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TUBERCULOSIS
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WHAT IS IT ? Bacterial infection
Caused by Mycobacterium tuberculosis (also called tubercle bacillus) Damages a person’s lungs or other parts of the body Fatal if not treated properly
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Mycobacterium – Slender, aerobic rods
Gram +ve, Acid fast M.tuberculosis – Reservoir- Humans M.bovis –Reservoir – contaminated milk M.Avium intracellulare-opportunistic (AIDS)
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TB flourishes in Poverty, Over crowding, Malnutrition DM, CRF Alcoholism Immunosuppression
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TRANSMISSION Spreads through the air when a
person with active TB (Inhalation) Coughs Speaks Laughs Sneezes Ingestion
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SPREAD OF TB Local Spread Lymphatic spread Haematogenous Spread
Natural passages – Pleurisy, Peritonitis (salpingitis), Laryngitis , Ileocaecal
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PATHOGENESIS Breath in infected air and bacilli go to lungs through bronchioles Bacilli infect alveoli Macrophages attack bacteria, but some survive Infected macrophages separate and form tubercles
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Hypersensitivity to tubercular antigens
Cell Mediated immunity Caseating granulomas, Cavitation
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Host response to lipids such as Mycosides
(cord factor) & glycolipids ( Wax-D) on the bacterial cell wall Type IV Hypersensitivity
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Primary cells infected
are MACROPHAGES
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ACTIVE INFECTION Unhealthy person Bacilli overwhelm immune system
Bacilli break out of tubercles in alveoli and spread through bloodstream
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LATENT INFECTION Initial infection controlled by immune system
Bacilli remain confined in tubercles for years
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DIAGNOSIS Mantoux test Medical history, x-rays, and smears for
AFB, Sputum culture, PCR
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SYMPTOMS Perpetual Cough Fever Weight loss Night sweats
Loss of appetite Fatigue Swollen glands Pain while breathing
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EVOLUTION OF TUBERCLE ( Granuloma)
PMN Macrophages Poorly degradable bacilli CD4+ T cells ( IFN, TNF) Epithelioid cells Hard Tubercle Soft Tubercle
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GRANULOMA Central caseous necrosis surrounded by
epithelioid cells, Langhan’s giant cells, Rim of lymphocytes and fibroblasts.
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FATE OF GRANULOMA Cold Abscess Sinus Formation Fibrosis Dystrophic calcification
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CLINICAL SPECTRUM Secondary – Previously sensitized person
Primary – previously unexposed, unsensitized person Secondary – Previously sensitized person - Follows primary, - Reactivation of dormant lesion, - Exogenous reinfection ( Large inoculum of virulent bacilli)
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Primary tuberculosis GHON’S COMPLEX( Primary complex)
Ghon’s Focus- Subpleural focus in the upper part of lower lobe/ lower part of upper lobe Lymphatic component Lymph node component – Hilar & Tracheo-bronchial
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Fate of Primary TB Fibrosis, calcification Progressive Pulmonary TB
Primary Miliary TB Secondary TB
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Secondary Tuberculosis
Initially -- small focus (2 cm) of consolidation in the apical pleura Develop a small area of caseation, fibrosis
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Fate of secondary TB Heal with fibrosis Fibrocavitary TB Pneumonia Miliary TB
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Progressive Pulmonary TB
Child, Elderly, Immunocompromised Erosion of blood vessels hemoptysis Erosion into bronchus Empyema, effusion, pleuritis
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MILIARY TUBERCULOSIS Miliary = ‘millet seeds’ Spread thro’ lymphatics Lesions- small / microscopic Liver, Spleen, Kidney, Brain, Bonemarrow adrenals, fallopian tubes, epididymis, etc.
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Isolated organ TB: Meningitis Renal Osteomyelitis Adrenals Salpingitis
Pott’s spine Lymphadenitis- Scrofula Intestinal
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IMMUNIZATION Bacilli Calmette Guerin ( BCG) [ Attenuated Strains of Bovine type of Bacilli]
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THANK YOU
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