BORDETELLA!!! MICROM 442 Deck 16 Flashcards

1
Q
  1. B. pertussis
  2. B. parapertussis
  3. B. bronchiseptica
  4. B. holmesii
  5. B. hinzii (rarest)
A

Five human pathogenic species

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2
Q

clinical diagnosis sometimes complicated because?

A

Overlapping clinical pictures for B. pertussis & B. parapertussis

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3
Q

gram negative and what shapes??

A

cocobacilli

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4
Q

what type of aerobe?

A

strict -> makes sense they like the lungs :)

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5
Q

what color pigment does parapertussis have?

A

brown

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6
Q

all of these are non-motile except?

A

B. bronchiseptica

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7
Q

Regan-Lowe, Bordet-Gengou, Stainer-Scholte

A

– Colonies: Small, shiny, round, domed, silvery (on RL)
– On BG slight hemolysis

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8
Q

these are encapsulated but also they do not produce?

A

spores

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9
Q

Recall CFUs decrease over time because

A

fastidious

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10
Q

oxidase positive or negative?

A

positive

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11
Q

exceptions

A

– B. bronchispetica is motile
– B. parapertussis has brown pigment
– B. bronchiseptica & rare Bordetella spp can grow on MacConkeys

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12
Q

who are resevoirs?

A

Adults, adolescents & older children = reservoir

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13
Q

Dz in unimmunized (too young, no immune system)

A

– esp < 1 yr
– < 6 mos most at risk

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14
Q

Clinical Pertussis Sx

A

> Prolonged cough
Distinct whoop, infants
CFU #’s decrease over time
Lymphocytosis
Infectious ~3 wks
– Most non-infx by 4 wks
– 90% non-infx by 5wks
Lower respiratory tract, large airway dz

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15
Q

what distinct shape does pertussis have?

A

CLUB

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16
Q

what are the phases of the dz?

A

catarrhal -> convulsive (intensity of coughing) -> convalescence

17
Q

when is it best to take a sample?

A

during the catarrhal bc that when the bactiera are in large numbers because the antibody receptors ahven’t started

18
Q

Filamentous hemagglutinin (FHA) -> virulence & adherence

A

> Fimbriae
Pertactin

19
Q

Toxins

A

– Adenylate Cyclase Toxin
– Pertussis Toxin
– Tracheal cytotoxin

20
Q

Laboratory Detection

A

> Culture
PCR
Serology

21
Q

when you would culture?

A

early, the CFUs tend to fall overtime

22
Q

PCR is done later in the dz because?

A

a. organism-specific assays more sensitive than broad-range
bacterial assays for that target only
b. multi-target, low-complexity panels “box & ship” to labs

23
Q

serology can be helpful two weeks of symptoms bc

A

examine for antibodies (probably?)

24
Q

clinical presentations

A
  1. Prolonged cough, runny nose (both contribute to spread)
  2. Whoop in infants
  3. Rare complications à bronchopneumonia and encephalopathy
  4. Increased lymphocytes
25
Q

increased lymphocytes is surprising/different bc???

A

they typically move from the circulating pool into the tissues

26
Q

pertussis can also cause???

A

kennel cough & other infx

27
Q

Kennel Cough

A
  1. Zoonotic disease milder than whooping cough
  2. Animal workers & immunocompromised most at risk
  3. Can progress to severe pneumoniae, but rare
28
Q

Other infections via pertussis

A

Rare, B. holmesii can cause both pertussis-like illness AND blood
stream infections

29
Q

pathogenesis -> toxins -> pertussis toxin (AB subunit)

A

End result -> disrupts immune cell function in multiple
ways

30
Q

mechanism of pertussis toxin

A

Toxin secreted form cyotosol to IM/PP/OM -> host cell retrograde trafficking after binging to golgi -> golgi to cell surface -> at cell-surface subunit cleaved and ADP-ribosylates GPCRs -> signaling shut down bc can no longer convert GDP to GTP -> shuts down cAMP signaling and leaves high concentration

31
Q

what is a key vaccine component?

A

Pertussis toxin

32
Q

binds to a complement receptor -> forms pores in cell -> cations pour in and lyse cells -> n-terminal AC domain converts ATP to cAMP

A

Adenylate cyclase (AC) toxin mechanism

33
Q

different results from the AC toxin

A

i. In macrophages, loss of reactive nitrogen species
(nitric oxide, NO)
ii. In neutrophils, loss of reactive oxygen species
(ROS

34
Q

Tracheal toxin (TCT)

A

Cytotoxin for airway epithelial cells: poisons cilia & stops
ciliary movement/bronchociliary ladder

35
Q

FHA

A

Type I pilus; extremely long polymer of Fim protein
subunits; anchored in OM

36
Q

Macrolides treatment

A

– Erythromycin for infants
– Weight-based dosing
– Fixed dosing adolescents & adults

37
Q

Respiratory distress ->

A

intubation & ventilation

38
Q

Minimal utility:

A

– Inhaled corticosteroids, anti-pertussis Ig, inhaled beta
blockade