1. TUBERCULOSIS

3. 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

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

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

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

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

8. 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

9. Hypersensitivity to tubercular antigens
Cell Mediated immunity
Caseating granulomas, Cavitation

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

11. Primary cells infected
are
MACROPHAGES

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

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

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

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

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

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

26. FATE OF GRANULOMA
Cold Abscess
Sinus Formation
Fibrosis
Dystrophic calcification

27. 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)

29. 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

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

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

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

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

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

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

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

44. THANK YOU