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Introduction: vancomycin-resistant Enterococcus faecium (VREfm) is a major public health problem worldwide. The aim of our study was to determine the microbiological, epidemiological and molecular characteristics of VREfm isolated in north-central, eastern and western Algeria. Methodology: a collection of 48 VREfm isolated from September 2010 to April 2017 in several Algerian hospitals were studied. Minimum inhibitory concentrations (MICs) were determined by E-test method according to CLSI guidelines. the detection of van genotype of all strains was performed by PCR. Clonal relationship of five VREfm targeted by region were characterized using multilocus sequence typing (MLST). Results: All isolates have multidrug-resistance (MDR) and were resistant to at least five classes of antibiotics; however, all were susceptible to tigecycline and daptomycin with MIC50 at 0.094 µg/mL and 2 µg/mL respectively. All strains belonged to vanA genotype and have high level of resistance to vancomycin and teicoplanin. MLST revealed two sequence types (STs): ST80 (from the four regions of Algeria) and ST789, both belonging to the former hospital-adapted clonal complex CC17. Conclusions: the alarming dissemination of MDR E. faecium vanA and the ST80 in several regions of Algeria suggest a clonal spread of VREfm strains, which urgently require implementation of adequate infection control measures.

We determined the clinical and molecular epidemiology of emerging nosocomial vancomycin-resistant Enterococcus faecium (VREfm)–causing serious bloodstream infections (BSIs) and the correlations between antibiotic resistance and virulence determinants among isolates. All isolates were confirmed by molecular methods (16SrRNA and E. faecium ddl genes) and tested for disk diffusion. PCR was used to detect aac(6′)-aph(2″), vanA and vanB resistance genes, and asa1, cylA, ace, esp, gelE and hyl virulence genes. VREfm and high-level gentamicin-resistant (HLGR) representative isolates were selected to characterize by pulsed-field gel electrophoresis (PFGE) and multi-locus sequence typing (MLST). Of 173 isolates, 73 (42.2%), 146 (84.4%), and 0 (0.0%) were vanA-containing VREfm, aac(6′)-aph(2″)–positive HLGR, and vanB-positive. Independent predictors of VREfm infection were hematological malignancies (P = 0.001) and previous hospitalizations (P = 0.007). Observed mortality rate was 34.7%. Independent predictors of BSI-related mortality were endotracheal intubations (P < 0.001), gastrointestinal diseases (P = 0.002), and pulmonary disease (P < 0.001). All VREfm were resistant to vancomycin, teicoplanin, ciprofloxacin, and erythromycin. The esp, hyl, ace, asa1, cylA, and gelE genes were detected at 55.9, 22.5, 2.9, 2.3, 1.7, and 1.2%, respectively. The esp gene was significantly associated with VREfm compared to VSEfm (P = 0.001). PFGE analysis revealed 23 clones, with 7 major clones. The MLST analysis revealed the following five sequence types: ST80, ST17, ST117, ST132, and ST280, all belonging to CC17. The emergence and expansion of VREfm CC17 with limited antibiotic options in our hospital present a serious public health menace and represent challenges to infection control.

This study aimed to investigate the antimicrobial resistance, virulence gene profile, and pathogenicity of Enterococcus faecium isolated from a large-scale cattle farm in Xinjiang, China, to provide a scientific basis for the prevention and control of E. faecium infections in the region. Nineteen rectal swabs were aseptically collected from diarrheic calves for bacterial isolation. Isolates were identified through morphological observation, biochemical characterization, and PCR amplification. Homology analysis was conducted using 16S rRNA gene sequencing. Antimicrobial susceptibility was evaluated by the disk diffusion method, and key virulence genes were detected using PCR. Pathogenicity was assessed through intraperitoneal inoculation of mice, followed by histopathological examination. Three isolates were identified as E. faecium, consistent with morphological and molecular results. Biochemical tests indicated that the strains could metabolize sucrose, maltose, lactose, melibiose, and raffinose, but not sorbitol. Phylogenetic analysis revealed that isolates SCQ3 and SCQ4 shared 99.3% homology with E. faecium strain MF678878.1, while SCQ11 showed 91% similarity to strain JP2. Antimicrobial susceptibility testing indicated that SCQ11 was resistant to vancomycin. PCR analysis identified the presence of multiple virulence genes, including psaA, hyp, asal, sprE, nuc, cbh, srtA, hyl, scm, and agg. In vivo pathogenicity testing demonstrated that the vancomycin-resistant strain exhibited strong virulence in mice, with gross lesions observed in the liver, spleen, and intestines. Histopathological examination confirmed varying degrees of tissue damage, particularly in the liver and spleen. All three E. faecium isolates exhibited multidrug resistance, with one strain showing vancomycin resistance and harboring a high number of virulent genes. This strain demonstrated significant pathogenicity in vivo. These findings highlight the potential public health threat posed by multidrug-resistant E. faecium in livestock and provide essential data for regional prevention and control strategies.

