Pulmonary Tuberculosis II

The pathophysiology of tuberculosis begins when a susceptible host inhales aerosolized droplets containing Mycobacterium tuberculosis.

The droplets reach the lungs' alveoli, where the bacteria multiply and encounter alveolar macrophages, which engulf them.

However, instead of destroying the bacteria, the macrophages allow them to survive and replicate within.

After 2-6 weeks, the body initiates a cell-mediated immune response, forming a specialized structure called a granuloma to contain the bacterial spread.

The granuloma comprises immune cells, live and dead bacterial cells, T-cells, and macrophages.

The bacteria can remain dormant within the granuloma, causing no symptoms and being non-contagious. This stage is known as latent tuberculosis infection.

If the immune system is compromised, latent tuberculosis can progress to active tuberculosis disease through the caseation process, where the center of a granuloma becomes necrotized, forming a cheese-like substance called caseum.

This caseous material then erodes into a bronchus, creating a cavity that facilitates rapid bacterial proliferation and the potential spread of the infection through blood or lymph.