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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%)
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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
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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
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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
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Causes of community acquired pneumonia
- Streptococcus pneumoniae
- Nontypeable Haemophilus influenzae
- Mycoplasma pneumoniae
- Chlamydia pneumoniae
- COMMUNITY ACQUIRED – THINK STREPTOCOCCUS PNEUMONIAE
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Streptococcus pneumonia – non-Lancfield groupable
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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)
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COPD pathogens
- Pneumococcus
- Haemophilus influenzae
- Moraxella catarrhalis
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Predisposition to aspiration
Mouth anaerobes
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Influenza in community
- Pneumococcus
- Haemophilus influenzae
- Staphylococcus aureus
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Exposure to birds
Chlamydia psittaci
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CF, Bronchiectasis
- Pseudomonas aeruginosa
- Burkholderia cepacia
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Airway obstruction
Anaerobes
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Early HIV infection
- Pneumococcus
- H. influenzae
- Tuberculosis
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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
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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)
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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
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otitis media
One of the important associations with early in life colonization with Haemophilus influenzae nontypeable
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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.
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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%)
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NTHI: Clinical manifestations in adults
- Exacerbations of COPD
- Sinusitis
- Community acquired pneumonia
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Most common cause of COPD exacerbations
Non typable haemophilus influenzae
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Hib enters the blood stream
And can get to CSF!!
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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
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Main reason for Hib causing hematogenous spread
- Type b capsule
- Not so in nontypeable
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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
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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
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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
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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
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Pertussis: clinical manifestation stages
- Catarrhal or prodromal stage: – not yet full-blown
- Paroxysmal stage: full-blown
- Convalescent stage: recovery
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Pertussis: Catarrhal or prodromal stage:
- lasts 7-14 days
- nonspecific, malaise, rhinorrhea, lacrimation, low grade fever
- then cough appears
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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)
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Pertussis: Convalescent stage
- Lasts 3-4 weeks
- Lymphocytes gradually decline
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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
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B. Pertussis virulence factors
- Adhesins: fimbriae, filamentous hemagglutinin
- Toxins: pertussis toxin
- Tracheal cytotoxin: causes ciliostasis, toxic to tracheal epithelial cells
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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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