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WHAT IS IT ? Bacterial infectionCaused 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 rodsGram +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 aperson with active TB (Inhalation) Coughs Speaks Laughs Sneezes Ingestion
SPREAD OF TB Local Spread Lymphatic spread Haematogenous SpreadNatural 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 antigensCell 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 infectedare MACROPHAGES
ACTIVE INFECTION Unhealthy person Bacilli overwhelm immune systemBacilli break out of tubercles in alveoli and spread through bloodstream
LATENT INFECTION Initial infection controlled by immune systemBacilli remain confined in tubercles for years
DIAGNOSIS Mantoux test Medical history, x-rays, and smears forAFB, Sputum culture, PCR
SYMPTOMS Perpetual Cough Fever Weight loss Night sweatsLoss 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 byepithelioid 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 personPrimary – 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 TBPrimary Miliary TB Secondary TB
Secondary TuberculosisInitially -- 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 TBChild, 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 SalpingitisPott’s spine Lymphadenitis- Scrofula Intestinal
IMMUNIZATION Bacilli Calmette Guerin ( BCG) [ Attenuated Strains of Bovine type of Bacilli]
Dr. Meg-angela Christi Amores
Outline Transmission Mycobacteria Pathogenesis LTBI LTBI vs TB Disease
Clinical Manifestations of TB
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Tuberculosis : Tuberculosis (TB) is an infectious disease caused by bacteria whose scientific name is Mycobacterium tuberculosis. It was first isolated.
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