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Etiology:

• The most common cause of TB is Mycobacterium tuberculosis.
• In patients with AIDS, a frequent causative agent is M. avium-intracellulare.
• In under-developed countries, M. bovis, the causative agent of bovine tuberculosis causes gastro-intestinal TB and is acquired through the ingestion of contaminated milk.

Pathogenesis:

• The bacterium enters the individual through inhalation of infectious sputum; in many under-developed countries, ingestion of contaminated milk is another source of infection.
• Irrespective of the poral of entry, the bacterium is ingested by macrophages and induces an output of cytokines responsible for the constitutional symptoms.

Epidemiology:
the macrophage.
• Multiplication within the macrophage follows, with subsequent lysis of the host cell permitting spread of infection.
• Macrophages also travel to local lymph nodes, carrying the infection to these structures.
• Development of an immune response aborts the spread of infection through unknown mechanisms and results in the formation of the typical granulomas.
• However, it appears that the mycobacteria are not killed within these granulomas.
• Later in life, if the level of immunity is lowered for any reason, reactivation of infection occurs.
• At this stage, the cell mediated immunity or delayed type hypersensitivity (DTH) contributes to tissue destruction.

General Gross Description:

• TB afflicts 33% of the world's population and is responsible for 3 million deaths a year.
• In the first world, with the reduction in over-crowding and improvements in sanitation and in the health care of milk-cow herds, the incidence of the disease has fallen through much of the 20th century.
• Recently, however, the reported incidence has climbed, mainly due to the frequency of the infection in patients with AIDS.

General Microscopic Description:

• Tuberculous lesions may occur in almost any organ of the body.
• The most common are the lungs and lymph nodes.
• The size of the lesion can vary from a few millimeters to the entire lobe of the lung or the entire node.
• Early lesions are characterized by small, white, soft nodules a few mm. in diameter.
• Larger lesions, especially in the lung are characterized by extensive necrosis and cavitation.
• The walls of the cavities contain ragged, white material that houses millions of mycobacteria and is intensely infectious.
• Late, healed lesions can be walled off by fibrosis and appear white and hard.
• Dystrophic calcification can also take place, giving rise to a white chalky appearance.

Clinical Correlations:

• Irrespective of the organ affected, tuberculosis is characterized by granulomas, with epitheloid cells and Langhans giant cells.
• Very early lesions may be non-caseating, but typically tubercular granulomas undergo central caseation necrosis.
• CASEATION IS CHARACTERISTIC BUT NOT PATHOGNOMONIC OF TB.
• When this necrotic material communicates with the exterior, as in tuberculosis of the lung, it is coughed up and helps spread the infection.

References:
•Tuberculosis can result in symptoms in almost any organ system; however, the most common manifestations relate to the respiratory tract. •Mycobacterium tuberculosis causes secretion of cytokines by macrophages, resulting in the typical constitutional reactions of fever and weight loss. •Spread of disease to the entire lobe of the lung, especially with the development of communcation with the exterior through the bronchial tree results in coughing, often with blood tinged sputum. •TB in the GI tract can manifest as obstruction.