Daniels-Pneumo, etc Flashcards

1
Q

Strep. pneumoniae characteristics

A
Gram + cocci
Diplococci
Aerotolerant anaerobe
Non-spore forming
Encapsulated
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2
Q

Main cause of pneumonia

A

S. pneumoniae

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3
Q

S. pneumoniae identification tests

A

Alpha hemolysis
Neg catalase test
Zone of inhibition

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4
Q

S. pneumoniae Reservoir and transmission

A

Young children are reservoir
Nasopharyngeal mucosa
Transmission via respiratory secretions/hands

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5
Q

S. pneumoniae pathogenesis

A

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

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6
Q

S. pneumoniae disease manifestations other than pneumonia

A
  • otitis media in children
  • Potential sequelae to pneumonia in adults
    • Pleural effusion-fluid in chest outside of lungs
    • bacteremia-meningitis
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7
Q

S. pneumoniae diagnosis

A

gram stained sputum and culture

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8
Q

S. pneumoniae therapy

A
  • Penicillins and other B-lactams (resistance is concern)
  • Macrolides (erythromycin, azithromycin)
  • Fluoroquinolones (levofloxacin)
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9
Q

S. pneumoniae vaccine

A

Made from polysaccharide (capsular) antigens from multiple strains of S. pneumoniae.
-Given to children and elderly

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10
Q

Legionella pneumophila characteristics

A
Gram -
Pleomorphic rod
Obligate aerobe
Fastidious
Cysteine requirement-imp. for identification
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11
Q

L. pneumophila encounter

A

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)
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12
Q

L. pneumophila multiplication

A
  • Bacteria in alveoli are phagocytosed

- Virulent strains multiply in autophagosomes

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13
Q

L. pneumophila pathogenesis

A

Inflammation->acute bronchopneumonia

  • Suppurative (neutrophils)
  • Recruitment of more macrophages (L. pneumophila multiply in autophagosomes)
  • Abscess formation
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14
Q

Immune response to L. pneumophila

A

Cell mediated immune response

  • Secretion of IFN-gamma
  • Iron sequestration (decreases replication of bacteria)
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15
Q

L. pneumophila virulence

A
  • Survival in macrophages
  • LPS
  • Flagellin (enhances inflammation via TLR-5 of innate immune system)
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16
Q

L. pneumophila therapy

A

Need antimicrobial drugs w/ good intracellular penetration
-Macrolides
-Fluoroquinolones
-Tetracyclines
Penicillins NOT effective b/c do not penetrate macrophages enough

17
Q

Bordetella pertussis and parapertussis characteristics

A

Gram - rod
Obligate aerobe
Causes whooping cough
Very contagious

18
Q

B. pertussis reservoir

A

Adults are reservoir

Nasopharynx

19
Q

B. pertussis entry/transmission

A
Access trachea/bronchi
 -Ciliary adherence via:
    *Filamentous hemagglutinin (Fha)
    *Pili
    *Pertactin protein
Think B. pertussis adheres w/ FhaPP
20
Q

B. pertussis vs B. parapertussis

A

*Difference-B. parapertussis does not have pertussis toxin
*Similarities
-Adenylate cyclase/ hemolysin
-Upregulate host cAMP
>Decreased neutrophil function
>Inc. capillary permeability (edema)
-Endotoxin

21
Q

B. pertussis pathogenesis

A

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

22
Q

B. pertussis diagnosis

A
  • 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
23
Q

B. pertussis vaccine

A
  • Contain acellular pertussis
  • dTAP-given to young
  • Tdap-given to older and during pregnancy
    • Lower dose of diptheria and pertussis
24
Q

B. bronchiseptica

A

Canine tracheobronchitis–kennel cough

Only affects immunocompromised humans

25
Q

Mycobacterium species

A
TB:
  -M. tuberculosis
  -M. bovis
  -M. avium
Leprosy:
  -M. leprae
Opportunistic deep wound infections:
  -RGM (rapidly growing mycobacterium)
26
Q

Mycobacterium spp.characteristics

A

Obligate aerobes
Non-spore formers
Thick, waxy cell wall–acid fast
*Mycolic acid binds carbol fuscin dye. Not gram stained!

27
Q

Mycobacterium spp.encounter, multiplication and spread

A

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

28
Q

M. tuberculosis pathogenesis/immune response

A
  • Multiplication in macrophages
  • Activation of CD4
  • Cytokines: IFN-gamma, IL-12, IL2
  • Macrophage recruitment forms granuloma
29
Q

M. tuberculosis diagnosis

A
Intradermal test:
  -Killed tuberculin antigen
  -DTH (type IV hypersensitivity)
     *Activation of specific CD4
Acid fast sputum exam
Culture-very slow growing
PCR
30
Q

M. leprae spread and disease characteristics

A
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
31
Q

Tuberculoid leprosy vs lepromatous leprosy

A
Tuberculoid leprosy:
  -Milder
  -May be self limiting
  -Few bacteria in lesions
Lepromatous leprosy:
  -Severe disfiguring
  -Many organisms in lesions
  -Cell mediated immunity significantly decreased
32
Q

M. leprae cultivation

A

Uncultivatable in vitro
Can inoculate mouse footpad
Armadillos are carriers