Primary Causes & Pathophysiology
Inhaled droplet nuclei (tiny airborne particles) reach alveoli (air sacs). Alveolar macrophages (lung eater cells) engulf bacilli but often fail to kill them. T cells (immune fighter cells) wall off foci into granulomas (rounded immune nests) with caseation (cheese-like necrosis). Ghon focus (healed lung focus) with hilar node (central chest gland) forms primary complex. Weak immunity allows liquefaction (tissue breakdown) with cavitation (hole formation) and spread.
Inhaled bacilli infect alveoli and persist in macrophages causing granulomas that later cavitate and spread
Repeated droplet exposure in crowded or poorly ventilated rooms raises inhaled dose and infection risk
Lost T-cell control allows latent foci to reactivate and new infection to disseminate rapidly
Impaired macrophage and T-cell function weakens granuloma walls favouring reactivation
Damaged macrophages with fibrotic lungs (scarred lungs) cannot contain bacilli so foci progress
Weak immunity plus high exposure dose allows infection to establish and progress to disease
Blocked granuloma signalling dissolves containment and releases dormant bacilli
Ingested or inhaled bovine bacilli cause lymph node and gut disease similar to tuberculosis