Target: UG medical students.

1. Pulmonary Infections
Dr.CSBR.Prasad, M.D.

2. Pulmonary infections
• Viruses Interstitial Pneumonias
• Mycoplasma
• Bacterial Bronchopneumonia
Lobar pneumonia.
• Fungal

3. Pulmonary infections
• Interstitial Pneumonia
• Atypical Pneumonia
• Viral Pneumonia
• Bronchopneumonia
• Lobar pneumonia.

4. Classification
1. Etiologic agent Pneumococcal
Staphylococcal
2. Nature of host reaction Suppurative
Fibrinous
3. Anatomic distribution
Lobular (bronchopneumonia)
Lobar
Interstitial

5. Bacterial pneumonia
• Bacterial invasion of the lung parenchyma
evokes exudative solidification (consolidation)
of the pulmonary tissue known as bacterial
pneumonia.

6. Pathogenesis
Defence mechanisms
1. Filtering function of nasopharynx
2. Mucociliary action of lower air passages
3. Phagocytosis and elimination by alveolar MØ

7. Pneumonia results when….
1. Clearing mechanisms are impaired
2. Resistance of the host in general is lowered.

8. Clearing mechanism interference
1.Loss or suppression of cough reflex
2.Injury to the mucociliary apparatus
3.Interference with phagocytic action of
alveolar MØ.
4.Pulmonary congestion and edema
5.Accumulation of secretions

9. Clearing mechanism interference
1- Loss or suppression of cough reflex
coma, anesthesia, neuromuscular disorders,
drugs / chest pain, aspiration of gastric
contents, Systemic sclerosis

10. Clearing mechanism interference
2.Injury to the mucociliary apparatus
impairment of ciliary function
destruction of ciliated epithelium
cigarette smoke, hot/corrossive gas
inhalation, viral diseases, immotile cilia
syndrome, Cystic fibrosis

11. Clearing mechanism interference
3. Interference with phagocytic action of
alveolar MØ.
Alcohol, Tobacco smoke, Anoxia,
intoxication.

12. Clearing mechanism interference
4. Pulmonary congestion and edema
CHF
Hypostatic pulmonary edema.

13. Clearing mechanism interference
4. Accumulation of secretions
Cystic fibrosis
Bronchial obstruction
Foreign bodies, Pul. fibrosis, Tumors

14. Factors affecting resistance of
individual
1. Chronic diseases
2. Immunologic deficiency
3. Immunosuppressive treatment
4. Leukemia
5. Unusually virulent infections.

15. Terminology
• If the consolidation is patchy and centered around the
terminal bronchiole the patient is said to have
bronchopneumonia.
• If the consolidation involves the whole of one or
more lobes, the disease is called lobar pneumonia.
• When the inflammation is predominantly in the
alveolar walls with only secondary changes in the
alveoli, the condition is termed interstitial
pneumonitis.

16. Bronchopnemonia
• Patchy consolidation of lung .
• Centered around the terminal bronchiole
• Common in extremes of age - infancy/old age
• An extension of bronchitis / bronchiolitis.

17. Etiology of bronchopneumonia
Any pathogen
• staphylococci,
• streptococci,
• pneumococci,
• haemophilus influenza,
• pseudomonas aeroginosa,
• coliform bacteia.

18. Gross pathology –
bronchopneumonia
1. Patchy distribution in ONE LOBE
2. Multiple, bilateral, and basal 3 to 4 cms,
slightly elevated dry granular grey red to
yellow with poor delimitation at margins.
3. Foci of consolidated areas of acute
suppurative inflammation
4. Confluence produces – lobar pneumonia.

19. Microscopy of bronchopneumonia
• Suppurative exudation involving, bronchi,
bronchioles and adjacent alveolar spaces -
PMN
• Central necrosis
• Abscess - fibrosis – resolution.

25. This slice of lung with
bronchopneumonia.
Find a row of subpleural
centrilobular nodules.
Find rosettes (2 are marked).
Find tree-in-bud patterns (1
is marked).

29. Complications of bronchopneumonia
1. Lung abscess
2. Spread to pleural cavity – empyema
3. Spread to pericardial cavity-suppurative
pericarditis.
4. Bacteremia – metastatic abscesses.

