Microbiology 13

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Microbiology 13: Pneumococcus and Bacterial Pneumonia
Key Concepts
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Pneumococcus is α-hemolytic streptococcus (nasopharynx)
Respiratory tract infections (otitis media, sinusitis, chronic bronchitis, and pneumonia)
Acute inflammatory response
Polysaccharide capsule resists phagocytic clearance
Multiple capsular types (antigenic and combined for vaccines)
Resistance to penicillin and other antibiotics
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Streptococcus pneumoniae = common in mucosa of nasopharynx sans disease until reaches lung
o Thick polysaccharide layer inhibits host clearance
Cases
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Heavy smoker, nasal congestion, muscle aches, fever, shaking chill, cough (blood-tinged
sputum), severe pain on R chest (worse with breathe), diminished breath sounds
(consolidation), high WBCs (leukocytosis), Gram + lancet-shaped diplococci = communityacquired pneumonia
o Treat with fluoroquinolone (levofloxacin)
Classic features of pneumococcal pneumonia = abrupt onset, ill appearance, rust-colored
sputum, homogeneous involvement of entire lobe of lung (lobar consolidation), leukocytosis,
and rapid response to antibiotics, bacteremia (more severe)
Streptococcus pneumoniae
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Characteristics
o Aerobic streptococci
o S. oralis, sanguis or mitis coinhabit nasopharynx
o Lacks catalase enzyme (generates copious amounts of hydrogen peroxide)
 With pneumolysin damages host tissue
o Thick cell wall with autolysin
o Capsule (polysaccharide) gives smooth appearance -> do not activate complement
 Important for survival in bloodstream
 In meningitis -> cross BBB via sustained presence in blood
 Nonencapsulated pneumococci rarely cause disease
 Antigenic differences in serotypes from chemical structure of polysaccharide
o Visualized with Quellung reaction: add antibody to cause antigen-antibody precipitation
Bacterial Capsules as Defenses against Opsonization and Phagocytosis
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Other encapsulated organisms = Str. pneumoniae (pneumococcus), pyogenes (group A strep),
agalactiae (group B strep), Staph. aureus, Neisseria meningitides (meningococcus), H. influenza,
Klebsiella pneumonia, E. coli, Bacteroides fragilis, Cryptococcus neoformans (fungi)
o H. influenza and Neisseria meningitidis with pneumococcus are most frequent cause of
bacterial meningitis
Complement system (lytic complex) highly efficient in eliminating extracellular bacteria
o Pneumococcus require complement + phagocytes via opsonization but polysaccharide
capsule doesn’t activate complement sans antibody
 Other components of innate immune system opsonize pneumococci
Epidemiology
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Pneumococcal pneumonia = most common form of bacterial pneumonia acquired in
community
o High in children (<5), adults (>40), blacks, Native Americans, impoverished and
debilitated, sickle cell anemia, alcoholism, Hodgkin disease, multiple myeloma, HIV
infection, absence of spleen
o Seasonal, winter and early spring
o May cause otitis media, acute sinusitis, chronic bronchitis, peritonitis, endocarditis,
septic arthritis, meningitis
Encounter
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Reservoir of S. pneumonia = humans (majority never have symptoms)
o Step 1: colonization of nasopharynx
 May remain in carrier state or progress to disease (strain virulence and host
defense determine outcome)
 Incidence declines with age
 Different serotypes due to serotype-specific immune response limiting
reacquisition of same serotype
o Transmission through airborne droplets (person-to-person)
Entry
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Lungs usually protected by 1) tortuous path, 2) epiglottis, 3) cough reflex, 4) mucus and cilia, 5)
alveolar macrophages
o Affected by unconscious aspiration, cigarette smoke, alcohol, virus or excess fluid
Spread, multiplication and damage
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Stage 1: serous fluid in alveoli
Stage 2: early consolidation (neutrophil and RBCs in alveoli)
o Chemotactic signals (from complement path)
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Some may have type-specific anticapsular antibodies opsonizing organism for
phagocytosis
o interaction of C-reactive protein (CRP) (acute phase reactant) with phosphorylcholine
on pneumococcal surface -> activates complement cascade
Stage 3: late consolidation (victorious neutrophils, few bacteria)
o Affected lung heavy = hepatization
Stage 4: resolution (neutrophils replaced by macrophages)
o Most cases, architecture of lung restored to normal
Complications = pleural effusion, empyema (purulent infection of pleural space), spread to
blood and distal (bacteremia)
o Direct seeding of blood from nasopharynx = occult bacteremia
Humoral factors assist spleen, liver, and lymph nodes in filtering function
Diagnosis
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Leading cause of lobar pneumonia, acute otitis media, chronic bronchitis, and acute sinusitis
Gram stain sputum = 10 lancet-shaped Gram + diplococcic and neutrophils
Antipneumococcal antibiotic = levofloxacin
Blood agar = α-hemolysis
Sensitivity to Optochin and soluble in bile salts
Definitive if found in blood sample
Treatment and Prevention
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Penicillin, erythromycin -> treatment fails because of rapid progression of infection (lyse cell
wall -> short-term increased inflammation)
Mild drug resistance can still use penicillin unless in CNS (3/4 of strains)
High resistant strains -> cannot use other β-lactams, macrolides, and sulfas, use levofloxacin
Penicillin-binding proteins confer resistance to penicillin
o Selective pressure from antibiotic presence + adaptation (transformation)
Antigenic diversity barrier to vaccine development
o Vaccine developed for common serotypes (elderly and predisposed individuals)
 Hodgkin disease and multiple myeloma pts (at risk) don’t make adequate
antibody to vaccine
 Contains capsular polysaccharide
o Pneumococcal conjugate vaccine = use in children (contains bacteria itself)
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