RESPIRATORY SYSTEM: PATHOLOGY OF PNEUMONIAS

RESPIRATORY SYSTEM: PATHOLOGY OF PNEUMONIAS

1. PNEUMONIAS Dr Vijay Shankar S

2. Case A 35 y.o . M presents with 2d cough, productive of green-yellow sputum. He complains of fever, chills, and dyspnea PE: T 38.7℃, RR 26/min, BP 110/65 mmHg, HR 125/min

3. Examination of the lungs reveals increased fremitus and dullness at the right posterior base. Crackles and bronchial breath sounds are audible at the right base Gram stain of the sputum reveals gram-positive cocci and numerous neutrophils

4. Pneumonia is the #1 killer of children under age 5 worldwide – responsible for nearly one in five global child deaths annually.

5. NOVEMBER 12 TH WORLD PNEUMONIA DAY

6. Raise awareness  about pneumonia, the world’s leading killer of children under the age of five; Promote intervention s to protect against, prevent and treat pneumonia; and Generate action  to combat pneumonia.

7. Pathology of Pneumonia

8. Normal Lung

9. Consolidation of the lung occurs in pneumonia What is consolidation? Consolidation is exudative solidification of lung parenchyma that occurs in bacterial invasion of the lung. This is known as pneumonia.

10. Defense mechanisms of the respiratory tree: Nasal clearance : Aerosolized particles carrying micro-organisms are normally removed by sneezing & blowing OR by swallowing. Tracheobronchial clearance : Accomplished by mucociliary action. Partcicles are either swallowed or expectorated. Alveolar clearance : Phagocytosis of bacteria or solid particles by alveolar macrophages.

11. Pneumonia can occur when any of these mechanisms are damaged OR When host immunity is lowered. OR When the organism is highly virulent.

12. Factors that interfere with defense mechanisms: Loss or suppression of cough reflex : Coma, general anaesthesia, neuromuscular disorders, drugs & chest pain. Injury to mucociliary apparatus : Smoking, corrosive gases, viral diseases, genetic (immotile cilia syndrome). Impaired phagocytic clearance : Alcoholism, cigarette smoke, anoxia, oxygen intoxication. Pulmonary congestion & oedema. Accumulation of secretions : Cystic fibrosis

13. Etiology: Decreased resistance - General/immune Virulent infection - Lobar pneumonia Defective Clearing mechanism Cough/gag Reflex – Coma, paralysis, sick. Mucosal Injury – smoking, toxin aspiration Low Alveolar defense - Immunodeficiency Pulmonary edema – Cardiac failure, embol. Obstructions – foreign body, tumors

14. Pathogenesis of Pulmonary Infections Step 1: Entry Aspiration ( ie Pneumococcus ) Inhalation ( ie M.TB and viral pathogens) Inoculation (contaminated equipment) Colonization (in patients with COPD) Hematogenous spread (patients with sepsis) Direct spread (adjacent abscess)

15. Pathogenesis:

16. Pathogenesis:

17. Pneumonia Types: Etiologic Types: Infective Viral Bacterial Fungal Tuberculosis Non Infective Toxins chemical Aspiration Morphologic types: Lobar Broncho Interstitial Duration: Acute Chronic Clinical: Primary / secondary. Typical / Atypical Community acquired / hospital acquired(nosocomial)

18. Lobar Pneumonia: whole lobe, exudation - consolidation 95% - Strep pneum.(Klebsiella in aged, DM, alcoholics) High fever, rusty sputum, Pleuritic chest pain. Four stages: ( * also in bronchopneumonia) Congestion – 1d – vasodilatation congestion. Red Hepatization 2d Exudation+RBC Gray Hepatizaiton 4d neutro & Macrophages. Resolution – 8d few macrophages, normal.

