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·
The
1st picture shows the alveolar membrane of a
normal lung which is a thin, single-cell layer, allowing
for good oxygen transfer from the lung into the
capillaries. The viral particles are seen in the
alveolar space.
·
The
2nd picture shows the infection of Type I
pneumocytes which are easily destroyed by the disease.
This process is called interstitial pneumonitis,
and as I mentioned earlier, it resolves in about a week.
·
The
3rd picture shows hyperplastic Type II
pneumocytes which try to adapt to the stimulus. The
thickened interstitium contains debris, edema, and
inflammatory cells and the capillaries are dilated and
congested. This particular schematic also shows
hyaline membrane. Hyaline membrane is not normally
seen patients who just have viral pneumonia; it’s seen
as a consequence of patients who have unresolved
pneumonia causing further complications.
·
(The
difference between Type I & II pneumocytes was taken
from the 2003 scribe notes, but wasn’t discussed in
class.)
So
what’s all this hype about the avian flu? The
reason for panic is because an infection with this agent
causes the patient’s condition to degrade quickly.
Resolution is rare and most patients rapidly
progress to ARDS which leads to death. The patient has
no time to develop symptoms before they’re very ill.
The
influenza epidemic (1917-18) which swept across
the world killed over half-million people (more
casualties than any of the World Wars or the Civil
War.) Attempts are being made to understand the genetic
material of the virus behind the 1918 flu to prevent a
recurrence of the epidemic.
Bacterial Lung Disease
(S. aureus, S. pneumoniae, H. influenzae)
·
There are 2 types: lobar pneumonia (mainly caused
by S. pneumonia) and bronchopneumonia (can
be caused by all 3 agents).
·
The
organism may be hard to visualize with Gram staining due
to surrounding dead tissue, debris, WBCs, and RBCs. The
slide shows a nice view of a long chain of Strep among
dead inflammatory cells.
·
Lobar Pneumonia
o
As
mentioned before, S. pneumoniae is the
etiological agent in 95% of the cases. Klebsiella
and other organisms can be the cause, but less
frequently.
o
Part
of the lobe or the entire lobe
is involved, and it is unilateral.
o
The
patients are usually debilitated or alcoholics,
which compromises the host.
o
In
the CXR you typically see a unilobar bulging
fissure, abscess with cavity formation, and pleural
effusion and empyema (pus in the pleural cavity).
Complete lobar consolidation is typically limited
to one lobe and the patient complains of pleuritic chest
pain in a focal area.
o
One
complication that could occur is that the organisms
could spread to the other lobes causing bronchopneumonia
of the other lung so the patient could present with this
as well. Additionally, the bacteria could easily
disseminate through the blood to the heart and brain
causing endocarditis or meningitis.
o
The
hallmark of bacterial pneumonia (lobar and broncho) is
that it’s an intra-alveolar process with acute
inflammatory (suppurative) infiltrate that commonly
results in destroyed alveoli septae (even though the
septae aren’t involved in the inflammatory response),
leading to scarring upon recovery. As with viral
pneumonia, the 3 possible outcomes of bacterial
pneumonia are resolution, scarring, or progressive
disease.
o
Other predisposing factors
to developing lobar pneumonia include cirrhosis, renal
failure, malignancy, diabetes, and sickle cell disease.
o
It’s
a very virulent disease with a high mortality rate
(about 20%). These patients need to be treated
immediately with antibiotics.
·
Bronchopneumonia
o
Bronchopneumonia is the most common form of bacterial
pneumonia. As mentioned before, the major causes are
Staph, Strep, and H. influenzae.
o
Bronchopneumonia tends to be more focused with
inflammation around the bronchioles while lobar
pneumonia involves an entire lobe.
o
The
pathological presentation is that of patchy
consolidation, while there are other areas that are
completely spared. The consolidation is usually
multilobar and bilateral.
o
The
viral infection can become more disseminating and
necrotizing, eventually resulting in complete
consolidation of the lung (patches become confluent).
o
As
the lung tries to resolve the infection, it goes through
a series of processes. The initial stage is an acute
inflammatory exudate in alveoli and bronchi. Some
fibrin maybe present in the exudate.
§
This
stage is followed by an acute congestive process called
red hepatization. The capillaries become dilated
which leads to congestion and blood in the area
(hyperemia). Red hepatization is characterized by
diffuse, homogeneous consolidation of PMNs & macrophages
(to clear out the lung), fibrin, and RBCs in the
alveoli. The lung becomes red, hard, and liver-like.
§
Grey
hepatization
appears 2-3 days after red hepatization when more
macrophages come in to consume the inflammatory cells,
RBCs, and bacteria. The lung remains firm, but is grey,
dry, granular due to the resolution process and
increased fibrin deposition. Following this, complete
resolution results. Antibiotics help to speed up the
process.
Gross cut of lung. The dark, tube-like structures are
the bronchioles. The black pigmentation is caused by
pollutants trapped in the bronchioles. The affected
bronchioles are surrounded by white patches which
represent inflammation. The spared bronchioles are
surrounded in red tissue (lack inflammation). In time,
the inflammation can become confluent leaving you with a
completely consolidated lung.
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