“What is the pathophysiology of tuberculosis?”

TB is a chronic communicable disease caused by Mycobacterium Tuberculosis. The lesion is characterized by a necrotizing granulomatosis (Caseating necrosis) in tissue where the organism is seeded. Transmission of TB is by inhalation of infected droplets from coughing or sneezing of infected individuals. The cell wall of lipids and carbohydrates of Mycobacterium Tuberculosis appear to enhance virulence by interfering with phagolysosomal fusion. This interference allows the intracellular survival of mycobacteria. Once the sensitization appears in patients during the infection, the nonspecific inflammatory response become granulomatous (granuloma), and abundant epithelioid histiocytes, occasional giant cells, peripheral mononuclear cells among others. There is often a central, caseous necrosis of the granuloma. Therefore, an increase resistant inhibiting intracellular replication of the bacilli. There are several forms of TB. Primary Pulmonary Tuberculosis – these are individual lacking previous contact with the bacilli. Secondary TB – means that the patient has an active infection in a previously infected individual. Miliary TB – present with myriad of minute foci of infection in many organs, preferentially liver, bone marrow, spleen, and kidneys. Isolated organ tuberculosis – when disseminated organism become established in only one or two organs or female genital tract (salpingitis, endometritis). Tuberculosis is caused by the aerobic, non-spore forming, non-motile bacillus M. tuberculosis, which has a waxy coat that stain red with acid-fast stain. The mycobacteria may block vacuolar acidification by nonactivated macrophages. The CD4+ helper T cells secretes tissue necrosis factor gamma (TNFγ), which activates macrophages to kill intracellular mycobacterium via reactive nitrogen intermediates and to form epithelioid granulomas. CD8+ suppresser T cell kill macrophages that are infected with mycobacteria, resulting in the formation of caseating (cheeselike) granulomas (delayed type of hypersensitivity reaction). The residual lesion is a calcified scar in the lung parenchyma and in the hilar lymph node (Ghon Complex). Thank you.