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The internalization of Staphylococcus aureus into non-professional phagocytic cells (NPPCs) is considered a key mechanism in the development of persistent infections. The primary internalization pathway has been clearly identified. However, the capacity for internalization and its underlying mechanism remain poorly studied in other Staphylococcus species. In this study, we demonstrated that half of the species within the Staphylococcus genus are capable of being internalized by osteoblasts using a mechanism similar to that of S. aureus . Internalization into NPPCs may therefore represent a partially conserved process within the Staphylococcus genus, raising important questions about the evolution of pathogenicity in staphylococci.

Past work has seen over-representation of Staphylococcus aureus clinical isolates in genome and biology studies on staphylococci. Here, we show by a selective plating analysis of municipal wastewater that independent isolates representing seven other species of Staphylococcus were recovered ( S. cohnii , S. equorum , S. lentus , S. nepalensis , S. sciuri, S. shinii, and S. xylosus ), as readily identified in the samples. Genome sequence analysis revealed some species-specific antibiotic resistance profiles across the strains, and a bacteriophage was isolated that had a cross-species host range. Using this broad biological approach to analyze staphylococci has identified a phage with a broad killing range, and this phage is morphologically distinct from the three known types of tailed phages.

Infections with Staphylococcus aureus pose a serious public health threat due to high levels of antibiotic resistance and limited efficacy of alternative therapeutics. There has been a great deal of interest in developing novel therapeutics that target virulence factors essential during infection. However, it remains largely unknown if these factors are required at specific stages of the infection, and whether all bacterial cells or a limited subset express them. Here, we sought to examine virulence factor expression using fluorescent reporter strains that would indicate activity of two master regulators of virulence in S. aureus , Agr and Sae. While Agr appeared inactive during kidney abscess development, the Sae system exhibited heterogeneity, increased expression at later stages, and was required for abscess progression. These results provide critical information for the development of virulence factor-targeting strategies for kidney abscess treatment.

To gain a full understanding of how bacteria infect tissues, it is necessary to characterize both the bacteria and the tissue at the time of infection. However, this analysis is very complex because it involves obtaining infected tissue directly from patients and analyzing it with minimal processing to preserve the characteristics of the natural state of infection. In this study, we examined the gene expression profiles of replaced heart valves from patients with Staphylococcus aureus infection and compared them with pig valves experimentally infected with the same bacteria. Our findings provide a detailed insight into the changes occurring in the infected tissue and the bacterial adaptations required for multiplication and survival on the valve tissue. Notably, the strong similarity observed between human and porcine valves confirms that the porcine endocarditis model closely mirrors the human condition, making it a valuable tool for testing new therapies against this serious infection.

Staphylococcus aureus is a major human pathogen that can cause life-threatening infections in humans. However, treatment options are limited due to the prevalence of antimicrobial-resistant isolates in the hospital and the community. The MarR-type repressor Sa MhqR was described to control resistance toward quinones and quinone-like antimicrobials. However, the redox-regulatory mechanism of Sa MhqR by quinones was unknown. In this work, we explored the DNA-binding and quinone-sensing mechanism of Sa MhqR and identified a quinone-binding pocket and an allosteric loop, which facilitates DNA binding activity via a helical wound conformation and adapts an unstructured coiled conformation upon quinone binding to inhibit DNA binding. A similar mechanism has been recently discovered for the regulation of uric acid resistance by UrtR family repressors (W. S. Song, D. U. Ki , H. Y. Cho, O. H. Kwon, H. Cho, S. I. Yoon, Nucleic Acids Res 52:13192–13205, 2024, https://doi.org/10.1093/nar/gkae922 ). Our results contribute to a better understanding of antimicrobial resistance regulation, which may be exploited for future drug design to combat multidrug-resistant S. aureus .

