A systematic review shows no evidence of harm or benefit of antibiotic combinations on resistance evolution as clinical data lack statistical power to draw definitive conclusions, highlighting a knowledge gap.

Dysregulated unsaturated fatty acids and saturated fatty acids contribute to bacterial phenotypic resistance to antibiotics.

High-level transposon insertional mutagenesis and a broader spectrum of resistance-conferring mutations for selected carbapenems facilitate the evolution of carbapenem resistance in Klebsiella pneumonia clinical isolates.

Sequential therapy with only β-lactam antibiotics achieves surprisingly high potency by exploiting both low rates of spontaneous resistance emergence and low rates of spontaneous cross-resistance among the drugs in sequence.

Disruption of disulfide bond formation sensitizes resistant Gram-negative bacteria expressing β-lactamases and mobile colistin resistance enzymes to currently available antibiotics.

Directed evolution of the resistance enzyme Cfr under antibiotic selection identifies increased Cfr expression and stability as strategies to boost resistance and reveals that Cfr modification of the ribosome confers resistance by sterically occluding binding of antibiotics.

A data-driven within-host model reveals that different antibiotics are associated with divergent effects on antibiotic resistance carriage and abundance in hospitalised patients, with important implications for antibiotic stewardship.

Antibiotic stewardship in the outpatient setting can substantially reduce exposures of potential pathogens to common antibiotics, and complementary efforts are needed to reduce remaining exposures that occur in 'necessary' contexts.

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.

Collapse of bacterial communities containing antibiotic-resistant and susceptible cells can be driven by increased population size or delayed drug exposure.