The pathogenicity of a microbe is defined by its ability to cause disease in a host organism. For Mycobacterium tuberculosis (Mtb), this ability has been shaped by its evolution within humans as both host and reservoir. Its pathogenicity has thus co-evolved with its physiology as a species.
Following infection, Mtb begins its life cycle within the terminal airspace, or alveolus, of the lung. Here, the pathogen is phagocytosed by resident alveolar macrophages and dendritic cells. Mtb is then believed to undergo a period of unrestricted replication, during which it migrates to the local draining lymph nodes, disseminates through the bloodstream, infects more macrophages, and reseeds additional regions of the lung. Infection is usually contained with the onset of cellular immunity and formation of granulomatous lesions, marking the transition to a chronic phase of infection.