In: Anatomy and Physiology
Pneumococcal pneumonia
More than 90% of all lobar pneumonias are caused by Streptococcus pneumoniae, a lancet-shaped diplococcus. Out of various types, type 3 S. pneumoniae causes particularly virulent form of lobar pneumonia. Pneumococcal pneumonia in majority of cases is community-acquired infection.
MORPHOLOGIC FEATURES
Laennec’s original descrip- tion divides lobar pneumonia into 4
sequential pathologic phases: stage of congestion (initial phase),
red hepatisation (early consolidation), grey hepatisation (late
consolidation) and resolution. However, these classic stages seen
in untreated cases are found much less often nowadays due to early
institution of antibiotic therapy and improved medical care.
In lobar pneumonia, as the name suggests, part of a lobe, a whole
lobe, or two lobes are involved, sometimes bilaterally. The lower
lobes are affected most commonly. The sequence of pathologic
changes described below represents the inflammatory response of
lungs in bacterial infection.
1 STAGE OF CONGESTION: INITIAL PHASE The initial phase represents
the early acute inflammatory response to bacterial infection that
lasts for 1 to 2 days. Grossly, the affected lobe is enlarged,
heavy, dark red and congested. Cut surface exudes blood-stained
frothy fluid. Histologically, typical features of acute
inflammatory response to the organisms are seen. These are as
under
i) Dilatationandcongestionofthecapillariesinthealveolar
walls.
ii) Paleeosinophilicoedemafluidintheairspaces.
iii) A few red cells and neutrophils in the intra-alveolar
fluid.
iv) Numerous bacteria demonstrated in the alveolar fluid by Gram’s
staining.
2. RED HEPATISATION: EARLY CONSOLIDATION
This phase lasts for 2 to 4 days. The term hepatisation in
pneumonia refers to liver-like consistency of the affected lobe on
cut section.
Grossly, the affected lobe is red, firm and consolidated. The cut
surface of the involved lobe is airless, red-pink, dry, granular
and has liver-like consistency. The stage of red hepatisation is
accompanied by serofibrinous pleurisy. Histologically, the
following features are observed
i) The oedema fluid of the preceding stage is replaced by strands
of fibrin.
ii) There is marked cellular exudate of neutrophils and
extravasation of red cells.
iii) Manyneutrophilsshowingestedbacteria.
iv) The alveolar septa are less prominent than in the first stage
due to cellular exudation.
3. GREY HEPATISATION: LATE CONSOLIDATION
This phase lasts for 4 to 8 days.
Grossly, the affected lobe is firm and heavy. The cut surface is
dry, granular and grey in appearance with liver-like consistency .
The change in colour from red to
grey begins at the hilum and spreads towards the periphery.
Fibrinous pleurisy is prominent.
Histologically, the following changes are present
i) Thefibrinstrandsaredenseandmorenumerous.
ii) The cellular exudate of neutrophils is reduced due to
disintegration of many inflammatory cells as evidenced by their
pyknotic nuclei. The red cells are also fewer. The macrophages
begin to appear in the exudate.
iii) The cellular exudate is often separated from the septal walls
by a thin clear space.
iv) The organisms are less numerous and appear as degenerated
forms.
4. RESOLUTION This stage begins by 8th to 9th day if no
chemotherapy is administered and is com- pleted in 1 to 3 weeks.
However, antibiotic therapy induces resolution on about 3rd day.
Resolution proceeds in a pro- gressive manner.
Grossly, the previously solid fibrinous constituent is liquefied by
enzymatic action, eventually restoring the
normal aeration in the affected lobe. The process of softening
begins centrally and spreads to the periphery. The cut surface is
grey-red or dirty brown and frothy, yellow, creamy fluid can be
expressed on pressing. The pleural reaction may also show
resolution but may undergo organisation leading to fibrous
obliteration of pleural cavity.
Histologically, the following features are noted:
i) Macrophages are the predominant cells in the alveolar spaces,
while neutrophils diminish in number. Many of the macrophages
contain engulfed neutrophils and debris.
ii) Granular and fragmented strands of fibrin in the alveolar
spaces are seen due to progressive enzymatic digestion.
iii) Alveolarcapillariesareengorged.
iv) There is progressive removal of fluid content as well as
cellular exudate from the air spaces, partly by expectoration but
mainly by lymphatics, resulting in restoration of normal lung
parenchyma with aeration.