1. Community-acquired pneumonia definition
    • Acute infection of the pulmonary parenchyma in a patient who is not hospitalized or residing in a long-term care facility for >14 days before the onset of symptoms and associated with:
    • Symptoms of acute infection
    • Acute infiltrate on chest X-ray
    • Particularly important disorder in the elderly
    • Mortality average 14% (2-30%)
  2. Community-acquired pneumonia – rationale for establishing etiology
    • Optimal antibiotic selection: activity, antimicrobial resistance, adverse drug reactions, cost
    • Identify pathogens of epidemiological significance
    • Legionella, penicilling-resistant pneumococcus, Hantavirus
    • Exclude selected pathogens
    • Average cost is <1% of average hospital bill
  3. Diagnostic tests for evaluation of community-acquired pneumonia
    • CXR
    • Complete blood count, chemistries
    • Gram stain and culture of sputum
    • Blood cultures
    • Urinary antigen for pneumococcus and Legionella
  4. Additional Diagnostic tests for evaluation of community-acquired pneumonia to sputum culture for Legionella
    • HIV serology especially in younger people
    • acid fast stain of sputum (Tb)
    • smear for Pneumocystitis carinii
    • Bronchoscopy
  5. Causes of community acquired pneumonia
    • Streptococcus pneumoniae
    • Nontypeable Haemophilus influenzae
    • Mycoplasma pneumoniae
    • Chlamydia pneumoniae
  6. Streptococcus pneumonia – non-Lancfield groupable
  7. Less common causes of community acquired pneumonia
    • Moraxella catarrhalis (elderly, COPD)
    • Staphylococcus aureus (post-influenza)
    • Legionella pneumophila (transplant, COPD)
    • Streptococcus pyogenes
    • Gram-negative rods (nursing home)
    • Neusseria meningitides
    • Influenza
    • Severe acute respiratory syndrome (SARS)
  8. COPD pathogens
    • Pneumococcus
    • Haemophilus influenzae
    • Moraxella catarrhalis
  9. Predisposition to aspiration
    Mouth anaerobes
  10. Influenza in community
    • Pneumococcus
    • Haemophilus influenzae
    • Staphylococcus aureus
  11. Exposure to birds
    Chlamydia psittaci
  12. CF, Bronchiectasis
    • Pseudomonas aeruginosa
    • Burkholderia cepacia
  13. Airway obstruction
  14. Early HIV infection
    • Pneumococcus
    • H. influenzae
    • Tuberculosis
  15. Haemophilus influenzae
    • Small gram negative coccobacillus, pleiomorphic
    • Six capsular serotypes – genetically distinc polysaccharide
    • Some are non-encapsulated or nontypable
    • Important human ones are: type b and nontypable strains
  16. Epidemiology of H. influenzae type b encapsulated
    • Low rate of nasopharyngeal colonization due to widespread use of conjugate vaccines
    • Spread by airborne droplets or direct contact with secretions and fomites
    • Unimmunized young children in same household with a child with Hib meningitis are at increased risk of meningitis
    • Certain populations have a higher risk of Hib meningitis: African-american children, native Americans (Apache, Navajo, Alaskan Eskimo children (10X)
  17. Epidemiology of H. influenzae nontypeable
    • Colonizes the nasopharynx of many healthy children and adults
    • Colonizes the lower respiratory tract of adults with COPD
    • Dynamic turnover of strains in the respiratory tract
    • Colonization early in life is associated with recurrent: otitis media
  18. otitis media
    One of the important associations with early in life colonization with Haemophilus influenzae nontypeable
  19. Haemophilus influenzae b Clinical Manifestations
    • Invasive disease in children under 6 years:
    • Infections cause by Hib
    • Meningitis: < 2yo. Fever, altered mental status
    • Epiglottitis: 2-7 yo. Fever and airway obstruction – cause of death
    • Cellulitis: face and neck are most common sites – generally by hemotogenous spread.
