The asymptomatic colonization and importation of methicillin-resistant Staphylococcus aureus (MRSA) in hospital settings can be inferred from observed cases using combined model-inference methods and used to inform improved interventions.
Reconstruction of transmission pathways of methicillin-resistant Staphylococcus aureus using multiple genomes per host reveals great variation in the size of the transmission bottleneck and limited evidence for body site/phylogeny association.
Neutrophil-dependent innate immune responses to the human pathogen, methicillin-resistant Staphylococcus aureus, are modulated by an interplay between interleukin-21 and type 1 interferons.
Mutations in several components of a bacterial ribosome are shown to broadly decrease antibiotic and stress sensitivity, and readily accessible reversion mutations allow these ribosomal mutations to serve as stepping stones to high level antibiotic resistance.
The absence of oxygen prompts Staphylococcus aureus cells to rupture resulting in increased formation of biofilms, which are the etiological agents of recurrent infections.
Identification and exploitation of interactions between the antifungal drug fluconazole and FDA- approved drugs has the potential to improve treatment for patients with difficult-to-treat systemic fungal infections.
The identification of horizontally transferred genes, and commonly transferred functions, can provide a window into the selective forces acting on species within an ecosystem.
Yersinia pseudotuberculosis and enteropathogenic Escherichia coli promote pathogenicity by deamidating the ubiquitin-like protein NEDD8 to block ubiquitin-dependent trafficking of Perforin-2, which is an effector of innate immunity.
