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TUBERCULOSIS
WHAT IS IT ? Bacterial infectionBacterial infection
Caused by Caused by Mycobacterium tuberculosis Mycobacterium tuberculosis (also(also called called tubercle bacillustubercle bacillus))
Damages a person’s lungs or other parts ofDamages a person’s lungs or other parts of the bodythe body
Fatal if not treated properlyFatal 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 aSpreads through the air when a person with active TB (Inhalation)person with active TB (Inhalation)
– CoughsCoughs
– SpeaksSpeaks
– LaughsLaughs
– SneezesSneezes
• IngestionIngestion
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 INFECTIONACTIVE INFECTION
Unhealthy personUnhealthy person
Bacilli overwhelm immune systemBacilli overwhelm immune system
Bacilli break out of tubercles in alveoli Bacilli break out of tubercles in alveoli
and spread through and spread through
bloodstreambloodstream
LATENT INFECTIONLATENT INFECTION
Initial infection controlled Initial infection controlled
by immune systemby immune system
Bacilli remain confined in Bacilli remain confined in
tubercles for yearstubercles for years
DIAGNOSIS
• Mantoux testMantoux test
• Medical history, Medical history,
x-rays, and smears forx-rays, and smears for
AFB, AFB, Sputum cultureSputum culture, ,
PCRPCR
SYMPTOMS• Perpetual CoughPerpetual Cough
• FeverFever
• Weight lossWeight loss
• Night sweatsNight sweats
• Loss of appetiteLoss of appetite
• FatigueFatigue
• Swollen glandsSwollen glands
• Pain while breathingPain 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
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]