Quantifiable bioenergetic parameters, determined from extracellular flux analyses, are distinct between macrophages infected with Mycobacteriumtuberculosis or vaccine strain M. bovis BCG, enabling assessment of future vaccine and drug efficacy.
The rapid killing of macrophages by Mycobacterium tuberculosis aggregates, and the subsequent proliferation of the bacteria inside the dead cell, leads to a cell death cascade and explains the coupling of necrosis and pathogen growth observed in active disease.
Systemic inflammation is greater in individuals with concurrent TB and diabetes than in euglycemic individuals with TB, and this disparity persists through the full 6-month course of anti-tubercular treatment.
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.
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.