Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
Dr. T. Prasad
Contents
1 Pathogenesis and clinical features of
tuberculosis.
2. Classification of tuberculosis and atypical
mycobacterial infections.
4. Pathological features: both macroscopic and
microscopic
5. Association of tuberculosis with HIV infection.
6. Complications of tuberculosis
Tuberculosis
• Introduction:
Is the most important communicable disease in the world.
It is important to differentiate between infection with
M. tuberculosis & the disease.
Infection with M. tuberculosis – development of delayed
hypersensitivity to M.tuberculosis antigens.
Can be detected by tuberculin (Mantoux) test.
- Test does not differentiate between infection and disease.
- False- negative reaction seen in certain viral infections,
sarcoidosis, Hodgkin disease, malnutrition, immunosuppressive
conditions, & in overwhelming active tuberculosis.
- False – positive reaction may be seen in infection by atypical
mycobacterium.
• The hall mark of tuberculosis :
- tubercle( small nodule) formation
- also called hard tubercle - nature of “Progressive
inflammation” (granulomatous inflammation).
- response to low bacillary mass( low dose x high virulence) in
a pt. with good resistance.
• Another type of response “Exudative inflammation”-
- response to large bacillary mass ( high dose x high virulence) in
a pt. with poor resistance.
• Other conditions – hard tubercle seen
- Mycotic inf, Tuberculoid leprosy, Syphilis, Brucellosis, Silicosis,
Foreign body granuloma & sarcoidosis.
• Diagnosis of TB :
- demonstration of TB bacilli in histopathology section & in
culture.
Evolution of Tubercle
• After ingestion of bacilli :-
• At the end of 24hrs. --- Neutrophils are dominant cells.
• At the end of 48 hrs --- Macrophages digest all the bacilli which
has escaped neutrophils. as well as neutrophils.
• At the end of 2– 3 wks. – focus grown to form a tiny seed—like
nodule, greyish-white in colour &
0.5—2mm in diameter (Miliary tubercle), compact & avascular.
• Microscopy : Langhan’s type of giant cell at the centre,
surrounded by epitheloid cell macrophages, & around epitheloid
cells, is a mantle(Cuff/collar) of lymphocytes.
– Bacilli can be seen in the cytoplasm of epitheloid cells.
– Later caseation, then healing.
• Healing : by Resolution, Fibrosis( takes wks.), Calcification (yrs.), &
ossification.
Langhan’s giant cell lymphocytes Epitheloid cell
Lympocytes
epitheloid cell
caseation
necrosis
PATHOGENESIS OF TUBERCLE
A. EXOGENOUS
INFECTION
Mechanism of evolution of a granuloma
Injury by M.tuberculosis
• Failure to digest the bacilli
• Activation
• Of CD4+ T cells (release of Lymphokines IL-1 & 2,
Growth factors, IFN—γ, & IFN—α ),Monocyte chemotactic factor.
• Mannose-capped glycolipids
M.bact.
endosomal manipulation: Bacteraemia
• Morphoogy :
Primary Tuberculosis : most affected organ:
- lung.
- Site – lower part of the upper lobe or upper part of
the lower lobe, usually close to pleura.
Ghon’s focus – 1 -1.5cmm.gray-white, inflammatory,
consodilated area.
Micro: lesion consists of tuberculous granuloma
with caseous necrosis.
- In most cases center undergoes caseous necrosis.
Ghon’s complex : consists of 3 components:
i)Pulmonary component: Ghon’s focus located
peripherally under a patch of pleurisy.
Ghon’s complex(ctd)
• Ii) Lymphatic vessel component : lymphatics draining the lung
lesion – bacilli – develop beaded, miliary tubercle along the path
of hilar nodes.
• Iii) LN component : enlarged hilar & tracheo-broncheal LN.
Involved LN are matted & show caseation necrosis.
- Micro: extensive caseation, tuberculous granuloma & fibrosis.
Nodal lesions are potential source of re- infection later.
Radiologically detectable calcification (Ranke complex).
• Fate of Primary tuberculosis :
Healing by fibrosis ,& in time undergo calcification &
ossification.
In some cases, caseous material disseminated through bronchi
to other parts of same lung or the opposite lung, called
Progressive primary tuberculosis.
Hematogenous spread – Primary Miliary tuberculosis.
Fate of primary tuberculosis –contd.
Spread along mucous & serous surfaces :
• from lung bacilli larynx during expectoration, or through
swallowed sputum to small intestine – tuberculous ulcers.
• Spread to pleura – tuberculous pleurisy with or without effusion,
pneumothorax or pyo-pneumothorax.
• Epithelioid cells
Firoblastic Langhan’s
proliferation giant cell
Lympho cytes
Caseation
necrosis