP SCSK lantibiotic has reduced activity against intestinal commensal bacteria. In patients at high risk of VRE infection, high abundance of the lantibiotic gene is associated with reduced density of E. faecium . In germ-free mice transplanted with patient-derived faeces, resistance to VRE colonization correlates with abundance of the lantibiotic gene. Lantibiotic-producing commensal strains of the gastrointestinal tract reduce colonization by VRE and represent potential probiotic agents to re-establish resistance to VRE. The gut commensal Blautia producta secretes a lantibiotic that reduces colonization of the gut by the major pathogen vancomycin-resistant Enterococcus faecium , and transplantation of microbiota with high abundance of the lantibiotic gene enhances resistance to colonization in mice.

Today, there is a continuous worldwide battle against antimicrobial resistance (AMR) and that includes vancomycin-resistant enterococci (VRE). Methods that can adequately and quickly detect transmission chains in outbreaks are needed to trace and manage this problem fast and cost-effectively. In this study, DNA-microarray-based technology was developed for this purpose. It commenced with the bioinformatic design of specific oligonucleotide sequences to obtain amplification primers and hybridization probes. Microarrays were manufactured using these synthesized oligonucleotides. A highly parallel and stringent labeling and hybridization protocol was developed and employed using isolated genomic DNA from previously sequenced (referenced) clinical VRE strains for optimal sensitivity and specificity. Microarray results showed the detection of virulence, resistance, and species-specific genes in the VRE strains. Theoretical predictions of the microarray results were also derived from the sequences of the same VRE strain and were compared to array results while optimizing protocols until the microarray result and theoretical predictions were a match. The study concludes that DNA microarray technology can be used to quickly, accurately, and economically detect specifically and massively parallel target genes in enterococci.

Vancomycin-resistant and (VRE) are increasingly recognized as major opportunistic pathogens in immunocompromised patients, where they may cause bloodstream infections (BSIs). The present study aimed to characterize a cohort of immunocompromised patients colonized or infected with VRE, performing genomic analysis of these isolates. Additionally, we investigated the impact of bacterial culture supernatants on Caco-2 epithelial cells, focusing on adhesion and cytotoxicity to elucidate mechanisms related to epithelial dysfunction and bacterial translocation. We conducted a retrospective study including 46 VRE from two Italian hospitals. Clinical and epidemiological data were collected, and isolates were characterized by antimicrobial susceptibility testing and whole-genome sequencing. Four representative isolates ( ST80, ST117, ST28, and ST179) and two reference strains (ATCC 29212™ and ATCC 51299™) were selected for analyses. Adhesion to Caco-2 monolayers was quantified, while cytotoxicity was assessed using MTT assays with bacterial cell-free supernatants (CS). Hydrogen peroxide (H O ) production was measured using the Amplex Red Hydrogen Peroxide/Peroxidase Assay Kit. The majority of isolates were (78.3%), predominantly ST80 and ST117, possessed multiple resistance determinants. isolates displayed greater sequence type diversity with a ST28 predominance, carrying virulence genes as , , and . , bloodstream-derived isolates ( 51, 52) and reference strain ATCC 29212™ adhered more strongly to Caco-2 cells than other isolates. CS from invasive isolates and ATCC 51299™ significantly reduced epithelial cell viability at 24 h (p < 0.01). In these isolates, H O higher quantification was documented in a cellular model. Our findings highlighted the convergence of antimicrobial resistance and virulence traits in VRE, alongside functional evidence of strain-dependent adhesion and secretion of cytotoxic metabolites. Elevated H O production provides a possible path between enterococcal secretomes and epithelial injury, suggesting oxidative stress as a contributor to epithelial dysfunction and potential translocation. These insights expand current understanding of VRE pathogenesis and point to novel therapeutic approaches aimed at preserving epithelial integrity and mitigating oxidative damage in high-risk patients.

We investigated genomic evolution of vancomycin-resistant Enterococcus faecium (VREF) during an outbreak in Shenzhen, China. Whole-genome sequencing revealed 2 sequence type 80 VREF subpopulations diverging through insertion sequence-mediated recombination. One subpopulation acquired more antimicrobial resistance and carbohydrate metabolism genes. Persistent VREF transmission underscores the need for genomic surveillance to curb spread.

