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Pathology of Pneumonia

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Presentation on theme: "Pathology of Pneumonia"— Presentation transcript:

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 damaged
OR 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

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