2. Pneumonia
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Introduction:
5000 sq meters
Filters >10,000 L of air / day…!
Normal lungs are sterile.
Delicate, thin resp. mem – gas exch.
Filter, humidify, sterilize, highly sensitive.
RTI – Resp. tract inf. commonest in medical
practice.
Enormous morbidity & mortality.
Pneumonia – inflammation of alveoli.
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Lung defense mechanisms
A, Innate defenses against infection:
1, In the normal lung, removal of microbial
organisms depends on entrapment in the mucous
blanket and removal by means of the mucociliary
elevator
2, phagocytosis by alveolar macrophages that can
kill and degrade organisms and remove them from
the air spaces by migrating onto the mucociliary
elevator
.
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3, phagocytosis and killing by neutrophils recruited
by macrophage factors.
4, Serum complement may enter the alveoli and
be activated by the alternative pathway to provide
the opsonin C3b, which enhances phagocytosis
5, Organisms, including those ingested by
phagocytes, may reach the draining lymph nodes
to initiate immune responses
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Additional mechanisms operate after
development of adaptive immunity.
1, Secreted IgA can block attachment of the microorganism
to epithelium in the upper respiratory tract.
2, In the lower respiratory tract, serum antibodies (IgM,
IgG) are present in the alveolar lining fluid. They activate
comple- ment more efficiently by the classic pathway,
yielding C3b (not shown). In addition, IgG is opsonic.
3, The accumulation of immune T cells is important for
controlling infections by viruses and other intracellular
microorganisms. PMN, polymorphonuclear cell
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CLINICAL FEATURES
CHILLS
FEVER
MALAISE
PLEURITIC CHEST PAIN
DYSPNOEA
COUGH WITH EXPECTORATION
HYPOXAEMIA
BRONCHOPNEUMONIA
INFECTION OF TERMINAL BRONCHIOLES
EXTENDING INTO SURROUNDING
ALVEOLI
RESULTING IN PATCHY CONSOLIDATION.
OCCURS IN EXTREMES OF LIFE.
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Streptococcus pneumoniae Infections
three subsets of patients:
those with underlying chronic diseases such as CHF, COPD, or
diabetes;
those with either congenital or acquired immunoglobulin
defects (e.g., with the acquired immune deficiency syndrome
[AIDS]); and
those with decreased or absent splenic function (e.g., sickle
cell disease or after splenectomy).
spleen contains the largest collection of phagocytes and is there-
fore the major organ responsible for removing pneumo- cocci
from the blood and also produces antibodies against
polysaccharides - against encapsulated bacteria.
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Lobar Pneumonia:
whole lobe, exudation - consolidation
95% - Strep pneum.(Klebsiella in aged, DM,
alcoholics)
High fever, rusty sputum, Pleuritic chest pain.
the lower lobes or the right middle lobe is most
frequently involved
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Four stages:
Congestion – 1d – vasodilatation
congestion.
Red Hepatization 2d Exudation+RBC
Gray Hepatizaiton 4d neutro & Macrophages.
Resolution – 8d few macrophages, normal.
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congestion
the affected lobe(s) is
(are) heavy, red, and
boggy;
histologically,vascular
congestion can be seen,
with proteinaceous fluid,
scattered neutrophils,
and many bacteria in
the alveoli
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red hepatization –
lung lobe has a liver-like
consistency; the
alveolar spaces are
packed with neutrophils,
red cells, and fibrin
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gray
hepatization-
lung is dry, gray, and
firm, because the red
cells are lysed and
fibrinosuppurative
exudate persists
within the alveoli
Resolution -uncomplicated
cases, as exudates within the alveoli
are enzymatically digested to
produce granular, semifluid debris
that is resorbed, ingested by
macrophages, coughed up, or
organized by fibroblasts growing
into it
The pleural reaction (fibrinous or
fibrinopurulent pleuritis) may
similarly resolve or under- go
organization, leaving fibrous
thickening or permanent adhesions.
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Complications of Pneumonia
Abscesses
Localized tissue destruction and necrosis may lead to
abscess
Right side often in aspiration.
Staphylococcus; Klebsiella; Pneudomonas
Pleuritis / Pleural effusion.
Inflammation of the pleura ( Streptococcus pneumoniae)
Blood rich exudate (esp. rickettsial diseases)
Empyema
Pus in the pleural space.
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Septicemia
bacteremic dissemination may lead to meningitis,
arthritis, or infective endocarditis. Complications are
much more likely with serotype 3 pneumococci
organization of the intra- alveolar exudate may
convert areas of the lung into solid fibrous tissue
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Bronchopneumonia (patchy)
Extremes of age. (infancy and old age)
Staph, Strep, Pneumo & H. influenza
Patchy consolidation – distributed in patches not limited to
lobes.
Suppurative inflammation
Usually bilateral
Lower lobes common
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Broncho-
pneumonia
GROSS-Well- developed
lesions up to 3 or 4 cm in
diameter are slightly elevated
and are gray-red to yellow;
lung substance immediately
surrounding areas of
consolidation is usually
hyperemic and edematous, but
the large intervening areas are
generally normal.
Pleural involvement is less
common than in lobar
pneumonia.
Histologically, the
reaction consists
of focal sup-
purative exudate
that fills the
bronchi,
bronchioles, and
adja- cent
alveolar spaces.
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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
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LUNG ABSCESS
LOCALISED AREA OF NECROSIS WITH
SUPPURATION.MORE COMMON IN RIGHT LUNG,
RIGHT APEX OF LOWER LOBE.
PRIMARY
SECONDARY
ETIOPATHOGENSIS
STAPHYLOCOCCUS,STREPTOCOCCUS ETC.
ASPIRATION
SECONDARY TO PNEUMONIA
BRONCHIAL OBSTRUCTION
SEPTIC EMBOLI
DIRECT EXTENSION
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GROSS –ABSCESS WALL SURROUNDED
BY ACUTE PNEUMONIA
CLINICAL FEATURES
• FEVER
• MALAISE
• LOSS OF WEIGHT
• COUGH
• PURULENT EXPECTORATION
• HAEMOPTYSIS
• CLUBBING OF FINGERS AND TOES.