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.

Killing their neighbors allows bacteria to steal genes, including antibiotic resistance genes, which we observed under a microscope, quantified, modeled, and predicted potentially guiding strategies to combat it.

We are writing to comment on the recent study by Olesen et al., 2018 on antibiotic use and antibiotic resistance.

We are writing to reply to the comment by Pouwels et al., 2019 about our recent study (Olesen et al., 2018) on antibiotic use and antibiotic resistance.

Population-level antibiotic resistance correlates with the breadth of antibiotic use, that is, the proportion of people taking an antibiotic, better than with intensity of use the amount of use among users.

Both within and between hosts, the key factor guiding whether increasing treatment strength will increase or decrease antibiotic resistance is whether inter-strain competition is effective, not whether it is present.

Drug-resistance declines in the laboratory in an antibiotic stress-free environment, indicating that restricting antimicrobial usage in the clinics could be a useful policy.

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

Conflicts between CRISPR-Cas systems and antibiotic resistance plasmids can be exploited to selectively eliminate antibiotic resistance from Enterococcus faecalis populations.