Hospitalized patients are often administered antibiotics that perturb the gastrointestinal commensal microbiota, leading to outgrowth of antibiotic‐resistant bacteria, like multidrug‐resistant Enterococcus faecium, subsequent spread, and eventually infections. However, the events that occur at the initial stage of intestinal colonization and outgrowth by multidrug‐resistant E. faecium within the antibiotic‐treated host have not been thoroughly studied. Here, we describe and visualize that only 6 hr after cephalosporin treatment of mice, the Muc‐2 mucus layer is reduced and E‐cadherin junctions were altered. In contrast, the cadherin‐17 junctions were unaffected in antibiotic treated mice during E. faecium colonization or in untreated animals. E. faecium was capable to colonize the mouse colon already within 6 hr after inoculation, and agglutinated at the apical side of the intestinal epithelium. During the primary stage of gastrointestinal colonization the number of IgA+ cells and CD11b+IgA+ cells increased in the lamina propria of the colon and mediated an elevated IgA response upon E. faecium colonization. The interaction of multidrug‐resistant Enterococcus faecium with the mouse colon during antibiotic treatment was studied. We show that 6 hr after cephalosporin antibiotic treatment of mice, the Muc‐2 mucus layer is reduced and E‐cadherin adherens junctions were altered. The cadherin‐17 junctions were unaffected in antibiotic‐treated mice during E. faecium colonization or in untreated animals. E. faecium was capable of colonizing the mouse colon within 6 hr after inoculation, and agglutinated at the apical side of the intestinal epithelium. During the primary stage of gastrointestinal colonization the number of IgA+ cells and CD11b+IgA+ cells increased in the lamina propria of the colon and mediated an elevated IgA response to E. faecium.

Enterococcus faecium is a common cause of nosocomial infections, of which infective endocarditis is associated with substantial mortality. In this study, we used a microarray-based transposon mapping (M-TraM) approach to evaluate a rat endocarditis model and identified a gene, originally annotated as \"fruA\" and renamed \"bepA\" putatively encoding a carbohydrate phosphotransferase system (PTS) permease (biofilm and endocarditis-associated permease A [BepA]), as important in infective endocarditis. This gene is highly enriched in E. faecium clinical isolates and absent in commensal isolates that are not associated with infection. Confirmation of the phenotype was established in a competition experiment of wild-type and a markerless bepA mutant in a rat endocarditis model. In addition, deletion of bepA impaired biofilm formation in vitro in the presence of 100% human serum and metabolism of β-methyl-D-glucoside. β-D-glucoside metabolism has been linked to the metabolism of glycosaminoglycans that are exposed on injured heart valves, where bacteria attach and form vegetations. Therefore, we propose that the PTS permease BepA is directly implicated in E. faecium pathogenesis.

The findings of this study shed light on ampicillin resistance in Enterococcus faecium clade A strains. They underscore the significance of alterations in the amino acid sequence of penicillin-binding protein 5 (PBP5) and the pivotal role of the psr region in PBP5 expression and ampicillin resistance. Notably, the presence of a full-length psrB leads to reduced PBP5 expression and lower minimum inhibitory concentrations (MICs) of ampicillin compared to the presence of a shorter psrA, regardless of the pbp5 allele involved. Additionally, clade B E. faecium strains exhibit lower AMP MICs when both psr alleles from clades A and B are present, although it is important to consider other distinctions between clade A and B strains that may contribute to this effect. It is intriguing to note that the divergence between clade A and clade B E. faecium and the subsequent evolution of heightened AMP MICs in hospital-associated strains appear to coincide with changes in Pbp5 and psr . These changes in psr may have resulted in an inactive Psr, facilitating increased PBP5 expression and greater ampicillin resistance. These results raise the possibility that a mimicker of PsrB, if one could be designed, might be able to lower MICs of ampicillin-resistant E. faecium , thus potentially resorting ampicillin to our therapeutic armamentarium for this species.

