Bordetella Pertussis Flashcards

1
Q

morphology and general characteristics

A

gram-negative coccobacilli - resembling Haemophilus influenzae.

  • strict aerobe
  • fastidious and will grow slowly only on charcoal blood agar or bordet -gengou agar - 3-7 days for growth
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2
Q

transmission and epidemiology

A

B. pertussis is found only in humans

  • survives briefly outside the human respiratory tract
  • highly communicable and is transmitted from person to person via respiratory secretions
  • common in infants and children -> dangerous if within first 6 months of life
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3
Q

virulence factors (5)

A
  1. Filamentous hemagglutinin (Fha)- mediates adhesion to ciliated epithelial cells of the upper
    respiratory tract. Pili and agglutinogens may play a similar role in adherence
  2. Tracheal cytotoxin - immobilization and destruction of ciliated epithelial cells
    -toxicity is through the inhibition of DNA synthesis.
  3. Pertussis Toxin (PT) -the major virulence factor of B. pertussis; an ADPR-transferase
    - classic A-B type exotoxin:
    - active or A subunit, transfers ADP-ribose from NAD to a G protein that regulates
    adenylate cyclase activity such that the host cell cannot turn off the production of cAMP.
    - binding or B subunits which mediate attachment to carbohydrate moieties on the host cell
    surface and translocates A subunit across the membrane
    - biological effects depend on cell type involved and include histamine sensitization,
    lymphocytosis, insulin secretion, and alteration of other immune effector cell functions (decreased
    oxidative killing capacity)
  4. Invasive adenylate cyclase - enters host cell and raises host cell cAMP levels
    - hemolytic and interferes with chemotaxis and superoxide production
    by PMNs
  5. B. pertussis produce a hemolysin and a dermonecrotic heat-labile toxin -role in disease is unknown.
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4
Q

Pathogenesis and clinical considerations

A

-extracellular organism -> initiates infection by colonizing the ciliated bronchial epithelium and rapidly multiplying - immobilization and destruction of the ciliated epithelial cells occurs with no tissue invasion or dissemination

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5
Q

3 stages of the disease

A

Three stages of disease -
a. catarrhal stage (1-2 weeks)
- malaise, fever, sneezing and anorexia may be present
- profuse and mucoid rhinorrhea
- highly communicable with a large number of organisms in the nasopharynx and mucoid secretions
b. paroxysmal coughing stage (2-4 weeks)
- coughing episodes 40-50 times per day, characteristic inspiratory whoop as air is drawn through
narrowed glottis
- due to coughing and disruption of breathing, child may turn red and sometimes blue, and may
result in vomiting or choking on respiratory secretions
-lymphocytosis - elevated white blood cell counts with 70-80% lymphocytes
c. convalescent stage (3-4 weeks) - gradual fade of symptoms
Infection is usually limited to the upper respiratory tract. Infrequent complications may include:
-Bronchopneumonia due either to B. pertussis or to superinfection with organisms such as
Staphylococcus, S. pneumoniae or H. influenzae.
- Acute encephalopathy, characterized primarily by convulsions resulting in death or life-long brain
damage.

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6
Q

Laboratory diagnosis

A

culture - nasopharyngeal swab- during 1st 4 weeks -> charcoal blood agar

  • direct immunofluorescent assay-> sent 50%
  • PCR for rapid ID followed by confirmation by culture is standard
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7
Q

Immunity

A

protective immunity but not life-long. second infections are mild if they occur. antibody that prevents attachment to ciliated epithelial cells or neutralize PT may be involved . Secretory IgA may be important in nasopharyngeal secretions

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8
Q

treatment

A

erythromycin is the drug of choice
only useful in the catarrhal stages of the infection
and for prophylaxis of their exposed and susceptible individuals

once paroxysmal coughing has begun - treatment is primarily supportive

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9
Q

prevention and control

A

Vaccination - part of the diphtheria, tetanus acellular pertussis DTaP
- vaccinated at 2,4 and 6 months
boosters at 15-18 months and at the time of school entry are recommended.

1st gen vaccine - heat-killed prep of whole virulent organism- post vaccinal encephalopathies occurs every 100,000-300,000

2nd gen acellular vaccine- DTaP is now used - neuro complication reduced. acellular vaccine consists of Fha, pertussis toxoid and outer membrane protein and 2 fimbrial hemagglutinating antigens

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