PULMONARY TUBERCULOSISPULMONARY TUBERCULOSIS

ByBy Dr. Abdelaty ShawkyDr. Abdelaty Shawky

Assistant professor of pathologyAssistant professor of pathology

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* 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.

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* 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.

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* Types of T.B:

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

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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. Nose. 2. Intestine. 3. Tonsil. 4. Skin.

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

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

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*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.

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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) & lymphotoxins8

• 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).

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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.

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* Gross picture of tubercle:

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

grey periphery.

* Microscopic picture of tubercle: Central caseating material (structureless, eosinophilic

material, epithelioid cells, macrophages, Langhan’s giant

cells, lymphocytes and peripheral fibroblastic reaction.

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Non-caseating tubercles

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Pulmonary TuberculosisPulmonary Tuberculosis

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Lung is a favorable site for T.B. (easy inhalation and

aeration).

Types:Types:

1. 1ry pulmonary T.B.

2. 2ry pulmonary T.B.

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1ry pulmonary T.B1ry pulmonary T.B

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* Age:

• Children.

* Mode of infection:

• Droplet infection.

* Lesions:

• More in the right lung than the left lung.

• 1ry pulomnary complex (Ghon’s triad).

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Primary pulmonary complex (Ghon’s triad)

Consists of 3 parts:

1. Parenchymatous lesion (Ghon’s focus):

- Tubercles which develop at the lower parts of upper

lung lobes or upper parts of lower lung lobes,

subpleural.

- Consists of non-caseating and caseating tubercles.

1. Tuberculous lymphangitis.

2. Tuberculous lymphadenitis.

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GhonGhon’’s focuss focus

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* Fate:* Fate:

A. Good fate: A. Good fate:

- Healing by fibrosis and dystrophic calcification.

- Formation of a dormant T.B focus.

B. Bad fate: B. Bad fate: Spread.

1. Local.

2. Lymphatic.

3. Hematogenous

4. Natural passage: through the lumen of bronchi20

2ry2ry PULMONARY T.B PULMONARY T.B

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* Age: adults who are infected or vaccinated before.

* Mode of Infection:

1. Reactivation of dormant focus.

2. Exogenous by inhalation.

* Lesions:

• It is only caseating tuberclous reaction (Assman’s focus or

Simon’s focus) develop at the apical portion of the lung.

• No complex formation.

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Apical pulmonary T.BApical pulmonary T.B

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* The Fate of 2ry pulmonary T.B:* The Fate of 2ry pulmonary T.B:

A. Good fate: A. Good fate:

- Regression and healing. In cases of good immunity.

B. Bad Fate: B. Bad Fate:

- Progression and spread in cases of poor immunity.

1. Cavitary Tuberculosis

2. Chronic fibrocaseous pulmonary tuberculosis

3. Acute tuberculous bronchopneumonia & acute

caseous pneumonia.26

ThanksThanks

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