Antibiotic resistance among enterococci and γ-proteobacteria is an increasing problem in healthcare settings. Dense colonization of the gut by antibiotic-resistant bacteria facilitates their spread between patients and also leads to bloodstream and other systemic infections. Antibiotic-mediated destruction of the intestinal microbiota and consequent loss of colonization resistance are critical factors leading to persistence and spread of antibiotic-resistant bacteria. The mechanisms underlying microbiota-mediated colonization resistance remain incompletely defined and are likely distinct for different antibiotic-resistant bacterial species. It is unclear whether enterococci or γ-proteobacteria, upon expanding to high density in the gut, confer colonization resistance against competing bacterial species. Herein, we demonstrate that dense intestinal colonization with vancomycin-resistant Enterococcus faecium (VRE) does not reduce in vivo growth of carbapenem-resistant Klebsiella pneumoniae. Reciprocally, K. pneumoniae does not impair intestinal colonization by VRE. In contrast, transplantation of a diverse fecal microbiota eliminates both VRE and K. pneumoniae from the gut. Fluorescence in situ hybridization demonstrates that VRE and K. pneumoniae localize to the same regions in the colon but differ with respect to stimulation and invasion of the colonic mucus layer. While VRE and K. pneumoniae occupy the same three-dimensional space within the gut lumen, their independent growth and persistence in the gut suggests that they reside in distinct niches that satisfy their specific in vivo metabolic needs.

The spread of vancomycin-resistant enterococci (VRE) is a major threat in nosocomial settings. A large-scale multiclonal VRE outbreak has rarely been reported in Japan due to low VRE prevalence. We evaluated the transmission of vancomycin resistance in a multiclonal VRE outbreak, conducted biological and genomic analyses of VRE isolates, and assessed the implemented infection control measures. In total, 149 patients harboring VanA-type VRE were identified from April 2017 to October 2019, with 153 vancomycin-resistant Enterococcus faecium isolated being grouped into 31 pulsotypes using pulsed-field gel electrophoresis, wherein six sequence types belonged to clonal complex 17. Epidemic clones varied throughout the outbreak; however, they all carried vanA -plasmids (pIHVA). pIHVA is a linear plasmid, carrying a unique structural Tn 1546 containing vanA ; it moves between different Enterococcus spp. by genetic rearrangements. VRE infection incidence among patients in the “hot spot” ward correlated with the local VRE colonization prevalence. Local prevalence also correlated with vancomycin usage in the ward. Transmission of a novel transferrable vanA -plasmid among Enterococcus spp. resulted in genomic diversity in VRE in a non-endemic setting. The prevalence of VRE colonization and vancomycin usage at the ward level may serve as VRE cross-transmission indicators in non-intensive care units for outbreak control.

Vancomycin-resistant enterococci (VRE), particularly Enterococcus faecium , represent a significant nosocomial threat worldwide. In Saudi Arabia, limited genomic data exist to support phenotypic surveillance findings, impeding the understanding of resistance mechanisms, clonal diversity, and plasmid dynamics. To investigate the genomic and phenotypic characteristics of vancomycin-resistant E. faecium and E. faecalis clinical isolates from a tertiary care center in Riyadh, Saudi Arabia, and to assess antimicrobial resistance genes, virulence factors, sequence types, and plasmid replicons. Seventy-five VRE isolates were collected between 2017 and 2019 and subjected to antimicrobial susceptibility testing per CLSI guidelines. The whole genome sequencing (WGS) was performed using the Illumina MiSeq platform. Species identification, MLST/cgMLST typing, resistome, virulome, and plasmidome analyses were conducted using established bioinformatics pipelines (e.g., CARD, VFDB, PlasmidFinder, pyMLST). Among 75 isolates, 50 E. faecium and 6 E. faecalis passed WGS quality thresholds. E. faecium isolates showed high resistance to vancomycin (100%), ciprofloxacin (98%), and ampicillin (96%), while linezolid retained activity (98% susceptible). The vanA gene was detected in 93.9% of E. faecium isolates; other resistance determinants included tet(M ), erm(B) , and liaR/liaS mutations associated with daptomycin non-susceptibility. MLST revealed multiple STs, including ST136, ST102, and ST252, with no dominant clone, supporting polyclonality. Plasmid analysis identified 20 replicon types, predominantly rep11a, rep2, and repUS15, some co-associated with AMR genes. Virulence profiling showed enrichment of bopD , acm , and cpsA/uppS genes. E. faecalis isolates exhibited limited resistance and no clonal clustering. This is the most comprehensive genomic study of VRE from Saudi Arabia to date. Our findings reveal a diverse, polyclonal population of E. faecium harboring high-risk resistance and virulence determinants disseminated via plasmids. These data underscore the need for routine genomic surveillance to guide infection control and antimicrobial stewardship.

