PNEUMONIAS

Dr Vijay Shankar S

CaseA 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

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

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

NOVEMBER 12TH

WORLD PNEUMONIA DAY

• Raise awareness about pneumonia, the world’s leading killer of children under the age of five;

• Promote interventions to protect against, prevent and treat pneumonia; and

• Generate action to combat pneumonia.

Pathology of Pneumonia

Normal Lung

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.

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.

• Pneumonia can occur when any of these mechanisms are damaged

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

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

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

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:

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)

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.

Stage Gross microscopy images Clinical features

Stage of Congestion

1st-2nd day

Heavy, dark red and firm

Alveolar capillaries: DilatedAir space: fluid, RBC, WBC

Fever, cough, cyanopathyChest painBacteremia Bacteria can be found in sputum

Stage of red hepatization

2nd-4th day

Red &Consolidated

Just likeLIVER!

A. Capillaries congestion

B. Exudation: Fibrin, large number of RBC C. Fibrinous pleurisy

Fever, cough, chest painRapid breathing, cyanopathyDullness, vocal fremitus enhancement Rusty sputum

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 .enhancementSputum: 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

BRONCHO PNEUMONIA

Broncho-pneumonia(Lobular pneumonia)

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

Broncho-pneumonia

Broncho-pneumonia

BronchoPneumonia

Bronchopneumonia - CT

Bronchopneumonia

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

INTERSTITIAL PNEUMONIA

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:

Interstitial Pneumonia:

Lymphocyte Infiltrate in alveloar wall

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

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.

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.

Abscess formation

Lung Abscess:

Abscess formation

Lung Abscess:

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