2. Pathophysiology
• Until recently it was thought that the lungs were sterile.
• New pathogens entered lower respiratory tract through micro
aspiration of oro-pharyngeal organisms and also had ability to
overcome innate & adaptive immunity, resulting in pneumonia.
• Now it has been observed that there is a diverse community of
bacteria in the lungs that constitutes Lung micro biota.
4. Pathogenesis
• (i) Entry through Impaired mechanical factors like..
• Hairs
• Turbinates of the nares
• Branching tracheobronchial tree
• Muco ciliary clearance
• Gag reflex
• Cough reflex, etc.,
5. Pathogenesis
• (ii) Entry through Bacteria
• Bacteria have easy access to lower airways through
• Inhalation
• Micro-aspiration
• Direct mucosal dispersion
7. Pathogenesis
• In CAP and HAP, trigger may be..
• viral infection with added micro aspiration of Oro-pharyngeal
organisms
At this stage,
Innate & Acquired immunity has
the potential to prevent the development of Pneumonia
9. Morphological stages of Pneumonia
1. Congestion
2. Red hepatization
3. Gray Hepatization
4. Resolution
10. 1. Congestion
This stage last less than 24 hrs
Gross appearance:
Lungs are heavy, boggy & red, blood-stained frothy fluid
oozes from cut surface
Microscopy:
Dilatation & Congestion of capillaries in the alveolar walls
Mild Edema can be seen
11. 2. Red Hepatization
It last for 2-3 days
Gross appearance:-
Lungs appear red, firm, airless which resembles liver; Pleura
show serofibrinous pleurisy.
Microscopy:-
Alveoli show exudate and interlacing strands of fibrin
Numerous neutrophils and red cells are found in the fibrin
meshwork.
13. 3. Gray Hepatization
Seen on 5–7 days.
Gross appearance
Lungs appear gray
Cut surface shows gray, dry granular appearance
Microscopy
Progressive disintegration of red cells
Fibrino-suppurative exudate in the alveoli in which neutrophils
are replaced by macrophages
14. 3. Gray Hepatization
There is a clear space between the alveolar wall and the
exudate due to contraction of the fibrin thread
There is successful containment of the infection and
improvement in gas exchange.
15. 4. Resolution
Liquefaction of the previously solid, fibrinous constituents of the
exudate in the air spaces
To produce granular and semifluid debris
Liquefied material is removed, partly by expectoration, but
mainly ingested by macrophages & drained through lymphatics.
Gross appearance
The affected lobe becomes more crepitant as the air spaces
reopen.
Cut section appears frothy
18. Risk Factors
• In the case of age >70 years:
• Decreased cough
• Gag reflexes
• Reduced antibody
• Toll-like receptor responses
• increase the likelihood of pneumonia
20. Risk Factors for Enterobacteriaceae
Hospitalization
Treated with antibiotics
Comorbidities such as alcoholism, heart failure or renal failure
for Pseudomonas aeruginosa
Severe structural lung disease
21. Risk Factors for Enterobacteriaceae
for Legionella
Diabetes
Hematologic malignancy
Cancer
Severe renal disease
HIV Infection
Smoking
Male gender, etc.