30. Bronchopneumonia
General Patchy pneumonia that is localized, often to the
Description bronchioles and surrounding alveoli.
One or more of the following symptoms:
coughing, chest pains, fever, blood-streaked
Clinical Signs
sputum, chills, and difficulty in breathing.
Signs of pulmonary congestion
Inhalation of organisms.
Pathophysiology
Scarring if alveoli destroyed.
Patchy distribution in and around small airways
Dense acute inflammatory exudate of PMNs,
fibrin and blood in bronchi, bronchioles and
Histopathology
adjacent alveoli.
FOCAL destruction of alveolar walls (you can
see normal parenchyma in other areas adjacent

31. Lobar pneumonia
Definition:
It’s an acute bacterial infection of a large
portion of a lobe or of an entire lobe, which
tends to occur at any age but relatively
uncommon in infancy and old age.

32. Etiology and pathogenesis
• Pneumococci ( streptococcus pneumoniae)
1,3,7 and 2
type 3 is virulent form
Staphylococci, Streptococci
Gram negative: Pseudomonas, Proteus,
Klebsiella, Haemophilus influenzae.

33. Pathogenesis of lobar pneumonia
• Exudate spread through pores of Kohn
• Mucoid encapsulation- protection from
phagocytosis. (Pneumococcus, Klebsiella,
Hemophilus)
Which disease is associated with recurrent
infections by capsulated organisms?

34. Alveolar Structure
Pores of Kohn

41. Microscopy of lobar pneumonia
• Wide spread fibrinosuppurative
consolidation of large areas and even whole
lobes of lung.
• Serous exudation
• Vascular engorgement
• Fibrinocellular exudation - resolution /
organisation.

46. Comparison of bronchopneumonia vs. lobar pneumonia
Bronchopneumonia Lobar Pneumonia
Location 1. often bilateral large area, even whole lobe involvement
2. basal (i.e. lower lobes)
Route of infection spreads from bronchioles to nearby both alveoli and bronchioles
alveoli
Spread of infection consolidation is patchy Whole lobe becomes consolidated
Susceptible group infants, elderly Adults especially alcoholics and
vagrants.
Causative Organism Dependent on circumstances Often caused by Pneumococcus or
predisposing to infection(i.e. Klebsiella.
nosocomial or community
acquired)
Recovery If treated, recovery usually involves If treated promptly, many recover with
focal organisation of lung by lungs returning to normal structure and
fibrosis. functioning by resolution. In other cases
the exudate in alveoli is organised,
leading to lung scarring and permanent
lung dysfunction.
Notes Patients who are immobile develop Patient are severely ill and usually
retention of secretions; thus, most associated bacteriemia.
commonly involves the lower
lobes.

47. Pneumonia syndromes
1. Community acquired acute pneumonia
2. Community acquired atypical pneumonia
3. Nosocomial pneumonia
4. Aspiration pneumonia
5. Chronic pneumonia
6. Necrotizing pneumonia & lung abscess
7. Pneumonia in immunocompromised host

48. Community acquired
acute pneumonia
• Sterptococcus pneumoniae
• Moraxella
• Haemophilus influenza
• Legionella

49. Community acquired
atypical pneumonia
• Mycoplasma pneumonia
• Chlamydia species
• Viruses --- RSV, parainfluenza,
Influenza A and B.
Adenovirus, SARS

50. RSV

51. Nosocomial pneumonia
• Gram negative rods
• Staph aureus.

52. Aspiration pneumonia
Anaerobic oral flora

54. Chronic pneumonia
• Nocardia, Actinomycosis
• Granulomatous:
Mycobacterium TB, Atypical mycobacteria,
Histoplasma, coccidides.
Note: Chronic bacterial pneumonias are usually caused by
obstrution of the bronchus supplying the region involved.
It’s most common in the part of a lung obstructed by a
bronchogenic carcinoma.

55. Necrotizing pneumonia
&
lung abscess
• Anaerobic organisms
• Staph aureus

56. Four stages
1. Stage of congestion
2. Stage of red hepatization
3. Stage of grey hepatization
4. Stage of resolution.

57. Stage of congestion
• Represents bacterial infection
• Lasts for 24 hrs
• Vascular engorgement
• Intraalveolar fluid with few PMN + bacteria
• Grossly: heavy, boggy, red and subcrepitant.

