(incomplete) Haemophilus and Bordetella Flashcards

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0
Q

Explain the meaning of non-typeable H. influenzae.

A
Typeable = antibodies can recognize the capsule
Non-typeable = has no capsule, so anti-capsule Abs cannot recognize it
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1
Q

Explain the role of capsule in Haemophilus infection.

A

Capsule made of carbohydrates; required for virulence

Antiphagocytic: protects against complement and phagocytosis

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2
Q

Describe clinical syndromes and manifestations of Haemophilus bacteria.

A

Encapsulated (Typeable)

  • -Respiratory tract infections
  • -Bacterial meningitis mainly in children <4 years old

Unencapsulated (Non-typeable)

  • -Ear aches
  • -Respiratory disease
  • -Other infections

Likely a secondary invader after flu

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3
Q

Explain the importance of toxins in disease and adhesins in disease.

A

a

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4
Q

What characteristics of H.i. cause difficulties in diagnosis? Memorize the particular growth conditions needed by H. influenzae.

A

Facultative anaerobe
NO diagnostic fermentation patterns
Fragile - susceptible to disinfectants and drying

FASTIDIOUS: requires specific growth factors (these are used for diagnosis)

  • -Will NOT grow on blood agar -> NOT hemolytic
  • —-WILL grow around other bacteria on blood agar b/c they release nutrients
  • -Must use CHOCOLATE agar (heated blood, releases nutrients)
  • -X factor: hemin (Haemophilus = “heme-loving”)
  • -V factor: NAD/NADP
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5
Q

What does “pleomorphic” mean?

A

The characteristic of having multiple different shapes in a single bacterial culture

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6
Q

List characteristic of H. influenzae.

A

Small, Gm-, non-motile, non-spore-forming bacillus or coccobacillus (pleiomorphic)

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7
Q

What types of capsules can Haemophilus influenza have? Which is most virulent, and what is different about it?

A

Include A, B, C, D, E, F
Each type has a capsule with a different sugar composition

Type B = the most virulent
–Contain ribose in capsule (others have hexose)

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8
Q

Epidemiology of Hi/Hib: reservoir, % carriers

A

Reservoir in nasopharynx of humans only
75% of people carry Hi, but 3-5% carry Hib
–Vaccine usage has reduced levels of carriage
Responsible for 500,000 deaths of children worldwide

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9
Q

Hib: Clinical syndrome

A

Acquired through aerosol
Starts with nasopharyngitis, can include otitis media or sinusitis
Can invade epithelium and enter bloodstream, progress to bacteremia and meningitis

Can also cause:

  • -Epiglotititis/obstructive laryngitis
  • -Cellulitis (inflammation of connective tissue)
  • -Joint infections
  • -Pneumonia
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10
Q

Pathogenesis of Hib:

A
  1. Portal into humans
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11
Q

Immunity against Hib:

A

Capsule (polyribosyl phosphate) linked to proteins (diphtheria toxoid) to enhance T cell memory
Used for 20 years
Extremely successful
Now made with strictly synthetic components

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12
Q

Treatment of Hib infections

A

Meningitis:
–3rd gen cephalosporins (cefotaxime, ceftriaxone) most common
–Ampicillin with clavulanate (beta-lactamase inhibitor) used
FINISH

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13
Q

Clinical manifestations of non-typeable Hi

A

Generally restricted to respiratory tract and ear in healthy individuals
Colonization starts in nasopharynx -> damaged epithelia, respiratory mucus
Causes otitis media in children (immune system not as effective, structure of Eustachian tube makes infections more likely)
Conjunctivitis
FINISH

Respiratory disease in pts with underlying respiratory issues
Meningitis in individuals with predisposing factors or in neonates

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14
Q

Pathogenesis of Non-typeable H.i.

A

Uses MANY different complements of adhesins (don’t need to know them)

Invades via 3 routes: both an extracellular and intracellular pathogen

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15
Q

Is there a vaccine for non-typeable H.i.?

A

Immunity is strain-specific
Passive immunity is also strain-specific and lasts only a few months
NO vaccine

16
Q

Treatment of non-typeable H.i.

A

Amoxicillin for otitis media and sinusitis
Resistant strains treated with amoxicillin + beta-lactamase inhibitor
Persistent infections may be due to biofilm formation or host cell invasion

17
Q

How is H.i.b diagnosed? (5)

A
History, age of pt
Culture blood and spinal fluid (on chocolate and blood agar; Gm stain spinal fluid sediment)
Presence of Type B capsular antigen
PCR detection of capsule genes
Biochemical tests
18
Q

H. ducreyi

A

a

19
Q

H. aegypticus

A

a

20
Q

H. parainfluenzae

A

a

21
Q

Characteristics of bordatella pertussis

A

Smal, Gm- coccobacillus
OBLIGATE aerobe
Causes whooping cough

22
Q

Epidemiology of Bordetella pertussis

A

Found only in humans (no animal reservoir)

FINISH

23
Q

Clinical features of Bordetella pertussis

A

a

24
Q

Pathogenesis of Bordetella pertussis - steps in infection

A
  1. Introduction via water droplets
  2. Interactions with ciliated epithelial cells in trachea and nasopharynx
  3. Adherence
  4. Local multiplication and toxin production -> acute local inflammation, increased mucous secretions, patchy ulceration of respiratory epithelium
    - -May cause pneumonia
    - -NO bacteremia, remain in respiratory tract
  5. Evasion of host defenses
  6. Spread of disease
25
Q

Pathogenesis of Bordetella pertussis - specific toxins

A

Pertussis toxin -> increased cAMP via ADP-ribosylation of inhibitory G protein

  • -Effects on innate immune system
  • -Increased insulin production
  • -Sensitization to histamine
  • -Lymphocytosis
  1. Adenylate cyclase toxin
    –Secreted into host cell cytoplasm
    FINISH
  2. Dermonecrotic toxin
    - -Causes local necrosis and inflammation
    - -Affects cytoskeleton, actin polymerization
    - -FINISH
  3. Tracheal cytotoxin
    - -Peptidoglycan fragment
    - -> Ciliostasis
    - -Kills tracheal epithelial cells
    - -Promotes release of some proinflammatory FINISH
  4. LPS
26
Q

Pathogenesis of Bordetella pertussis - physical interactions with host

A
  1. Pili
  2. Filamentous hemagglutinin (Fha)
  3. Pertactin
    - -FINISH
  4. Tracheal colonization factor
    - -Surface molecule, anchored in OM
27
Q

Is there a vaccine against Bordetella pertussis?

A

YES - subunit/component vaccine: acellular pertussis vaccine
Doesn’t have the side effects of whole cell vaccine
Given as part of DTaP (Diphtheria, Tetanus, acellular Pertussis)
–Presence of surface components prevents infection
–Presence of pertussis toxoid prevents symptoms
FINISH

28
Q

Why is pertussis reemerging? (5)

A
Waning immunity
Antigenic divergence
--Mutation of PTX or its regulation
--Mutation of pertactin
Decreased vaccination
29
Q

Diagnosis of Bordetella pertussis

A

Pt symptoms and history -> classic cough

Lymphocytosis

30
Q

Detection of Bordetella pertussis

A

Needs VERY fresh media for growth

FINISH

31
Q

Treatment of Bordetella pertussis

A

FINISH

32
Q

Bordetella parapertussis

A

a

33
Q

Bordetella bronchiseptica

A

FINISH