Pathology of
Pneumonia
Pneumonia
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Normal
Lung
Pneumonia
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:
Pneumonia
1.
2.
3.
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.
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Pneumonia



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:
Pneumonia
1.
2.
3.
4.
5.
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
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Pneumonia
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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Pneumonia
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)
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Pathogenesis:
Pathogenesis:
Pneumonia
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)
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Pneumonia
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.
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Grey Hepatization
Resolution
Pathogenesis of Pneumonia
Congestion
Red Hepatisation
Pneumonia
Lobar
Pneumonia: Red
hepatization, lobe
of lung is heavy,
boggy & red
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Pneumonia
Lobar
Pneumonia,
grey
hepartization:
Greyishbrown, dry
surface
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Pneumonia
Lobar Pneumonia – Gray hep…
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Pneumonia
Lobar Pneumonia:
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Pneumonia
Lobar Pneumonia: Congestion
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Pneumonia
Lobar Pneumonia: Red hepat.
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Pneumonia
Lobar Pneumonia: Grey hepat.
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Pneumonia
Pneumonia-stages
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Pneumonia
Bronchopneumonia
(Lobular
pneumonia)
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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
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Pneumonia
Bronchopneumonia
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Pneumonia
Bronchopneumonia
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Pneumonia
Broncho
Pneumonia
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Pneumonia
Bronchopneumonia:
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Pneumonia
Bronchopneumonia - CT
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Pneumonia
Bronchopneumonia
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Pneumonia
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
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Broncho – Pneumonia - Lobar
Pneumonia
Interstitial / atypical Pneumonia


Primary atypical pneumonia in the
immunocompetant host (Mycoplasma or
Chlamydia)
Interstitial pneumonitis



Gross features:


immunocompromised host : Pneumocystic carinii; CMV
Immunocompetant host: Influenza A
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
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Interstitial
Pneumonia:
Pneumonia
Interstitial Pneumonia:
Lymphocyte
Infiltrate in
alveloar wall
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Pneumonia
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, preexisting 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
Mycoplasma
pneumoniae
Chlamydia
Coxiella burnetti
•
Coliform bacteria
•
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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Pneumonia
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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Pneumonia
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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Pneumonia
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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Pneumonia
Abscess formation
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Pneumonia
Lung Abscess:
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Pneumonia
Abscess formation
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Pneumonia
Lung Abscess:
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Pneumonia
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Pneumonia
Thank you
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