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 freely available computer program that takes into account specific local conditions enables users to predict the impact of adopting different diagnostic strategies on the spread of tuberculosis in their region.

Ending the TB epidemic requires scaling up access to new TB tools so that they can benefit the patients in low- and middle-income countries that need them the most.

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.

Genome sequence analysis of Mycobacterium tuberculosis clinical isolates and subsequent validation in laboratory and animal infection models identify previously unrecognized genetic mutations in DNA repair genes that contribute to the development of drug resistance.

Bulk whole genome sequencing data can be used to study the genetic variation present in pathogenic bacterial populations over the time-course of a single infection within a host.

Isoniazid resistance in Mycobacterium tuberculosis is linked to higher rifampicin tolerance, necessitating evaluation and potential adjustment of treatment regimens to combat emerging multi-drug resistant variants.

A modified BPaL regimen for tuberculosis treatment replaces linezolid with inhaled spectinamides without showing linezolid associated adverse effects.

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.

Kasugamycin potentiates rifampicin killing of Mycobacterium tuberculosis by targeting adaptive mistranslation.