59. Stage of red hepatization
• Neutrophils + fibrin precipitation
• Red cell extravasation
• Exudate confluence - obscures pulmonary
architecture
• Grossly: Lung appears distinctly red, firm
airless with liver like consistency.

61. Stage of grey hepatization
• Accumulation of fibrin
• Disintegration of WBCs and RBCs.
• Clear zone adjacent to alveolar septa.
• Grossly: grayish brown dry surface.
• Spread to pleural cavity – empyema.

63. Stage of resolution
• Progressive enzymatic digestion to produce
granular semifluid debris - resorbed.
• Ingestion by MØ -- coughed up .
• Gross: normal lung
• Pleura: fibrous thickening.

64. Complications of lobar pneumonia
1. Abundant mucinous secretion
2. Abscess formation
3. Organization of exudate.
4. Bacterial dissemination.

66. Clinical features of lobar pneumonia
1. Rusty sputum
2. X-ray opaque shadows
3. Limitation of breath sounds
4. Bronchial breath sounds.
5. Fever.

67. Viral / Mycoplasma pneumonia
• Primary atypical pneumonia (PAP)
• Acute febrile respiratory disease
characterized by patchy inflammatory
changes in the lungs, largely confined to
alveolar septa and pulmonary interstitium.
• Atypical – lacks alveolar exudate.

68. Etiology of PAP
• Mycoplasma pneumonia
• RSV
• Influenza virus type A & B
• Adenovirus
• Rhinovirus
• Rubeola
• Varicella
• Chlamydia
• Coxiella burnetti (Q fever)

69. Morphology of PAP
• Patchy, may involve whole lobe
unilateral / bilateral.
• Red blue, congested, subcrepitant
• No obvious consolidation
• Pleura – normal.

70. Microscopy of PAP
• Interstitial inflammatory reaction
• Alveolar septa widened, edematous, L,Hi,pl cells.
• Alveoli are free of exudate. NO EXUDATE.
• Intraalveolar proteinacious material, cellular
exudate.
• Characteristic PINK HYALINE EMEMBRANE
LINING alveolar damage similar to ARDS.

73. CMV

74. RSV

75. Microscopy of PAP contd.,
1- Bacterial infection- Ulcerative bronchitis
Bronchiolitis.
2- Herpes virus, varicella –Necrosis.
Giant cells
Intranuclear inclusions.

76. Clinical features of PAP
• Dry hacking cough
• Lab: elevated cold agglutinin titres in
mycoplasma pneumonia.

77. Lung abscess
• Local suppurative process within in the lung
characterised by necrosis (liquifactive
necrosis) of lung tissue.
• Common in males.

78. Etiology of lung abscess
• Any pathogen
• Staphylococcus aureus
• Gram negative organisms
• Anaerobic Bacteroides
Fusobacterium

79. Etiology contd.,
1. Aspiration of infective material
2. Antecedent primary bacterial infection
3. Septic embolism
4. Neoplastic
5. Miscellaneous
6. Primary cryptogenic

80. Aspiration of infective material
• Coma
• Alcoholism
• Anesthesia
• Sinusitis
• Gingivodental sepsis

81. Antecedent primary bacterial
infection
• Post pneumonic Staph aureus
Klebsiella
• Bronchiectasis

82. Septic embolism
• Thrombophlebitis
• Infective endocarditis

83. Neoplastic
• Secondary to inflammation by obstruction.

85. Miscellaneous
• Direct trauma
• Esophagus, spine, diaphragm, pleura etc.,

86. Morphology of lung abscess
• mm to 5 to 6 cms
• Common on right side, mostly single.
• In pneumonia / bronchiectasis
– Multiple, basal, diffusely scattered.
• Cavity with or without suppurative debris
• Contd infection-large fetid, green black multilocular
cavity with poor margins
• GANGRENE OF LUNG.

94. Causes of pulmonary infiltrates in
immunocompromised hosts
Diffuse infiltrates Focal infiltrates
Common Common
CMV, P.carinii, Drugs GN rods, Staph.aureus
Aspergillus, Candida, Malignancy
UNCOMMON UNCOMMON
Bacteria, Aspergillus, Cryptococcus, Mucor, P.carinii,
Cryptococcus, Malignancy Legionella pneumophila.

95. E N D
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