  20. NTHI: Clinical Manifestations-children
    • Otitis media in children under age 6 years:
    • Otitis media:
    • 80% of all children have at least one episode by age 3
    • recurrent otitis is associated with delay in speck and language development and learning problems
    • Etiology of otitis media:
    • Streptococcus pneumoniae (35-40%)
    • NTHI (25-30%)
    • Moraxella cararhalis (15-20%)
  21. NTHI: Clinical manifestations in adults
    • Exacerbations of COPD
    • Sinusitis
    • Community acquired pneumonia
  22. Most common cause of COPD exacerbations
    Non typable haemophilus influenzae
  23. Hib enters the blood stream
    And can get to CSF!!
  24. Hib meningitis: Pathogenesis
    • Colonizes the upper respiratory tract of children
    • Invasion into respiratory epithelial cells
    • Replication in submucosa
    • Bacteremia
    • Bacteria enter CSF through choroid plexus
    • Replicate in CSF-meningitis
    • Type b capsule (polyribose phosphate-PRP) – critical virulence factor
  25. Main reason for Hib causing hematogenous spread
    • Type b capsule
    • Not so in nontypeable
  26. NTHI: pathogenesis of otitis media
    • NTHI expresses several different adhesins which mediate attachment to host cell receptors
    • NTHI causes localized infections around the upper respiratory mucosa in contrast to Hib which causes invasive disease
    • Otitis media occurs when NTHI migrates from the nasopharynx to the middle ear via the eustacian tube
  27. Moraxella cararrhalis: Epidemiology
    • Recovered exclusively from humans
    • Strong relationship btw age and colonization rate: 1-5% healthy adults, while ~50% of infants before age 1.
    • Nasopharyngeal colonization is associated with otitis media
  28. Bordetella pertussis
    • Whooping cough
    • Tiny, gram negative cocobacilli, strictly aerobic
    • Does not survive outside the body
    • Slow-growing requires 3-6 days for visible colonies on media
    • Non-enteric gram negative rods
    • Elaborates powerful toxins
    • Highly contagious – attack rates 50-100% of susceptibles
    • Transmission by aerosol droplets
    • No animal reservoir and organism cannot survive in the environment
  29. Bordetella pertussis: epidemiology
    • Increased rate infants <1yo. Due to loss of maternal antibody
    • Increased rate in adults – due to limited duration of vaccine efficacy
    • In the U.S. adults constitute the majority of people infected with B. Pertussis
  30. Pertussis: clinical manifestation stages
    • Catarrhal or prodromal stage: – not yet full-blown
    • Paroxysmal stage: full-blown
    • Convalescent stage: recovery
  31. Pertussis: Catarrhal or prodromal stage:
    • lasts 7-14 days
    • nonspecific, malaise, rhinorrhea, lacrimation, low grade fever
    • then cough appears
  32. Pertussis: Paroxysmal stage
    • Lasts 1-2 weeks
    • Paroxysms of cough
    • Looks normal btw paroxysms. Minimal fever
    • Tenacious mucus due to ciliostasis
    • Marked lymphocytosis (up to 200,000)
  33. Pertussis: Convalescent stage
    • Lasts 3-4 weeks
    • Lymphocytes gradually decline
  34. Pathogenesis of pertussis:
    • Systemic: toxin production, lymphocytosis
    • Local: ciliary loss and thick mucus, severe cough, bronchial obstruction
    • Colonization of upper airway – growth on ciliated respiratory epithelium
  35. B. Pertussis virulence factors
    • Adhesins: fimbriae, filamentous hemagglutinin
    • Toxins: pertussis toxin
    • Tracheal cytotoxin: causes ciliostasis, toxic to tracheal epithelial cells
  36. Acellular pertussis vaccines
    • All contain inactivated pertussis toxin
    • Component antigens in purified form: pertussis toxin, filamentous hemagglutinin, pertactin, fimbriae
    • Antigens are protective in animal models
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