HIV co-infection does not affect Mycobacterium tuberculosis mutation rates and does not drive the emergence of antimicrobial resistance within patients in the largest outbreak of multidrug-resistant tuberculosis in Latin America to date.
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 genetic make-up of dominating MDR-TB clades in Central Asia is shaped by programmatic and socio-economic changes that led to fixation of resistance and bacterial fitness related mutations in the Soviet era.
A transport mechanism is uncovered in the major drug-efflux system in E. coli involving two remote alternating-access conformational cycles, which could provide the basis for the development of allosteric inhibitors against multidrug 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.