Persistence of in response to infection burden and host-induced stressors.

Introduction: As infection with Mycobacterium tuberculosis progresses, the bacilli experience various degrees of host stressors in the macrophage phagosome such as low pH, nutrient deprivation, or exposure to toxic agents, which promotes cell-to-cell phenotypic variation. This includes a physiologically viable but non- or slowly replicating persister subpopulation, which is characterised by a loss of growth on solid media, while remaining metabolically active. Persisters additionally evade the host immune response and macrophage antimicrobial processes by adapting their metabolic pathways to maintain survival and persistence in the host.

Phenotypic adaptation of to host-associated stressors that induce persister formation.

exhibits a remarkable ability to interfere with the host antimicrobial response. The pathogen exploits elaborate strategies to cope with diverse host-induced stressors by modulating its metabolism and physiological state to prolong survival and promote persistence in host tissues. Elucidating the adaptive strategies that employs during infection to enhance persistence is crucial to understanding how varying physiological states may differentially drive disease progression for effective management of these populations.

Recent Developments in the Application of Flow Cytometry to Advance our Understanding of Mycobacterium tuberculosis Physiology and Pathogenesis.

The ability of the bacterial pathogen Mycobacterium tuberculosis to adapt and survive within human cells to disseminate to other individuals and cause active disease is poorly understood. Research supports that as M. tuberculosis adapts to stressors encountered in the host, it exhibits variable physiological and metabolic states that are time and niche-dependent.