Background. Daptomycin has become a front-line antibiotic for multidrug-resistant Enterococcus faecium bloodstream infections (BSIs). We previously showed that E. faecium strains with daptomycin minimum inhibitory concentrations (MICs) in the higher end of susceptibility frequently harbor mutations associated with daptomycin resistance. We postulate that patients with E. faecium BSIs exhibiting daptomycin MICs of 3–4 μg/mL treated with daptomycin are more likely to have worse clinical outcomes than those exhibiting daptomycin MICs ≤2 μg/mL. Methods. We conducted a multicenter retrospective cohort study that included adult patients with E. faecium BSI for whom initial isolates, follow-up blood culture data, and daptomycin administration data were available. A central laboratory performed standardized daptomycin MIC testing for all isolates. The primary outcome was microbiologic failure, defined as clearance of bacteremia ≥4 days after the index blood culture. The secondary outcome was all-cause in-hospital mortality. Results. A total of 62 patients were included. Thirty-one patients were infected with isolates that exhibited daptomycin MICs of 3–4 μg/mL. Overall, 34 patients had microbiologic failure and 25 died during hospitalization. In a multivariate logistic regression model, daptomycin MICs of 3–4 μg/mL (odds ratio [OR], 4.7 [1.37–16.12]; P = .014) and immunosuppression (OR, 5.32 [1.20–23.54]; P = .028) were significantly associated with microbiologic failure. Initial daptomycin dose of ≥8 mg/kg was not significantly associated with evaluated outcomes. Conclusions. Daptomycin MICs of 3–4 μg/mL in the initial E. faecium blood isolate predicted microbiological failure of daptomycin therapy, suggesting that modification in the daptomycin breakpoint for enterococci should be considered.

This research was conducted using 50 samples of popular traditional cheeses and 160 enterococcal clinical isolates. Phenotypic and genotypic methods used for identification of enterococci. Then, the incidences of antibacterial resistance and virulence traits were investigated. In total, 165 E. faecalis and 43 E. faecium obtained from traditional cheeses and different clinical isolates were analyzed in the study. Antibiotic susceptibility testing revealed 175(84.1%) isolates with multi-drug resistance (MDR) patterns, which was more common among clinical sources. The predominant virulence profile, including gelE, asa1 and cpd was detected within 47 (22.6%) of the MDR isolates. Our results showed that traditional cheeses and clinical E. faecalis isolates have distinct patterns of virulence traits. The identified enterococci with antibiotic resistance and associated virulence factors, could provide a potential risk to the public health.

The aim of this study was to characterize virulence determinants and antibiotic resistance profiles in enterococci obtained from various clinical sources in the northwest of Iran. A total of 160 enterococcal clinical isolates from various wards of University Teaching Hospitals were collected and specified by biochemical test, from September 2014 to July 2015. Identification of enterococci was confirmed by multiplex PCR in the genus and species level. Antibiotic resistance properties and virulence determinants were examined by phenotypic and molecular methods. Of 160 enterococcal isolates, 125 (78.12%) and 35 (21.88%) isolates were identified as Enterococcus faecalis and Enterococcus faecium , respectively. The most common antibiotic nonsusceptible pattern observed was resistance toward rifampicin [ n  = 122 (76.25%)] followed by erythromycin [ n  = 117 (73.12%)]. Among all isolates, gel E [ n  = 140 (87.5%)], cpd [ n  = 137 (85.6%)], and asa 1 [ n  = 118 (73.8%)] were the most prevalent virulence genes studied. Thirty isolates (11 E. faecalis , 19 E. faecium ) were found to be resistant to vancomycin, with minimum inhibitory concentration of ≥256 μg/ml. Twenty-seven isolates carried the van A gene, whereas none of the isolates carried van B. E. faecalis had a considerable ability to show virulence genes and drug resistance. Emergence of antibiotic-resistant enterococci and the high prevalence of virulence traits in our study could be regarded as an alarming situation.

Vancomycin-resistant enterococci are an important cause of healthcare-associated infections and are inherently resistant to many commonly used antibiotics. Linezolid is the only drug currently approved by the US Food and Drug Administration to treat vancomycin-resistant enterococci; however, resistance to this antibiotic appears to be increasing. Although outbreaks of linezolid- and vancomycin-resistant Enterococcus faecium (LR-VRE) in solid organ transplant recipients remain uncommon, they represent a major challenge for infection control and hospital epidemiology. We describe a cluster of 4 LR-VRE infections among a group of liver and multivisceral transplant recipients in a single intensive care unit. Failure of treatment with linezolid in 2 cases led to a review of standard clinical laboratory methods for susceptibility determination. Testing by alternative methods including whole genome sequencing (WGS) and a comprehensive outbreak investigation including sampling of staff members and surfaces was performed. Review of laboratory testing methods revealed a limitation in the VITEK 2 system with regard to reporting resistance to linezolid. Linezolid resistance in all cases was confirmed by E-test method. The use of WGS identified a resistant subpopulation with the G2376C mutation in the 23S ribosomal RNA. Sampling of staff members' dominant hands as well as sampling of surfaces in the unit identified no contaminated sources for transmission. This cluster of LR-VRE in transplant recipients highlights the possible shortcomings of standard microbiology laboratory methods and underscores the importance of WGS to identify resistance mechanisms that can inform patient care, as well as infection control and antibiotic stewardship measures.