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PULMONARY TUBERCULOSIS By Dr. Abdelaty Shawky Assistant professor of pathology 1.

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Presentation on theme: "PULMONARY TUBERCULOSIS By Dr. Abdelaty Shawky Assistant professor of pathology 1."— Presentation transcript:

1 PULMONARY TUBERCULOSIS By Dr. Abdelaty Shawky Assistant professor of pathology 1

2 * 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. 2

3 * 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. 3

4 * Types of T.B: I.Primary (1ry) T.B. II.Secondary (2ry) T.B. 4

5 Primary tuberculosis (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. 5

6 * Methods of infection: 1. Inhalation 2. Ingestion 3. Direct contact. * Tissue reaction (Reaction of the body against T.B bacilli): proliferative (tubercle formation). 6

7 *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. 7

8 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 8

9 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). 9

10 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. 10

11 * 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. 11

12 Non-caseating tubercles 12

13 Pulmonary Tuberculosis 13

14 Lung is a favorable site for T.B. (easy inhalation and aeration).Types: 1.1ry pulmonary T.B. 2.2ry pulmonary T.B. 14

15 1ry pulmonary T.B 15

16 * Age: Children. * Mode of infection: Droplet infection. * Lesions: More in the right lung than the left lung. 1ry pulomnary complex (Ghon’s triad). 16

17 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. 17

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19 Ghon ’ s focus 19

20 * 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 bronchi 20

21 2ry PULMONARY T.B 21

22 * 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. 22

23 Apical pulmonary T.B 23

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26 * The Fate of 2ry pulmonary T.B: A. Good fate: - Regression and healing. In cases of good immunity. 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

27 Thanks 27

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