Immunology of Pulmonary TB Pulmonary Tuberculosis Caused by Mycobacterium tuberculosis (MTB) When MTB is inhaled, it is phagocytised by alveolar macrophage (innate

immunity) Normal alveolar macrophages cannot control infection MTB live and multiply (intracellular bacteria) Immune system (lymphocyte) will be activated to build immunity against TB In most individuals, the bacteria is controlled from spreading (clear the infection) Immune Response to Mycobacterium tuberculosis

Normal macrophage will phagocytise MTB 8-10% of individuals exposed to MTB will developPulmonary TB (active TB) y Acute 1° TB symptoms in 1st 2 years y Bacteria reproduce & spread If uncontrolled/ untreated in certain individuals, acute pulmonary TB can become chronic & disseminated into other organs (extra-pulmonary/ TB military) y Bone y Kidney y Brain In some individuals, infection is controlled (no symptoms) but experience latent infection (latent tuberculosis) y Production of granuloma y Recruitment of T cells & macrophages Latent infection can become activated when y Immunocompromised old age y Immunodeficiency HIV Course of MTB Infection MTB cannot be destroyed & can spread As APC, macrophage activate Th1 cell (CD4+) (by secreting cytokines) Activated Th1 cell (CD4+) release IL-2 IL-2 activate Tc cell (CD8+) Activated Tc cell (CD8+) destroy infected MTB cells (cytolysis) Released IFN , TNF macrophage microcidal activity (most active macrophage) Release (NO) Nitric Oxide Kill MTB intracell MTB infection can induce Type 4 Hypersensitivity reaction (Slow) (destroy lung tissue)(immunopathologic effect) Destruction of lung tissue by cytokines released (eg. TNF ) Immunological Laboratory Tests Mantoux Test (Tuberculin Test) y Delayed type hypersensitivity y +ve in BCG vaccinated patients Culture Acid Fast Bacilli (AFB) stain Polymerase Chain Reaction (PCR) Control & Prevention of TB (Vaccination) BCG

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