PULMONARY TUBERCULOSIS-1 Dr. WASIF ALI KHAN MD-PATHOLOGY (UNIVERSITY OF BOMBAY) AL MAAREFA COLLEGE

PULMONARY TUBERCULOSIS-1PULMONARY TUBERCULOSIS-1Dr. WASIF ALI KHANDr. WASIF ALI KHAN

MD-PATHOLOGY (UNIVERSITY MD-PATHOLOGY (UNIVERSITY OF BOMBAY)OF BOMBAY)

AL MAAREFA COLLEGEAL MAAREFA COLLEGE

* Definition: chronic infective granuloma affecting nearly all body systems but mainly the lungs.

* Predisposing factors:a) Environmental: low socioeconomic level, bad general hygiene, overcrowding.b) Personal factors: cases of low resistance e.g. malnutrition – AIDS - D.M.

* Causative Agents: T.B. bacilli

* Structure o f T.B. bacilli:

Tuberculoprotein core covered by glycolipid.

* Types of TB Bacilli:

• Human type: transmitted from human to human by

droplet infection.

• Bovine type: transmitted from cows to human by

ingestion of infected milk.

* Characters of T.B bacilli: • Gram + ve, Non-motile, • Non-toxin producing, not killed by macrophages.• Acid and alcohol fast. i.e resist discoloration by acid

and alcohol.• Resist dryness for months but killed by sun rays.

T.B bacilli detected by bacteriologic examination

* Types of T.B:

I. Primary (1ry) T.B.II. Secondary (2ry) T.B.

Primary tuberculosisPrimary tuberculosis(childhood type)(childhood type)

* Age:- Occurs in young persons < 3 years, who are: non immunized, and infected for the first time.* Sites:

1. lung 2. Intestine 3. Tonsil 4. Skin.

* Methods of infection: 1. Inhalation 2. Ingestion 3. Direct contact.

* Tissue reaction (Reaction of the body against T.B bacilli): proliferative (tubercle formation).

*Pathogenesis of tubercle (T.B granuloma) formation:

A. In the first 24 hours:•Carbohydrate coat of the bacilli recruits neutrophils, which fails to kill it.•Bacilli are taken by surface macrophages to the deep parts of the tissues, draining lymphatics & L.Ns. •Macrophages process the bacilli releasing the purified protein derivative PPD, then express it on the surface carried on MHC class II molecules.

B. After 10-15 days:•T.B granuloma is formed as follow;•Macrophages secrete IL-12 which activate the naïve CD+4 T lymphocytes to T helper (TH1) cells.•TH1 cells release lymphokines:

1. INF-y (interferon Gama) leads to macrophage activation.2. IL-2 (interleukin-2) leads to lymphocyte proliferation.3. TNF (tumor necrosis factor) & lymphotoxins: secrete prostacyclin, cheomkines (IL-8) & adhesion molecules.

• The accumulated macrophages undergo a morphologic transformation into epitheial-like cells (epithelioid cells). Some epithelioid cells coalesce to each other to form langhan’s giant cells. Collections of epithelioid cells, langhans giant cells and a collar of lymphocytes is termed (non-caseating tubercle).

C. After 2-3 weeks:•The tubercles undergo central caseation necrosis (very rare with 1ry T.B), the causes are:

1. Relative central ischemia.2. Lymphotoxins.3. Proteolytic enzymes of neutrophils.

* N/E of tubercle:

Small, 1-3 mm, with central yellow caseation and

grey periphery.

* M/E of tubercle: Central caseating material (structureless, eosinophilic

material, epithelioid cells, macrophages, Langhan’s giant

cells, lymphocytes and peripheral fibroblastic reaction.

Non-caseating tubercles

* Pathology of primary T.B:

• Is primary complex consists of:1. Parenchymatous lesion.2. Tuberclous lymphangitis.3. Tuberclous lymphadenitis.

1. Parenchymatous lesion: - The tubercles (caseating or non-caseating)

which develop at site of entrance of the bacilli.

2. Tuberculous lymphangitis: - The tubercles which develop along the

draining lymphatics.- The lymphatics appear thick and beaded.

3. Tuberculous lymphadenitis: - The tubercles which develop inside the draining

lymph nodes.• Early the lymph nodes appear enlarged, firm,

and discrete. Microscopically show non-caseating tubercles.

• Late, the lymph nodes appear enlarged, soft and fused to each other. Microscopically show caseating tubercles.

* Fate of primary complex:1. Good fate: - Healing by fibrosis.- Formation of a dormant focus. Some bacilli are not

killed and could be activated in the future if the patient’s immunity depress.

2. Bad fate: spread:1. Local.2. Lymphatic.3. Hematogenous 4. Natural passage. through e.g. the lumen of bronchi

Secondary tuberculosisAdulthood type

* Age: adults.* Sites:

Any site, mainly the lung & intestine are affected.* Methods of infection:

1. Endogenous by reactivation of dormant focus.2. Exogenous by inhalation or ingestion.

* Tissue reaction of the body against bacilli in secondary infection.

1. Proliferative reaction:

- Occurs in solid organs.

- Characterized by tubercles formation.

1. Exudative reaction:

- Occurs in serous sacs and sometimes in soft parenchymatous

organs e.g. lung and brain.

- Characterized by formation of tubercles exudate.

* Fate of secondary T.B:

1. Good fate: Healing by fibrosis.

2. Bad fate: Spread:

1. Local.

2. Natural passages.

3. Blood (rare)

4. Lymphatic.

TuberculomaTuberculoma

* Definition: Tumor-like tuberculous lesion formed

of inspissated caseating material surrounded by

fibrous capsule.

* Sites: Lung, brain, kidney, and spinal cord.

Miliary TuberculosisMiliary Tuberculosis* Definition: acute hematogenous dissemination

of large dose of T.B bacilli with wide spread involvement of multiple organs due to depressed patient’s immunity.

* Gross features: Multiple, scattered, uniform, small size (3mm)

tubercles separated from each other, by normal tissue and not surrounded by area of congestion and present on outer and cut surface of organs.

Miliary T.B of the lung

* MICROSCOPIC EXAMINATION:

Poorly developed tubercle with central caseation

necrosis and absent giant cells.

TB INTESTINE

Miliary TB

TB Intestine TB Peritonitis + liver Miliary TB

TB

Prostate TB Spinal TB - Potts Disease