ETIOLOGY

Mycobacteria belong to the family of Mycobacteriacea and the order Actinomycetales.

Mycobacteria comprises eight distinct subgroups, the most common of human disease is M.
Tuberculosis. M.Tuberculosis is a rod shaped, non-spore forming, thin aerobic bacterium by the
size of 0.5 µ by 3 µ. M.Tuberculosis are often neutral on gram staining. It’s cell wall, the lipids
are linked to underlying arabinogalactan and peptidoglycan which results in a very low
permeability of the cell wall and reducing the effectiveness of most of drugs.
Lipoarabinomannan, one of the molucle in cell’s wall is involved In the poathogen-host
interaction and promotes survival within macrophages.

Loscalzo, J. (2017). Harrison's pulmonary and critical care medicine. 3rd ed. Boston: McGraw-
Hill Education, p.121.

PATHOPHYSIOLOGY

M.Tuberculosis infection begins when a person inhaled a droplet nuclei containing viable
microorganisms that propelled into the air by infectious patients. Most bacilli are trapped in the
mucus secreting goblet cells parts. Frieden TR, Sterling TR, Munsiff SS, Watt CJ, Dye C.
Tuberculosis. Lancet.2003;362: 887-899. Bacteria that bypass the mucociliary system reach the
alveoli and quickly engulfed by alveolar macrophages. Jensen PA, Lambert LA, Iademarco MF,
Ridzon R; Centers for Disease Control and Prevention. Guidelines for preventing the
transmission of Mycobacterium tuberculosis in health-care settings, 2005. MMWR Recomm
Rep.2005;54(RR-17):1-141The Mycobacterial lipoarabinomannan is a key for a macrophage
receptor and activate the complement system to phagocyte the bacteria. When the bacteria is
engulfed they become dormant, the mycobacteria continue to multiply slowly with bacterial cell
division occurring every 25 to 32 hours. (Porth CM. Alterations in respiratory function:
respiratory tract infections, neoplasms, and childhood disorders. In: Porth CM, Kunert MP.
Pathophysiology: Concepts of Altered Health States.Philadelphia, PA: Lippincott Williams &
Wilkins; 2002:615-619.) Initial development invlolve production of proteolytic enzymes and
cytokines by macrophages in an attempt to degrade the bacteria. The released cytokines attract T
lymphocytes to the site this immune process continues for 2 to 12 weeks. van Crevel R,
Ottenhoff THM, van der Meer JWM. Innate immunity to Mycobacterium tuberculosis. Clin
Microbiol Rev.2002;15: 294-309 For persons with intact cell-mediated immunity, the next
defensive step is foffrmation of granulomas from accumulation of activated T lymphocytes and
macrophages. This environment destroys macrophages and produces solid necrosis at the center
of the lesion Dheda, K, Booth H, Huggett JF, et al. Lung remodeling in pulmonary tuberculosis.
J Infect Dis.2005;192:1201-1210.. By 2 or 3 weeks the necrotic environment resembles soft
cheese, often called caseous necrosis, and characterized by low oxygen levels, low pH, and
limited nutrients. For less immunocompetent persons, granuloma formation is initiated yet
ultimately is unsuccessful in containing the bacilli. The necrotic tissue undergoes liquefaction,
and the fibrous wall loses structural integrity. The semiliquid necrotic can drain into bronchus or
nearby blood vessel, leaving an air-filled cavity at the original site. If goes to bronchus the
person becomes infectious, if goes to blood vessel the occurrence of extrapulmonary tuberculosis
is likely. Dheda, K, Booth H, Huggett JF, et al. Lung remodeling in pulmonary tuberculosis. J
Infect Dis.2005;192:1201-1210.