Samuel A. Shelburne

This study identifies SpxA1 and SpxA2 as regulators of virulence gene expression in GAS, showing their stoichiometric balance determines transcriptional programs through interactions with CovR.

This paper evaluates the reproducibility and accuracy of nanopore-only versus hybrid-assembly methylation calling in bacterial genomes, showing high concordance and precision.

The paper characterizes recalcitrant enterococcal bacteremia through clinical and genomic analysis, finding species-specific genetic adaptations in persistent infections.

The paper identifies R5 pyocin production as a factor contributing to the dominance of high-risk Pseudomonas aeruginosa ST111 strains by exploiting O-antigen deficiency in competitors.

This study shows that asparagine (Asn) availability regulates Streptococcus pyogenes virulence and metabolism by controlling intracellular ATP levels and CovR/S signaling.

The paper assesses how ESBL-positive ST131 E. coli adapts to carbapenem exposure, finding increased ESBL gene copy numbers and Omp gene mutations correlate with resistance development.

This study examines TBDR mutations in P. aeruginosa clinical isolates and their association with cefiderocol resistance and heteroresistance.

This study identifies a survival strategy in emm4 group A Streptococcus strains through downregulation of SLO and upregulation of msrAB, enabling better macrophage survival without increased virulence.

The paper analyzes WGS data of E. coli isolates to show that blaTEM gene amplification correlates with resistance to AMC and TZP but not SAM, highlighting the need for comprehensive analysis of genetic determinants in BL/BLI resistance.

This study identifies non-carbapenemase-producing CRE mechanisms in recurrent Enterobacterales infections driven by porin loss and β-lactamase gene amplification.

VAMPr predicts antibiotic resistance using genomic data by analyzing variant associations and building machine learning models.

The paper identifies a chimeric M4 protein and a novel Emm pattern in emm4 GAS strains due to an emm/enn gene fusion, which replaced pattern E strains in Houston over four years.