TUBERCULOSIS

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

Mycobacterium – Slender, aerobic rods Gram +ve, Acid fast M.tuberculosis – Reservoir- Humans M.bovis –Reservoir – contaminated milk M.Avium intracellulare-opportunistic (AIDS)

TB flourishes in Poverty, Over crowding, Malnutrition DM, CRF Alcoholism Immunosuppression

TRANSMISSION Spreads through the air when a person with active TB (Inhalation) Coughs Speaks Laughs Sneezes Ingestion

SPREAD OF TB Local Spread Lymphatic spread Haematogenous Spread Natural passages – Pleurisy, Peritonitis (salpingitis), Laryngitis , Ileocaecal

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

Hypersensitivity to tubercular antigens Cell Mediated immunity Caseating granulomas, Cavitation

Host response to lipids such as Mycosides (cord factor) & glycolipids ( Wax-D) on the bacterial cell wall Type IV Hypersensitivity

Primary cells infected are MACROPHAGES

ACTIVE INFECTION Unhealthy person Bacilli overwhelm immune system Bacilli break out of tubercles in alveoli and spread through bloodstream

LATENT INFECTION Initial infection controlled by immune system Bacilli remain confined in tubercles for years

DIAGNOSIS Mantoux test Medical history, x-rays, and smears for AFB, Sputum culture, PCR

SYMPTOMS Perpetual Cough Fever Weight loss Night sweats Loss of appetite Fatigue Swollen glands Pain while breathing

EVOLUTION OF TUBERCLE ( Granuloma) PMN Macrophages Poorly degradable bacilli CD4+ T cells ( IFN, TNF) Epithelioid cells Hard Tubercle Soft Tubercle

GRANULOMA Central caseous necrosis surrounded by epithelioid cells, Langhan’s giant cells, Rim of lymphocytes and fibroblasts.

FATE OF GRANULOMA Cold Abscess Sinus Formation Fibrosis Dystrophic calcification

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)

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

Fate of Primary TB Fibrosis, calcification Progressive Pulmonary TB Primary Miliary TB Secondary TB

Secondary Tuberculosis Initially -- small focus (2 cm) of consolidation in the apical pleura Develop a small area of caseation, fibrosis

Fate of secondary TB Heal with fibrosis Fibrocavitary TB Pneumonia Miliary TB

Progressive Pulmonary TB Child, Elderly, Immunocompromised Erosion of blood vessels hemoptysis Erosion into bronchus Empyema, effusion, pleuritis

MILIARY TUBERCULOSIS Miliary = ‘millet seeds’ Spread thro’ lymphatics Lesions- small / microscopic Liver, Spleen, Kidney, Brain, Bonemarrow adrenals, fallopian tubes, epididymis, etc.

Isolated organ TB: Meningitis Renal Osteomyelitis Adrenals Salpingitis Pott’s spine Lymphadenitis- Scrofula Intestinal

IMMUNIZATION Bacilli Calmette Guerin ( BCG) [ Attenuated Strains of Bovine type of Bacilli]

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