Daniels-Pneumo, etc Flashcards
Strep. pneumoniae characteristics
Gram + cocci Diplococci Aerotolerant anaerobe Non-spore forming Encapsulated
Main cause of pneumonia
S. pneumoniae
S. pneumoniae identification tests
Alpha hemolysis
Neg catalase test
Zone of inhibition
S. pneumoniae Reservoir and transmission
Young children are reservoir
Nasopharyngeal mucosa
Transmission via respiratory secretions/hands
S. pneumoniae pathogenesis
1) Alveoli fill w/ fluid
2) Early consolidation phase
- Suppurative (neutrophils) inflammation
3) Late consolidation phase
- Alveoli and airways packed w/ neutrophils
- Affected tissue is solid instead of spongy
4) Recovery phase
- Macrophages phagocytose debris
- Normal architecture re-established
S. pneumoniae disease manifestations other than pneumonia
- otitis media in children
- Potential sequelae to pneumonia in adults
- Pleural effusion-fluid in chest outside of lungs
- bacteremia-meningitis
S. pneumoniae diagnosis
gram stained sputum and culture
S. pneumoniae therapy
- Penicillins and other B-lactams (resistance is concern)
- Macrolides (erythromycin, azithromycin)
- Fluoroquinolones (levofloxacin)
S. pneumoniae vaccine
Made from polysaccharide (capsular) antigens from multiple strains of S. pneumoniae.
-Given to children and elderly
Legionella pneumophila characteristics
Gram - Pleomorphic rod Obligate aerobe Fastidious Cysteine requirement-imp. for identification
L. pneumophila encounter
Think hot tub:
- Contaminated water
- L. pneumophila is a parasite of protozoa
- Biofilms w/ protozoa and other bacteria
- Thermotolerant
- Environmental aerosol spread (not by cough)
L. pneumophila multiplication
- Bacteria in alveoli are phagocytosed
- Virulent strains multiply in autophagosomes
L. pneumophila pathogenesis
Inflammation->acute bronchopneumonia
- Suppurative (neutrophils)
- Recruitment of more macrophages (L. pneumophila multiply in autophagosomes)
- Abscess formation
Immune response to L. pneumophila
Cell mediated immune response
- Secretion of IFN-gamma
- Iron sequestration (decreases replication of bacteria)
L. pneumophila virulence
- Survival in macrophages
- LPS
- Flagellin (enhances inflammation via TLR-5 of innate immune system)
L. pneumophila therapy
Need antimicrobial drugs w/ good intracellular penetration
-Macrolides
-Fluoroquinolones
-Tetracyclines
Penicillins NOT effective b/c do not penetrate macrophages enough
Bordetella pertussis and parapertussis characteristics
Gram - rod
Obligate aerobe
Causes whooping cough
Very contagious
B. pertussis reservoir
Adults are reservoir
Nasopharynx
B. pertussis entry/transmission
Access trachea/bronchi
-Ciliary adherence via:
*Filamentous hemagglutinin (Fha)
*Pili
*Pertactin protein
Think B. pertussis adheres w/ FhaPPB. pertussis vs B. parapertussis
*Difference-B. parapertussis does not have pertussis toxin
*Similarities
-Adenylate cyclase/ hemolysin
-Upregulate host cAMP
>Decreased neutrophil function
>Inc. capillary permeability (edema)
-Endotoxin
B. pertussis pathogenesis
1) Catarrhal stage (1-2 weeks)
- Looks like bad cold, really runny nose
- Organisms spreading down respiratory tract
- Extremely contagious
2) Paroxysmal stage (1-6 weeks)
- Fits of whooping coughs w/ vomiting
3) Convalescent stage (2-3 weeks)
- Gradual recovery
B. pertussis diagnosis
- Tricky b/c fewer organisms are shed in paroxysmal stage, when clinical suspicion is high.
- Deep nasal swab or nasal flush
- Can diagnose 3 weeks prior to cough
B. pertussis vaccine
- Contain acellular pertussis
- dTAP-given to young
- Tdap-given to older and during pregnancy
- Lower dose of diptheria and pertussis
B. bronchiseptica
Canine tracheobronchitis–kennel cough
Only affects immunocompromised humans
Mycobacterium species
TB: -M. tuberculosis -M. bovis -M. avium Leprosy: -M. leprae Opportunistic deep wound infections: -RGM (rapidly growing mycobacterium)
Mycobacterium spp.characteristics
Obligate aerobes
Non-spore formers
Thick, waxy cell wall–acid fast
*Mycolic acid binds carbol fuscin dye. Not gram stained!
Mycobacterium spp.encounter, multiplication and spread
1) Ingestion->localization in intestine->adequate cell mediated immunity should kill via macrophages->Latency->Reactivation by 2nd TB->Dissemination in intestine and spread to other organs
2) Inhalation->lesion in lung->adequate cell mediated immunity should kill via macrophages->Latency->Reactivation by 2nd TB->Dissemination in lung and spread to other organs
M. tuberculosis pathogenesis/immune response
- Multiplication in macrophages
- Activation of CD4
- Cytokines: IFN-gamma, IL-12, IL2
- Macrophage recruitment forms granuloma
M. tuberculosis diagnosis
Intradermal test:
-Killed tuberculin antigen
-DTH (type IV hypersensitivity)
*Activation of specific CD4
Acid fast sputum exam
Culture-very slow growing
PCRM. leprae spread and disease characteristics
Granulomatous disease -Similar immunology to TB (granulomas) Affects skin b/c bacteria prefers cooler temps Spread via respiratory route Two forms: 1)Tuberculoid leprosy 2)Lepromatous leprosy
Tuberculoid leprosy vs lepromatous leprosy
Tuberculoid leprosy: -Milder -May be self limiting -Few bacteria in lesions Lepromatous leprosy: -Severe disfiguring -Many organisms in lesions -Cell mediated immunity significantly decreased
M. leprae cultivation
Uncultivatable in vitro
Can inoculate mouse footpad
Armadillos are carriers