Staphylococcus aureus is a primary pathogen of chronic airway disease yet is also found in the upper airways of 30%–50% of the population to no obvious detriment. Thus, identifying the host and/or microbial factors that tip the balance between its commensal and pathogenic states may be key to its control. Here, we reveal that short-chain fatty acids produced by commensal microbiota promote a marked remodeling of the S. aureus lipid membrane that, in turn, sensitizes the pathogen to antimicrobials, disrupts accessory gene regulator quorum signaling, and reduces its competitive fitness. Altogether, these data suggest that co-colonizing microbiota and the metabolites they exchange with S. aureus may be key players in the microbial ecology of airway disease.

Bacteria colonize surfaces in the environment and can also penetrate tissues and materials by entering micro- and nano-scale cracks and pores. has been observed within nanoscale channels in bone that are 2-3 times smaller than cell diameter. Inside the bone, bacteria are protected from host immunity and systemic antibiotics, potentially contributing to chronic and recurrent infections. The physical mechanisms that enable bacteria to enter channels smaller than the cell width are unclear. It has been proposed that bacteria traverse narrow passages through division, such that daughter cells form within small channels and proliferate in chains down the channel length. Here, we use microfluidics to test the idea that can traverse submicrometer channels through growth. We examined the net migration of growing cell chains within tapered nanochannels (width ~1.5-0.3 μm). We found that proliferation can facilitate migration, but only to cell deformations of 600 nm (65% cell width). Below 600 nm, mechanical confinement significantly slows or completely inhibits division in single cells. Interestingly, growth arrest occurs independent of the Z-ring assembly and is unrelated to the initial orientation of the division plane. Thus, our findings suggest that it is unlikely for to traverse nanoscale channels via division. Bacteria that colonize materials and tissues within the body can be difficult to remove, even with thorough cleaning and application of antibiotics. Recent studies show that bacteria not only colonize the surfaces of tissues in the body but can also squeeze into naturally occurring pores and channels and thereby gain protection from immune cells and antibiotics. Here, we ask how physical forces and cell growth might enable bacteria to enter small pores within materials. We use microfluidic devices to study the growth and migration of the human pathogenic bacteria, .

The pressure of the coronavirus disease 2019 (COVID-19) pandemic on global healthcare systems and societies was unprecedented in the modern era. Social restrictions, containment measures, and disruptions in antimicrobial prescriptions and consumption during the pandemic have been reported to alter the epidemiology of bacterial diseases, although these effects likely differed markedly between locations. Here, we compare the clinical, clonal distribution, and genomic features of bloodstream isolates before, during, and after COVID-19 in two hospitals on different continents: Parc Taulí University Hospital (Spain) and Dartmouth-Hitchcock Medical Center (USA). We hypothesize that pandemic-related environmental perturbations, such as those due to infection control practices and antimicrobial exposure, may have contributed to shifts in the diversity of circulating bacterial lineages and genomic elements. Our findings revealed changes in the distribution of low-frequency clones, antimicrobial resistance genes, and virulence factors, potentially reflecting changes in selective pressures in clinical environments.

There have been limited studies on the fatty acid degradation (Fad) pathway of Staphylococcus aureus . The fadXDEBA operon has been shown to contain all the genes necessary for β-oxidation, and the FadD and FadBA proteins have been shown to perform their canonical functions. This study demonstrates that the full S. aureus Fad pathway is functional and capable of degrading exogenous fatty acids. These data bring to light a second exogenous fatty acid utilization pathway, expanding our knowledge on how this pathogen metabolizes environmental fatty acids.

The prevalence and propagation of Staphylococcus aureus clonal complex 59 (CC59) in Asia are serious public health concerns. To understand its adaptation to hosts and worldwide evolutionary success, we analyzed the genomic population structure of all CC59 isolates and traced their evolutionary history. Our research indicates that CC59 lineages developed through unique evolutionary routes that vary across time and space, highlighting their adaptation to diverse ecological environments. This study presents a comprehensive genomic epidemiology framework that integrates extensive metadata analysis with evolutionary assessment. It serves as a model for future S. aureus monitoring and provides insights into potential targets for interventions focused on reducing virulence.