Vancomycin-resistant Enterococcus faecium (VREfm) is a major nosocomial pathogen. Identifying VREfm transmission dynamics permits targeted interventions, and while genomics is increasingly being utilised, methods are not yet standardised or optimised for accuracy. We aimed to develop a standardized genomic method for identifying putative VREfm transmission links. Using comprehensive genomic and epidemiological data from a cohort of 308 VREfm infection or colonization cases, we compared multiple approaches for quantifying genetic relatedness. We showed that clustering by core genome multilocus sequence type (cgMLST) was more informative of population structure than traditional MLST. Pairwise genome comparisons using split k-mer analysis (SKA) provided the high-level resolution needed to infer patient-to-patient transmission. The more common mapping to a reference genome was not sufficiently discriminatory, defining more than three times more genomic transmission events than SKA (3729 compared to 1079 events). Here, we show a standardized genomic framework for inferring VREfm transmission that can be the basis for global deployment of VREfm genomics into routine outbreak detection and investigation. Vancomycin-resistant Enterococcus faecium is an important healthcare-associated pathogen and genomic analyses could inform targeted interventions. Here, the authors optimise an analysis pipeline for identification of putative transmission events using core genome multilocus sequence type clustering and split kmer analysis.

Background. Treatment options for vancomycin-resistant enterococci (VRE) bloodstream infection (BSI) are limited. Daptomycin, although not currently approved for this indication, is frequently used for the treatment of VRE-BSI. Its optimal dose still needs to be determined. Methods. We conducted a prospective, observational, cohort study during 2010–2015. We included patients who received a daptomycin dose of ≥6 mg/kg for the treatment of VRE-BSI caused by daptomycin-susceptible VRE. The primary endpoint was 14-day mortality, and multivariable logistic regression was performed for outcome analysis. Results. We included 112 patients treated with daptomycin for VRE-BSI and with evaluable clinical outcomes. The daptomycin minimum inhibitory concentration (MIC) was 4 mg/L in 78 (69.6%) and ≤2 mg/L in 34 (30.4%) isolates. The overall mortality was 40/112 (35.7%). The unadjusted mortality was 18/36 (50.0%) for a daptomycin dose of <7 mg/kg, 17/51 (33.3%) for a dose of 7–9 mg/kg, and 5/25 (20%) for a dose of ≥9 mg/kg (P = .05). The best outcomes were associated with a daptomycin dose of ≥9 mg/kg compared to doses of <7 mg/kg (adjusted odds ratio [aOR], 10.57; 95% confidence interval [CI], 2.25–49.62; P=.003) and 7–9 mg/kg (aOR, 5.01; 95% CI, 1.14–21.98; P=.03). There was no significant difference in mortality with respect to the daptomycin MIC. There was no association between daptomycin dose and elevated creatinine kinase. Conclusion. Higher daptomycin doses (≥9 mg/kg) were associated with lower mortality in patients with VRE-BSI. Our results suggest that higher daptomycin doses need to be considered for VRE-BSI treatment.

Vancomycin-resistant enterococci infection is a worrying worldwide clinical problem. To evaluate the accuracy of GeneXpert vanA/vanB in the diagnosis of VRE, we conducted a systematic review in the study. Experimental data were extracted from publications until May 03 2021 related to the diagnostic accuracy of GeneXpert vanA/vanB for VRE in PubMed, Embase, Web of Science and the Cochrane Library. The accuracy of GeneXpert vanA/vanB for VRE was evaluated using summary receiver to operate characteristic curve, pooled sensitivity, pooled specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio. 8 publications were divided into 3 groups according to two golden standard references, vanA and vanB group, vanA group, vanB group, including 6 researches, 5 researches and 5 researches, respectively. The pooled sensitivity and specificity of group vanA and vanB were 0.96 (95% CI, 0.93-0.98) and 0.90 (95% CI, 0.88-0.91) respectively. The DOR was 440.77 (95% CI, 37.92-5123.55). The pooled sensitivity and specificity of group vanA were 0.86 (95% CI, 0.81-0.90) and 0.99 (95% CI, 0.99-0.99) respectively, and those of group vanB were 0.85 (95% CI, 0.63-0.97) and 0.82 (95% CI, 0.80-0.83) respectively. GeneXpert vanA/vanB can diagnose VRE with high-accuracy and shows greater accuracy in diagnosing vanA.