Tuberculosis

Tuberculosis
“The Biggest Disease Today Is Not Leprosy Or
Tuberculosis, But Rather The Feeling Of Being
Unwanted”

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What Is Tuberculosis?
 An infectious disease characterized by the growth of
nodules(tubercles) in the tissues, especially lungs.
 It represents classical example of chronic granulomatous
inflammation in humans.

Other Known Strains:
• M.Tuberculosis hominis[(Human strain)
most common]
• M.Tuberculosis Bovis(Bovine Strain)
• M.microti, M.africanum, M.canettii.
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Causative Organism
Mycobacterium tuberculosis (Koch’s
Bacillus) causes tuberculosis in lungs and
other issues of the human body.
The Organism Is a strict Aerobe and
thrives in the tissues with high oxygen
tension such as in the apex of the lungs.

Staining Of M.Tuberculosis Hominis: 4
1.Acid Fast (Ziehl-Neelsen) Staining:
 Acid fastness of tubercule bacillus is due to mycolic
acid, fatty acids and other lipids.
 It takes up stain by heated carbon fuchsin.
 It resists decolourisation by acids and alcohols.
 It can be decolourised by 20% sulphuric acid.
 False positive AFB staining due to Nocardia,
Rhodococcus, Legionella.

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2. Fluorescent Dye Methods
3. Culture from sputum in Lowenstein-Jensen medium.
4. Guinea Pig Method (Subcutaneous injection)
5. Molecular Method [PCR (Polymerase Chain Reaction]

Atypical Mycobacteria:
(Non –Tuberculosis Mycobacteria)
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 This term is generally used for
mycobacterial species other than
M.tuberculosis complex and M.Leprae.
 They are widely distributed in environment
and thus are referred to as environmental
mycobacteria.
 Human Tuberculosis is generally caused by
those bacterias which are non-pathogenic
to guinea pigs and resistant to anti-
tubercular drugs.

Classification On The Basis Of Color Of
Colony And Their Speed Of Growth:
1.Rapid Growers: These organisms grow fast on solid media(within 7days) and are less
pathogenic.
Eg:- M.Abscessus, M.Fortuitum, M.Chelonae.
2.Slow Growers: These organisms grow slow on solid media (in 2-3 weeks).
Eg:- M.Avium-Intracellulare, M.Kansassi, M.Fortuitum.
Further Classified on the basis of colour of the colony:
A. Photochromogens: Produce Yellow Pigment Only in light .
B. Scotochromogens: Produce pigment irrespective of light and dark.
C. Non-Chromogens: No Pigment is produced in light or dark.
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 The infection by atypical mycobacteria is acquired directly
from environment, unlike person-to-person transmission
in classical tuberculosis.
 Produce human disease called atypical mycobacteriosis
which is generally much less virulent.
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Mode Of Transmission: 10
Inhalation (Fresh Droplets or Sputum).
Ingestion (Self- Swallowing).
Inoculation ( Direct invasion into skin).
Transplacental route (From infected
mother to Foetus).

