Pneumonia
Barriers to infection:
• Epiglottis: protects airway from aspiration.
• Cough reflex*.
• Mucociliary escalator.
• Alveolar macrophage & antimicrobial.
compounds: lysozyme, lactoferrin, complement
and IgA.
Pneumonia:
Inflammation of the lung parenchyma:
Inflammation of alveoli, alveolar ducts, bronchioles,
and interstitial tissue of lung, induced by microbial
invasion of natural barriers.
Classification of pneumonia:

•
Clinical Classification:
Acute: less than three weeks duration
• Chronic pneumonias.
 Acute pneumonia is further classified
according to place where it was acquired,
source of transmission, and etiology.
Classification of Acute Pneumonia:
 Community acquired:
o Person to person
 Classical bacterial pneumonia
 Atypical bacterial pneumonia
 Viral pneumonia
o Animal, or Environmental Exposure.
 Nosocomial acquired.
Community-acquired acute pneumonia:
Person-to-Person:
 A- Classic bacterial pneumonia:
• Streptococcus pneumoniae.
• Haemophilus influenzae.
• Klebsiella pneumoniae.
• Moraxella catarrhalis.
• Aspiration pneumonia* (mixture of bacteria
including gram negatives, anaerobes and
Staphylococcus aureus).
Person to Person:

B- Atypical bacterial pneumonia:
• Chlamydophila pneumoniae
• Mycoplasma pneumoniae.

C- Viral pneumonia:
• Influenza virus type A, B, and C
• Coronaviruses.
• Others: RSV, measles , adenoviruses,
CMV…..
 Environmental
o
o
o
o
o
Legionellosis.
Tularemia.
Plague.
Q fever.
Anthrax.
or Animal Exposure:
Streptococcus pneumoniae :

Reservoir: nasopharynx of children and
adults.(patients or asymptomatic carriers).
 Transmission: droplets inhalation.
Pathogenesis and microbial virulence:
o Colonization of the nasopharynx then spread to the
bronchi and alveoli.
o Polysaccharide capsule resist phagocytosis.
o Production of pneumolysin: cholesterol-binding
toxin; epithelial cell-damage.
o Production of hydrogen peroxide; cell damage, and
inhibition of other bacteria.
o Inflammation: production of cytokines; TNFα,IL-1,
IL-8 by alveolar macrophage
(stages of pneumonia):
 Filling of alveoli by fluids*: many bacteria, and
few inflammatory cells.
 Early consolidation* stage; infiltration of
alveoli by neutrophils, activation of complement
and CRP which interact with bacterial teichoic
acid. (battle b/w the bacteria and the immune
system).
 Late Consolidation stage: heavy infiltration by
neutrophils which kill the microbe,
(Hepatization).
 Infection eradication (resolution): Replacement
of neutrophils by alveolar macrophages.
 Clinical presentation: Acute lobar pneumonia.
Classic bacterial pathogenesis:
Lobar Pneumonia
Complications of Streptococcus pneumonia:
 Local complications:
 Pleural effusion; Outpouring of fluid into pleural
space in 25% of cases.
 Empyema (pus in the pleura): in 1% of cases,
require drainage of fluid.
 Systemic complications
• Bacteremia (Pneumococcemia): through
lymphatic vessels of the lung to thoracic duct.
• Positive blood culture in only 25% of cases
(transient bacteremia).
• Defense: humoral factors and lymphatic system to
remove the bacteria from the blood.
• Meningitis esp. in splenectomy, sickle cell anaemia
Diagnosis of S. pneumoniae:
•
Clinical specimens:
Sputum, transtracheal aspirate, broncheoalveolar
lavage and lung biopsy.
• Direct Microscopy:
Streptococcus pneumoniae are Gram positive
lanceolate (lancet) shaped diplococci arranged in
pairs or chains, and capsulated.
• Cultural characteristics:
Facultative anaerobic bacteria, alpha hemolytic
on blood agar, optochin sensitive.
Blood agar: α hemolysis & optochin sensitive
Haemophilus influenzae
-Gram negative coccobacilli, rod-shaped to
pleomorphic.
- Epiglottitis, tracheobronchitis and pneumonia.
-
Isolation of Haemophilus influenzae :
-Aerobic or facultative anaerobic bacteria.
-Isolated on chocolate agar with factor X (hemin)
and factor V (NAD).
-Satellitism phenomenon.
Treatment of S. pneumoniae and H. influenzae:
• Beta-lactam antibiotic.
• If the patient is allergic to penicillin or the
bacteria is not sensitive: macrolide or
fluoroquinolones.
• Penicillin-resistant streptococcus due to
mutation in penicillin-binding protein by
transformation.
Vaccine:
-Conjugated capsular antigen vaccines for S.
pneumoniae and H. influenzae type b.
Atypical bacterial pneumonia:
Chlamydophila pneumoniae:
• Infective stage: Elementary bodies.
-Target cells: columnar epithelial cells,
endothelial cells of the vessels and
macrophages.
- Receptor-mediated endocytosis (intracellular
infection).
- Lymphocytic infiltration; IF-γ creates
persistence infection by slowing the growth of
the RB.
• Diagnostic stage: Reticulate bodies.
Life cycle of C. pneumoniae

Clinical presentation:
 Acute tracheobronchitis.
 Bronchopneumonia (patchy infiltrates on
radiography).
 C. pneumoniae is associated with Coronary
artery disease (CAD):
o Adults with CAD have a high antibodies titer
against this bacterium.
o The microbe can be isolated from
atherosclerotic lesions.
o The microbe established CAD in animal
model studies.
Diagnosis:
• Immunofluorescent microscopy for antigen and
antibodies detection.
• PCR.
Treatment:
- Macrolide: Long-term Cmax (maximum serum
concentration) of azithromycin.
- Or doxycycline for 7 days.
- Pregnant women: erythromycin or azithromycin.
Mycoplasma pneumoniae:
• Smallest prokaryotes that lack cell-wall.
• Infect mainly individuals aged 5-20 years old.
• Pathogenesis:
Tip structure mediated attachment to
carbohydrate containing receptor on columnar
epithelial cells
The infection is not highly destructive but the
ciliary function is impaired.
Exotoxins:
• ADP-ribosyltransferase: inhibition of neutrophils
chemotaxis and phagocytosis.
• Vacuolating toxin: apoptosis of ciliated cells.
• Monocytic infiltration. (few neutrophils)
Clinical presentation:
• Tracheobronchitis (persistent dry cough).
• Bronchopneumonia; (infiltration of
monocytes with few neutrophils); patchy
infiltrate on radiography.
• In 50% of severe mycoplasma infections;
mild-autoimmune hemolytic anemia* due to
cold hemagglutinin formation.
Complications:
• Encephalitis, renal disease and arthritis
(antibody complex), autoimmune
thrombocytopenic purpura* erythema
multiforme).
Diagnosis:
-Direct: PCR or Immunofluorescent microscopy.
-Indirect: serology: Complement fixation or
cold agglutinin test.
Treatment:
-Macrolide.
-Resistance strains; Tetracycline or
Fluoroquinolones.