19. Stage Gross microscopy images Clinical features Stage of Congestion 1st-2nd day Heavy, dark red and firm Alveolar capillaries: Dilated Air space: fluid, RBC, WBC Fever, cough, cyanopathy Chest pain Bacteremia Bacteria can be found in sputum Stage of red hepatization 2nd-4th day Red & Consolidated Just like LIVER! A. Capillaries congestion B. Exudation: Fibrin, large number of RBC C. Fibrinous pleurisy Fever, cough, chest pain Rapid breathing, cyanopathy Dullness, vocal fremitus enhancement Rusty sputum

20. Stage Gross microscopy images Clinical features Stage of Grey hepatization 5th-6th day Dry Gray Firm Consolidation Capillary is not dilated anymore. Alveolar space is filled with neutrophil and fibrin Consolidation: dullness, vocal fremitus . enhancement Sputum: mucus purulent sputum Dyspnoea : is not obvious Stage of Resolution 7 days later Friable and mottled The fibrin and cell debris are digested by enzymatic The exudation is removed Improvement in above clinical features

21. BRONCHO PNEUMONIA

22. Broncho-pneumonia (Lobular pneumonia)

23. Bronchopneumonia (patchy) Extremes of age. (infancy and old age) Staph, Strep, Pneumo & H. influenza Patchy consolidation – not limited to lobes . Suppurative inflammation Usually bilateral Lower lobes common

24. Broncho-pneumonia

25. Broncho-pneumonia

26. Broncho Pneumonia

27. Bronchopneumonia - CT

28. Bronchopneumonia

29. Broncho Pneumonia Extremes of age. Secondary to other disorders. Staph, Strep, H.influenzae Patchy consolidation Around Small airway Not limited by anatomic boundaries. Usually bilateral. Middle age – 20-50 Primary in a healthy males common. 95% pneumoc ( Klebs .) Entire lobe consolidation Diffuse Limited by anatomic boundaries. Usually unilateral Lobar Pneumonia

30. INTERSTITIAL PNEUMONIA

31. Interstitial / atypical Pneumonia Primary atypical pneumonia in the immunocompetant host (Mycoplasma or Chlamydia) Interstitial pneumonitis immunocompromised host : Pneumocystic carinii; CMV Immunocompetant host: Influenza A Gross features: Lungs are heavy but not firmly consolidated Microscopic features: Septal mononuclear infiltrate Alveolar air spaces either ‘empty’ or filled with proteinaceous fluid with few or no inflammatory cells

32. Interstitial Pneumonia:

33. Interstitial Pneumonia: Lymphocyte Infiltrate in alveloar wall

34. Lobar pneumonia Broncho pneumonia Atypical (interstitial pneumonia) Age group Any age group Infancy & old age common Any age group Predisposing factors Highly virulent organisms CCF, disseminated malignancy, pre-existing bronchitis, bronchiolitis Malnutrition, alcoholism, underlying debilitating illnesses Etiologic agents 90-95% of cases caused by pneumococci (Strep.pneumoniae) Staphylococci Streptococci Pneumococci H. Influenzae Pseudomonas aeruginosa Coliform bacteria Mycoplasma pneumoniae Chlamydia Coxiella burnetti Distribution Consolidation of large areas of one lobe or the whole lobe Patchy consolidation of more than one lobe of the lung Involvement maybe patchy or involve whole lobes unilaterally or bilaterally Microscopic features Involvement of all alveoli of one lobe by inflammatory exudate; The 4 classical stages of consolidation are best seen in lobar pneumonia Patchy involvement of alveoli around the bronchioles in more than one lobe by inflammatory exudate Interstitial inflammation composed of lymphocytes, virtually localized within alveolar walls

35. Community acquired – Pneumonia – Nosocomial In healthy adults Gram positive. Streptococcus pneumoniae (90%) Strep. Pyogenes, Staph, H. influenzae and Klebsiella in elderly or with COPD. In *sick patients. gram-negative bacilli Pseudomonas aeruginosa, Escherichia coli, Enterobacter, Proteus, and Klebsiella.

36. Complications of Pneumonia Abscesses Localized suppurative necrosis, Right side often involved in aspiration. Common etiologic agents are Staphylococcus, Klebsiella, Pneudomonas Pleuritis / Pleural effusion. Inflammation of the pleura ( Streptococcus pneumoniae) Blood rich exudate (esp. rickettsial diseases) Empyema Pus in the pleural space. Septicemia: with bacteremic dissemination to heart valves, pericardium, brain, spleen, kidneys or joints causing metastatic abscesses, endocarditis, meningitis or suppurative arthritis. Organization of the exudate resulting in fibrosis.

37. Abscess formation

38. Lung Abscess:

39. Abscess formation

40. Lung Abscess:

41. Thank you