Enterococcus gallinarum
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA813694 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| JALBDB01.dat.gz | Other | |||
| JALBDB01.fasta.gz | Fasta.gz | |||
| JALBDB01.master.dat | Other | |||
| SRR19138401_1.fastq.gz | Fastqsanger.gz |
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Project description:Enterococcus faecium from bloodstream infection
| PRJNA901969 | ENA
Project description:This study aimed to evaluate the clinical outcomes of vancomycin-resistant enterococcal bloodstream infections (VRE BSI) caused by Enterococcus gallinarum or Enterococcus casseliflavus. Variables associated with treatment failure were determined and treatment options were compared. This was a national retrospective study of hospitalised Veterans Affairs patients with non-faecium, non-faecalis VRE BSI. The primary outcome was treatment failure, defined as a composite of: (i) 30-day all-cause mortality; (ii) microbiological failure; and (iii) 30-day VRE BSI recurrence. Stepwise Poisson regression was conducted to determine variables associated with treatment failure. In total, 48 patients were included, with 29 cases (60.4%) caused by E. gallinarum and 19 cases (39.6%) caused by E. casseliflavus. Among these cases, 20 (41.7%) were treated with an anti-VRE agent (linezolid or daptomycin) and 28 (58.3%) were treated with an anti-enterococcal ?-lactam. Overall, 30-day mortality was 10.4% (5/48) and composite treatment failure was 39.6% (19/48). In multivariate analysis, treatment with an anti-enterococcal ?-lactam was associated with increased treatment failure in comparison with anti-VRE therapy (adjusted risk ratio = 1.73, 95% confidence interval 1.06-4.97; P = 0.031). Overall, treatment with linezolid or daptomycin for vancomycin-resistant E. gallinarum or E. casseliflavus BSI resulted in improved clinical outcomes in comparison with anti-enterococcal ?-lactam treatment.
| S-EPMC4889110 | biostudies-literature
Project description:Glycopeptide-resistant enterococci of the VanC type synthesize UDP-muramyl-pentapeptide[D-Ser] for cell wall assembly and prevent synthesis of peptidoglycan precursors ending in D-Ala. The vanC cluster of Enterococcus gallinarum BM4174 consists of five genes: vanC-1, vanXY(C), vanT, vanR(C), and vanS(C). Three genes are sufficient for resistance: vanC-1 encodes a ligase that synthesizes the dipeptide D-Ala-D-Ser for addition to UDP-MurNAc-tripeptide, vanXY(C) encodes a D,D-dipeptidase-carboxypeptidase that hydrolyzes D-Ala-D-Ala and removes D-Ala from UDP-MurNAc-pentapeptide[D-Ala], and vanT encodes a membrane-bound serine racemase that provides D-Ser for the synthetic pathway. The three genes are clustered: the start codons of vanXY(C) and vanT overlap the termination codons of vanC-1 and vanXY(C), respectively. Two genes which encode proteins with homology to the VanS-VanR two-component regulatory system were present downstream from the resistance genes. The predicted amino acid sequence of VanR(C) exhibited 50% identity to VanR and 33% identity to VanR(B). VanS(C) had 40% identity to VanS over a region of 308 amino acids and 24% identity to VanS(B) over a region of 285 amino acids. All residues with important functions in response regulators and histidine kinases were conserved in VanR(C) and VanS(C), respectively. Induction experiments based on the determination of D,D-carboxypeptidase activity in cytoplasmic extracts confirmed that the genes were expressed constitutively. Using a promoter-probing vector, regions upstream from the resistance and regulatory genes were identified that have promoter activity.
| S-EPMC89929 | biostudies-literature
Project description:Vancomycin resistance in enterococci is an increasing clinical problem, and several phenotypes have been identified. We demonstrate here that the resistance mechanism in the constitutively vancomycin-resistant Enterococcus gallinarum BM4174 involves an altered pathway of peptidoglycan synthesis and hydrolysis of the normal precursors in the vancomycin-sensitive pathway. A ligase encoded by the vanC gene catalyses synthesis of D-Ala-D-Ser and substitutes this dipeptide for D-Ala-D-Ala in peptidoglycan precursors. It is presumed that this substitution lowers the affinity of vancomycin for its target site. Destruction of D-Ala-D-Ala (D,D-peptidase activity) and of UDP-MurNAc-L-Ala-D-isoGlu-L-Lys-D-Ala-D-Ala by removal of the terminal D-Ala residue (D,D-carboxypeptidase activity) ensures that the normal vancomycin-sensitive pathway of peptidoglycan synthesis cannot function in the resistant strain.
| S-EPMC1137133 | biostudies-other
Project description:In this study we describe the immunostimulatory properties of Enterococcus gallinarum MRx0518, a candidate live biotherapeutic agent with anti-tumorigenic properties. Here we demonstrate that strain MRx0518 elicits a strong pro-inflammatory response in intestinal epithelial cells. Treatments with metabolically active cells, inactivated cells or culture supernatants were found to induce distinct host responses. Microarray analysis was used to investigate and compare changes in the gene expression of intestinal epithelial cells in response to live MRx0518, heat-killed MRx0518 and MRx0518 culture supernatant.
2019-02-06 | GSE122232 | GEO
Project description:Enterococcus faecalis, a member of the human gastrointestinal microbiota, is a Gram-positive, opportunistic pathogen associated with hospital-acquired wound, bloodstream, and urinary tract infections. E. faecalis can suppress or evade immune-mediated clearance by macrophages to promote persistent infection, although the exact mechanisms and bacterial factor(s) involved are not well-defined. In this study, we examined E. faecalis factor(s) involved in suppressing macrophage activation, as well the macrophage pathways modulated by E. faecalis to suppress activation. We observed that E. faecalis prevents ERK and p65 phosphorylation and reduces MyD88 expression leading to a reduction in NF-κB activity. We identified E. faecalis lactate dehydrogenase, which is important for lactic acid production by E. faecalis, to be necessary for macrophage suppression and demonstrated that E. faecalis lactate dehydrogenase-mediated immune suppression promotes E. coli survival during polymicrobial wound infection. Taken together, these results suggest that that E. faecalis-derived lactic acid is involved in macrophage subversion and may help to promote the virulence of co-infecting bacteria.
2024-11-01 | GSE188916 | GEO
Project description:Gene expression in human umbilical vein endothelial cells (HUVEC) was investigated by microarray analysis after 4 h infection with S. aureus isolated from healthy nasal carriers (n=5) and from blood (n=5) of septic patients. All bacterial isolates were spa-typed and characterized with a DNA microarray to determine the presence of virulence genes. Keywords: infection studies, pathogen, S. aureus
2009-04-01 | GSE13736 | GEO
Project description:Genomes, metagenomes and transcriptomes of Enterococcus gallinarum
| PRJNA743649 | ENA