Antimicrobial Resistance in Staphylococcus

The paper investigates how capsular polysaccharide (CP) in Staphylococcus aureus affects wall teichoic acid (WTA) functions, finding that CP interferes with WTA-mediated processes like phage binding and adhesion but enhances virulence.

This study identifies SasG-II, a variant of the S. aureus surface protein, which binds to a broader range of ligands, enhancing its ability to colonize skin.

This study develops a cost-effective media to mimic the human skin environment and shows it enhances the expression of virulence factors in MRSA.

This study identifies that mutations in PBP4 and GdpP synergistically confer high-level, broad-spectrum β-lactam resistance in mecA-deficient Staphylococcus aureus strains.

This study identifies Desemzia incerta as a skin commensal that reduces MRSA colonization through secreted antimicrobial proteins and decreased biofilm formation in a murine model.

This paper predicts S. aureus antimicrobial resistance using interpretable genomic space maps generated by generative topographic mapping (GTM) applied to genomic data from the PATRIC database.

This study shows that SCCmec transfer in biofilms is significantly enhanced by using living donor cells, with frequencies up to 10^-2, and is mediated by the Ccr-attB system.

This study uses NMR spectroscopy to determine the substrate specificities of lysostaphin and LytM, showing they prefer D-Ala-Gly cross-linked parts of peptidoglycan, with LytM also acting as a D-alanyl-glycine endopeptidase.

The paper shows nasal commensals reduce S. aureus growth by consuming its siderophores, revealing inter-species competition and potential for probiotic strategies.

This study characterizes a putative staphylococcal enterotoxin, SEl26, showing its structural similarity to conventional SAgs and its ability to bind MHC-II and modulate cytokines.

The paper shows that inhibiting host deoxycytidine kinase with (R)-DI-87 reduces Staphylococcus aureus abscess formation by protecting phagocytes and enhancing immune response.

This study characterizes neonatal Staphylococcus capitis NRCS-A isolates and compares them with non-NRCS-A isolates from neonates and adults, identifying genetic and phenotypic traits associated with their success in NICUs.

The paper identifies a new family of chromosomal islands shared between Staphylococcus agnetis and Staphylococcus aureus that may contribute to pathogenicity in chickens.

The paper describes a novel repression-derepression mechanism for Staphylococcus aureus pathogenicity islands (SaPIs) involving tetrameric repressors and an inducing protein.

This study identifies genome degradation and convergent mutations in Staphylococcus aureus during severe infections, linking them to adaptation and clinical outcomes.

The paper systematically evaluates key parameters affecting SNP-based transmission inference of MDROs, finding that using a closely-related reference genome and sliding-window analysis improves accuracy.

The paper sequenced S. aureus isolates from the Philippines to analyze MRSA clones and resistance patterns, finding a limited number of genetic clones and high concordance between phenotypic and genotypic resistance.

This study quantifies the modes of vanA-type vancomycin resistance dissemination in Dutch hospitals, finding clonal spread as the dominant mechanism with significant contributions from horizontal gene transfer.

The paper presents a Bayesian model to estimate bacterial acquisition and clearance rates by accounting for within-host genetic variation and sampling intervals, validated using simulations and applied to MRSA isolates.

This study compares the pathogenicity of Staphylococcus aureus and Streptococcus pyogenes isolates toward human myoblasts and keratinocytes, finding higher internalization and cytotoxicity by NSTI-SA in myoblasts.

rPinecone defines sub-lineages in low-variant bacterial populations using phylogenetic trees to improve outbreak and endemic disease analysis.

The paper analyzes genomic evolution in persistent Staphylococcus aureus bacteraemia, identifying a molecular signature with low mutation frequency and high non-silent mutations.

Severe S. aureus infections arise from the nasal microbiome through adaptive evolution, with specific mutations enriched in infecting bacteria compared to colonizing ones.