Pathology of Pathology of PneumoniaPneumonia

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Normal Lung

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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.

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Defense mechanisms of the respiratory tree:

1. Nasal clearance: Aerosolized particles carrying micro-organisms are normally removed by sneezing & blowing OR by swallowing.

2. Tracheobronchial clearance: Accomplished by mucociliary action. Partcicles are either swallowed or expectorated.

3. Alveolar clearance: Phagocytosis of bacteria or solid particles by alveolar macrophages.

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Pneumonia can occur when any of these mechanisms are damaged

OR When host immunity is lowered. OR When the organism is highly virulent.

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Factors that interfere with defense mechanisms:

1. Loss or suppression of cough reflex: Coma, general anaesthesia, neuromuscular disorders, drugs & chest pain.

2. Injury to mucociliary apparatus: Smoking, corrosive gases, viral diseases, genetic (immotile cilia syndrome).

3. Impaired phagocytic clearance: Alcoholism, cigarette smoke, anoxia, oxygen intoxication.

4. Pulmonary congestion & oedema.5. Accumulation of secretions: Cystic

fibrosis

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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

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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)

Pathogenesis:

Pathogenesis:

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Pneumonia Types:

Etiologic Types: Infective

Viral Bacterial Fungal Tuberculosis

Non Infective Toxins chemical Aspiration

Morphologic types: Lobar Broncho InterstitialDuration: Acute ChronicClinical: Primary / secondary. Typical / Atypical Community acquired /

hospital acquired(nosocomial)

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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.

CongestionRed Hepatisation

Grey HepatizationResolution

Pathogenesis of Pneumonia

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

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

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Lobar Pneumonia – Gray hep…

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Lobar Pneumonia:

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Lobar Pneumonia: Congestion

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Lobar Pneumonia: Red hepat.

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Lobar Pneumonia: Grey hepat.

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Pneumonia-stages

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Broncho-pneumonia(Lobular pneumonia)

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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

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Broncho-pneumonia

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Broncho-pneumonia

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BronchoPneumonia

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Bronchopneumonia:

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Bronchopneumonia - CT

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Bronchopneumonia

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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

Broncho – Pneumonia - Lobar

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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

Interstitial Pneumonia:

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Interstitial Pneumonia:

Lymphocyte Infiltrate in alveloar wall

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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 pneumoniaeChlamydiaCoxiella 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

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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.

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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.

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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.

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Abscess formation

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Lung Abscess:

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Abscess formation

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Lung Abscess:

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