7- Infectious Pulmonary Diseases

1. 7- Infectious Pulmonary Diseases Dr Tarek Atia

2. Introduction: Respiratory tract infections – commonest in medical practice. Pneumonia: Inflammation of the lung tissue. High morbidity & mortality rate.

3. Etiology: Decreased general resistance Virulent infection : Lobar pneumonia Defect in clearing mechanisms Decreased Cough Reflex Injury of the cilia and mucosa Low alveolar defense Pulmonary edema or congestion Bronchial Obstructions The common pathogens are: Viral Bacterial Mycoplasmal Fungal

4. Patterns of infections Airwayinflammation: Bronchitis, Brocheolitis, Bronchiectasis Parenchyma inflammation: Pneumonia Bronchopneumonia Lobar pneumonia Lung abscess Tuberculosis

5. Pneumonia • Pathology: • Alveolar • Bronchopneumonia (Strept. pneumoniae, Haemophilus influenza, Staph. aureus) • Lobarpneumonia (Strept. pneumoniae) • Interstitial (Influenza virus, Mycoplasma pneumoniae) • Pathogenesis • Inhalation of infected air droplets • Aspiration of infected secretions or objects • Hematogenous spread

6. Pneumonia Symptoms • “Typical” pneumonia: sudden onset of fever, cough productive of purulent sputum, pleuritic chest pain • “Atypical”: gradual onset, dry cough, prominence of extra-pulmonary symptoms: headache, myalgias, fatigue, sore throat, nausea, vomiting.

8. Bronchopneumonia Suppurative inflammation of the lung tissue. Caused by Staph, Strept, Pneumococci & H. influenza Patchy consolidation of the lung tissue, not limited to lobes, and usually bilateral Lower lobes are commonly affected, but it can occur anywhere in the lung.

9. Complications: • Lung Abscess • Empyema • Dissemination

10. Bronchopneumonia Macroscopic picture of the lung showing multiple patches of suppurative inflammation of the lung tissue

11. Bronchopneumonia Microscopic picture of the lung alveoli filled with inflammatory cells; with intact alveolar septa.

12. Bronchopneumonia

13. Lobar Pneumonia Whole lobe affected Fibrino-suppurative consolidation Rare due to antibiotic treatment. ~95% - Strept. pneumoniae • The course of the disease runs in four stages: • Congestion. • Red Hepatization. • Gray Hepatization. • Resolution.

14. Lobar pneumonia Lobar pneumonia: whole lobe involved, grey and red hepatization

15. Lung Abscess: Focal suppurative inflammatory condition with necrosis of lung tissue Organisms commonly cultured: Staphylococci Streptococci Gram-negative Anaerobes Frequent mixed infections

16. Mechanism: • Commonly after bronchopneumonia • Aspiration • Septic embolism • Neoplasms • Productive Cough, prolonged fever • Clubbing, if chronic • Complications: Systemic spread, septicemia.

17. Lung Abscess:

18. Lung Abscess Microscopic picture of the lung tissue showing localized aggregation of inflammatory cells with destruction of the lung tissue.

19. Tuberculosis (TB) Communicable disease It is a chronic granulomatous disease Causative organism: acid-fast bacilli; Mycobacterium tuberculosis The bacilli are of two types (human and bovine), Typically results in caseous necrosis and granulation tissue formation.

20. Route of infection - Route of infection:- • Respiratory tract: Inhalation of infected droplets from patient with open TB. • Intestinal tract: Ingestion of infected milk • Skin by inoculation: (butchers). • Congenital by transplacental spread

21. Epidemiology • ~ 1/3 of the world’s population are infected • A leading single cause of death globally (~ 6% of deaths worldwide); 3 million deaths / year • The lung is the most common important clinical site of infection.

22. Microorganism • The bacilli are non-motile, acid fast, and very resistant organisms. • M. tuberculosis hominis • Transmitted by inhalation of infective droplets into the air or by exposure to contaminated secretions • M. bovis • Transmitted by milk from diseased cows • M. avium-intracellulare • Very low virulence  rarely cause disease in hosts

23. Predisposing Factors • Access of organism: close contact with open cases of disease • Susceptibility of individual: - Old or very young age - Black and/or Asian • Malnutrition, Crowding. • Occupation: increased incidence of TB in health workers.

24. Primary TB In Non Immunized individuals (Children) • Primary Tuberculosis: • Self Limited disease • Ghons focus, Primary complex. • Primary Progressive TB • Miliary TB and TB Meningitis. • Common in Immuno-suppressed individuals

25. Sites of 1ry TB - 1ry cervical complex: TB tonsillitis, TB lymphadenitis, TB lymphangitis. - 1ry pulmonary complex: Ghon`s focus, TB hilar lymphadenitis, TB lymphangitis . -1ry intestinal complex: TB enteritis, TB lymphadenitis, TB lymphangitis.

26. Ghon`s Focus • Small rounded about 1cm focus, present anywhere in the lung, commonly peripheral and subpleural. • Central caseation and cold abscess may occur.

27. Primary or Ghon’s Complex • Primary tuberculosis is the pattern seen with initial infection with tuberculosis in children. • Reactivation, or secondary tuberculosis, is more typically seen in adults.

28. Secondary Tuberculosis: • Post Primary in immunized individuals. • Reactivation or Reinfection • Caseous necrosis, cavity - soft granuloma • Pulmonary or extra-pulmonary • Local or systemic spread • Vein – via left ventricle to whole body • Artery – miliary spread within the lung

29. Tissue reaction to Tb bacilli Cellular (proliferative) reaction: occurs in 1ry TB, and leads to a tubercle (granuloma) formation , which is microscopically formed of:- - Epitheloid cells (macrophages) - Caseous necrosis - Multinucleated Giant Cells - Lymphocytes - Fibroblasts

30. Cavitary Tuberculosis • When necrotic tissue is coughed up  cavity. • Cavitation is typical for large granulomas. • Cavitation is more common in the secondary reactivation tuberculosis - upper lobes.

31. Morphology of granuloma • Collection of chronic inflammatory cells. • Central caseousnecrosis. • Active macrophages - epithelioid cells. • Outer layer of lymphocytes, plasma cells & fibroblasts. • Langhans giant cells – fused macrophages.

32. Epitheloid cells in granuloma Lung Fibrocaseous necrosis Caseation necrosis