RESPIRATORY SYSTEM: PATHOLOGY OF PNEUMONIAS

1. PNEUMONIAS
Dr Vijay Shankar S

2. Case
A 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

3. 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

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

6. NOVEMBER 12TH
WORLD PNEUMONIA DAY

7. • 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.

8. Pathology of
Pneumonia

10. Normal Lung

11. 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.

12. 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.

13. • Pneumonia can occur when any of these
mechanisms are damaged
OR
 When host immunity is lowered.
OR
 When the organism is highly virulent.

14. 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

15. 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

16. 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)

17. Pathogenesis:

18. Pathogenesis:

19. 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)

20. 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.

21. Stage Gross microscopy images Clinical features
Stage of
Congestion
1st-2nd day
Heavy, dark
red and firm
Alveolar
capillaries:
Dilated
Air space: fluid,
RBC, WBC
Fever, cough,
cyanopathy
Chest pain
Bacteremia
Bacteria can be
found in sputum
Stage of red
hepatization
2nd-4th day
Red &
Consolidated
Just like
LIVER!
A. Capillaries
congestion
B. Exudation:
Fibrin, large
number of RBC
C. Fibrinous
pleurisy
Fever, cough,
chest pain
Rapid breathing,
cyanopathy
Dullness, vocal
fremitus
enhancement
Rusty sputum

22. 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 .
enhancement
Sputum: 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

23. BRONCHO PNEUMONIA

24. Broncho-
pneumonia
(Lobular
pneumonia)

25. 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

26. Broncho-
pneumonia

27. Broncho-
pneumonia

28. Broncho
Pneumonia

31. Bronchopneumonia - CT

32. Bronchopneumonia

33. 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

37. INTERSTITIAL PNEUMONIA

38. 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

39. Interstitial
Pneumonia:

40. Interstitial Pneumonia:
Lymphocyte
Infiltrate in alveloar
wall

41. 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
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

42. 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.

43. 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.

44. Abscess formation

45. Lung Abscess:

46. Abscess formation

47. Lung Abscess:

53. Thank you