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.

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.

Environmental specialization of bacterial cell wall synthases influences intrinsic resistance to cell wall active antibiotics.

The absence of oxygen prompts Staphylococcus aureus cells to rupture resulting in increased formation of biofilms, which are the etiological agents of recurrent 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.

Tannic acid acts as an ‘antidote’ against the negative effects of a bacterial enzyme, which can both aggravate cystic fibrosis and enable the anthrax bacteria to evade the immune responses elicited by a typical live vaccine.

To avoid recognition by the immune system, bacteria use autolysins to trim fragments of peptidoglycans that are exposed on the bacterial cell wall.