A fluoroquinolone resistant variant of Salmonella Typhi has emerged that is likely to be widespread in the Indian subcontinent; therefore fluoroquinolones should not be recommended for empirical typhoid fever therapy in this setting.

The major evolutionary routes to drug resistance in Salmonella Typhi are associated with fitness benefits, not fitness costs, implying that prudent antimicrobial use will have no effect as a public health intervention in controlling typhoid fever.

Penetration of the fluoroquinolones in tuberculosis lesions is heterogeneous even in fully cellular areas, is driven by macrophage content and decreases as the distance from lesion outer rim increases.

A mechanism whereby aminoglycosides-mediated SOS induction in Escherichia coli also promote high-level fluoroquinolone resistance.

Horizontal gene transfer can potentially merge genomes from distinct bacterial species, but isolation in different hosts creates a physical barrier to gene flow.

Building on previous work (Wilkinson et al, 2016), it is shown that inhibition of RecBCD-induced DNA break repair can be used as a co-antibacterial strategy with quinolones.

Bacteria growing in biofilms evolve antimicrobial resistance via different pathways and generate greater genetic diversity than well-mixed populations, selecting fitter but less resistant genotypes.

An analysis of the largest Salmonella Typhi genome collection to date (n=13,000) provides an updated overview of global genome diversity and antimicrobial resistance trends over time to inform public health action.

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.