Spread Of
Tuberculosis:
 Local Spread (Macrophages
Carrying Bacteria).
 Lymphatic Spread (follicles of
pharynx, bronchi, intestine, or
regional lymph nodes).
 Hematogenous Spread (drainage of
lymphatics into the venous system).
 By The Natural Passangers
(invasion into different parts of
body).
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Hypersensitivity And
Immunity In Tuberculosis
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 Hypersensitivity plays a major role in development of lesions in tuberculosis.
 The bacteria (Tubercle Bacilli) do no produce any toxins.
 The specified tissue changes occur not due to exotoxins or endotoxins but occur as
a result of exaggerated response of CMI and hypersensitivity against the bacteria.
This responses occur as a result of several lipids present inside bacteria:
1. Mycosides : ‘Cord Factor’ essential for growth and virulence of organism.
2. Glycolipids : present in mycobacterial cell wall ‘WAX-D’ which increases the
response in the presence of tuberculoprotein
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Reaction Of Tubercule Bacilli In
Healthy Animal (Robert Koch):
1. Primary Infection :
 Injection in Guinea Pig.
 No reaction till 10-14 days.
 Nodule develops which heals poorly
in guinea pig.
 Regional Lymph Nodes also
develop.
 This is delayed type of
hypersensitivity, however healing
occurs in childrens.
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2. Secondary Infection:
 Injection in early infected guinea pig (4-6 weeks).
 The site of infection becomes dark in 1-2 days.
 In this infection the ulcerated lesion undergoes healing and regional lymph
nodes are not affected, known as Koch’s Phenomenon indicating
hypersensitivity in host.
 Similar changes can be produced with Old Tuberculin (OT).
 Hypersensitivity is produced through specific antigens against tuberculin in
CD-4 T Lymphocytes.
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Tuberculin (Mantoux) Skin Test:
 Intradermal injection of 0.1ml tuberculoprotein , purified protein derivative
(PPD).
 Delayed hypersensitivity in earlier affected individuals.
 Indurated Area of about 15mm in 72hrs.
 A negative test if patient suffers from disseminated tuberculosis due to
release of large amount of tuberculin.
 A positive test when CMI hypersensitivity is observed against
tuberculoprotein.
Immunization = Bacille- Calmette- Guerin (BCG)
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Pathogenesis Of Tuberculosis
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Types Of Tuberculosis:
1. Primary Tuberculosis
 Infection of an individual who has not been previously infected or
immunised is called Primary Tuberculosis or Ghon’s Complex or
Childhood Tuberculosis.
 Ghon’s complex is a lesion produced on the entry of foci in draining
lymphatic vessels and lymph nodes.
 Commonly involved organs are lungs and hilar lymph nodes.
 If ingested orally , it might produce lesions in small intestine and
mesenteric lymph nodes.
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 Disseminated form of tuberculosis is generally high in
immunocompromised patients i.e, in the patients of AIDS.
Primary Complex or Ghon’s Complex consists of 3 components:
1. Pulmonary Component: include lesions in the lungs that is primary
focus or Ghon’s focus.
2. Lymphatic Vessel Component: Draining lymph might get infected
causing infection in hilar lymph nodes.
3. Lymph Node Component: Includes enlarged hilar and tracheo-Bronchial
lymph nodes.
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2. Secondary Tuberculosis: 21
The infection of an individual who has been
previously infected or sensitised is called
Secondary or Post-Primary or Reinfection or
Chronic Tuberculosis.
Secondary Tuberculosis occurs most
commonly in lungs but can invade to tonsils,
pharynx, larynx, small intestine and skin.
The lesion produced may heal with fibrous
scar or undergo calcification. Further, it
might coalesce with each other to form
larger lesion, with following Pulmonary and
Extra- Pulmonary involvements:

1. Fibrocaseous
Tuberculosis:
 The original area may undergo caseation
necrosis in following manner:
1. Either, break into bronchus forming a
Cavity.
2. Remain, as a soft caseous lesion
without drainage into a bronchus, or
bronchiole to produce a non-cavitary
lesion.
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2. Tuberculous Caseous Pneumonia: The caseous
material may spread to various different parts of lungs
producing caseous pneumonia.
3. Miliary Tuberculosis: The spread of tuberculosis from
primary focus or later stages of tuberculosis through
lymphohematogenous spread to other parts of body such
as spleen, kidney, brain, bone marrow.
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 Productive Cough with
1. Haemoptysis (rupture of RBC’s)
2. Pleural Effusion (water in lungs)
3. Dyspnoea (difficulty in breathing)
4. Orthopnoea (shortness of breathing
when lying flat)
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Other Symptoms Of
Lungs:

Diagnosis Of Tuberculosis
1. Positive Mantoux Skin Test.
2. Positive Sputum For AFB (Acid – Fast Bacilli).
3. Complete Hemogram (Complete raised
lymphocytes and ERR).
4. Chest X-ray.
5. Fine Needle Aspiration Cytology Of An
Enlarged Peripheral Lymph Node.

Tuberculosis

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