- First, Mtb bacilli are inhaled by their victim and phagocytosed by resident alveolar macrophages in the lung, e.g. through exhaled droplets.
- Following, the infected cells invade the subtending epithelium. This recruits monocytes from the blood circulation, leads to neovascularization, and the formation of granulomas.
- Many of the granulomas persist in a balanced state, whereas progression towards disease is characterized by the loss of vascularization and the increase of necrosis.
- Finally, infectious bacilli are released into the airways after the cavitation of the granulomas and its collapse into the lungs.
Facts & Figures
The Life Cycle of M. tuberculosis
Tuberculosis is an old but re-emerging global health threat caused by mycobacteria belonging to the Mycobacterium tuberculosis (Mtb) complex. One third of the world’s population is infected with Mtb and new infections occur at a rate of one per second (World Health Organization Report, 2008). Less than 5% of individuals develop active disease within 1-2 years after infection. In the remaining 95%, it is thought that Mtb persists in the face of an active immune response in a metabolically highly reduced stage of dormancy (latent infection), where it rarely replicates if at all. At later times, about one in ten of the latent infections will eventually progress to active disease, which, if left untreated, kills more than half of its victims. Such prolonged persistent interactions between the host and the pathogen present a major challenge in disease control. Even more frightening is the rapid emergence of Multi-Drug-Resistant (MDR) and Extensively-Drug-Resistant (XDR) strains along with the dangerous liaison between the Human Immunodeficiency Virus (HIV) and Mtb. In Sub-Saharan Africa, Mtb is the number one killer of HIV-infected individuals.