1. Pathology of Pneumonia

3. Normal Lung

4. 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.

5. 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.

6. Pneumonia can occur when any of these mechanisms are damagedOR
When host immunity is lowered.
When the organism is highly virulent.

7. 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

8. 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

9. 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)

10. Pathogenesis:

11. Pathogenesis:

12. Pneumonia Types: Etiologic Types: Infective Non 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)

13. 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.

14. Pathogenesis of Pneumonia
Grey Hepatization
Resolution
Pathogenesis of Pneumonia
Congestion
Red Hepatisation

15. Lobar Pneumonia: Red hepatization, lobe of lung is heavy, boggy & red

16. Lobar Pneumonia, grey hepartization: Greyish-brown, dry surface

17. Lobar Pneumonia – Gray hep…

18. Lobar Pneumonia:

19. Lobar Pneumonia: Congestion

20. Lobar Pneumonia: Red hepat.

21. Lobar Pneumonia: Grey hepat.

22. Pneumonia-stages

23. Broncho-pneumonia (Lobular pneumonia)

24. 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

25. Broncho-pneumonia

26. Broncho-pneumonia

27. Broncho
Pneumonia

28. Bronchopneumonia:

29. Bronchopneumonia - CT

30. Bronchopneumonia

31. Broncho – Pneumonia - Lobar
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

32. Broncho – Pneumonia - Lobar

33. 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

34. Interstitial Pneumonia:

35. Interstitial Pneumonia:
Lymphocyte Infiltrate in alveloar wall

36. Etiologic agents Distribution Microscopic features Lobar pneumonia
Broncho pneumonia
Atypical (interstitial pneumonia)
Age group
Any age group
Infancy & old age common
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

37. 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.

38. Pathogenesis of Clinical features:
*Alveolar inflammation.
Tachypnoea, Dyspnoea, Resp Acidosis  Solid/airless lungs – decreased oxygenation.
Dull percussion - Consolidation – Exudation
Rusty sputum - RBC & Inflammatory cells.
Fever – Inflammatory mediators.

39. 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.

40. Abscess formation

41. Lung Abscess:

42. Abscess formation

43. Lung Abscess:

45. Thank you