Lecture 18 - TB Flashcards
TB demographics
Migrants from South Asia
HIV
Homeless
Drug users
Causative pathogen
Mycobacterium tuberculosis
M Bovis - cattle
M Africanum
M tuberculosis
Rod shaped
Obligate aerobe - normally in right apex as receives most O2
Long chain fatty acids, glycolipids and wax in cell wall so cant be stained
Slow growing
Stain
Acid alcohol fast stain
Red on Ziegler’s Neelson stain
Transmission
Respiratory droplets
Coughing
Sneezing
- small dose (1-10 bacilli)- contagious but not easy to acquire
- remain in air for long time
- Prolonged exposure for atleast 8 hours/day for 6 months
Pathogenesis
- Inhales aerosol
- Engulfed by macrophages and phagocytosed.
- MTB is deposited in alveoli as unable to kill
- Spread to local lymph nodes
- Primary complex formed in Ghon’s focus and the primary lymph nodes are drained into the hilar lymph nodes
- Can progress to active disease where the primary complex does not heal (5%)
- Or there is initial containment of the infection
- Latent infection can occur where TB persists within host without causing disease for years
- Reactivation - post primary TB (5%) or heals 95%
Primary complex -
MTB in a phagosome is not killed initiates cell mediated immunity.
Activated macrophages try and kill MTB but exceeds capacity therefore granuloma formation (6 weeks)
Granuloma reaction - Ghon focus
- spherical granuloma with central casseation - cheese like core necrosis
- surrounded by Langerhan giant cells
- casseation of lymph nodes + ghon focus = ghon complex
Fibrosis and calcification
Why is MTB not phagocytosed
Due to cell wall lipids blocking phagolysosome formation
Primary progression to active disease
TB bacilli in alveoli cause damage and spread
Generally asymptomatic with minimal damage
Post primary TB
Occurs when:
- immunosuppressed
- malnourished
- Old
- HIV
- Drugs
Symptomatic
Latent infection
Before healing via lymph drainage to venous system, some bacilli enter the blood stream
Seeding in other parts of the lung and extra pulmonary sites
When immunocompromised, MTB can spread to the upper lobes (more oxygenated)
Memory T cells release cytokines and more caseous necrosis occurs, causing cavitation
TB can disseminate
- via bronchial arteries and lymph channels to other parts of lung - can cause bronchopneumonia
- via vascular system - military TB
Clinical TB infection
Symptomatic
Subclinical TB infection
Asymptomatic
Latent TB presentation
Inactive TST and IFN +ve CXR - normal Sputum smear - -ve No symptoms Not infectious Not a case of TB
TB presentation
Active - multiplying TST or blood test - +ve CXR - cavity formation in shadowing Sputum - +ve Symptoms Infectious A case of TB
Symptoms of TB
Cough Fever Weight loss Night sweats Malaise
Haemoptsis occasionally
Breathless with pleural effusion
Miliary TB
Carried to all parts of the body through the blood stream
Multiple organs involved
- Kidneys - sterile pyuria - WBCs in urine
- brain meninges - meningitis
- lumbar vertebrae - Pott disease
- adrenal glands - Addison’s disease
- liver - hepatitis
Diffuse specks on CXR
Rare
Lung sounds
Maybe crackles
Effects of TB
Can cause pleural effusion if pleura is affected
Lung fibrosis and cavitation if extensive
Investigations
CXR - if positive IGRA or TST
Sputum - 3 early morning samples
Induced sputum
Microscopy
Bronchoscopy - patients with dry cough
NAAT
CXR
Often right apex with patchy consolidation
Cavitation in consolidation
Healing causes fibrosis
Sputum culture
Gold standard
Tuburcle bacillus
Rapid and cheap
Cannot differentiat MTB with non TB mycobacterium
NAAT
Nucleic acid amplification tests
- rapid diagnosis
- drug resistant mutations
Tuberculin sensitivity test (Montoux test)
TST
Protein derived from MTB (tuberculin) is injected intradermally
2-3 days later if there is presense of a skin reaction at the site, indicated previous exposure to TB or latent TB
