Bordetella Pertussis: Whooping Cough

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Questions and Answers

During which stage of a Bordetella pertussis infection is an individual most contagious, posing the highest risk to close contacts?

  • Paroxysmal stage, characterized by intense coughing fits that expel large quantities of bacteria.
  • The stage following vaccination, when individuals may be asymptomatic carriers.
  • Convalescent stage, due to the lingering presence of the bacteria in the respiratory tract.
  • Catarrhal stage, marked by common cold-like symptoms which facilitate unwitting transmission. (correct)

What is the primary mechanism by which tracheal cytotoxin (TCT) contributes to the pathogenesis of Bordetella pertussis infection?

  • Inducing excessive mucus production, leading to airway obstruction.
  • Promoting the ADP-ribosylation of host cell proteins, disrupting cellular signaling pathways.
  • Increasing intracellular cAMP levels, leading to fluid secretion and edema.
  • Directly inhibiting cilia movement and causing damage to ciliated epithelial cells. (correct)

A researcher is investigating potential therapeutic targets to mitigate the effects of Bordetella pertussis infection. Which virulence factor would be the MOST effective target to simultaneously address both the initial colonization and subsequent tissue damage?

  • Pertussis toxin, due to its role in ADP-ribosylation and systemic effects.
  • Adenylate cyclase toxin, due to its role in inhibiting phagocyte activity.
  • Filamentous hemagglutinin, due to its critical role in attachment to ciliated epithelial cells. (correct)
  • Tracheal cytotoxin, due to its direct damage to ciliated cells.

Why is it important to diagnose Bordetella pertussis during the catarrhal phase?

<p>To administer azithromycin when it can have the greatest impact on the disease course. (B)</p> Signup and view all the answers

A patient presents with a persistent cough, and Bordetella pertussis is suspected. If initial culture results are inconclusive, which subsequent diagnostic approach would provide the MOST rapid and specific confirmation of infection?

<p>Fluorescent antibody staining of nasopharyngeal swab to directly visualize the bacteria. (C)</p> Signup and view all the answers

Consider a scenario where a new strain of Bordetella pertussis emerges with a mutated pertussis toxin that exhibits reduced ADP-ribosylating activity. What is the MOST likely clinical manifestation that would be observed in individuals infected with this new strain?

<p>A milder form of whooping cough with reduced severity of coughing fits. (A)</p> Signup and view all the answers

What is the DISTINCT role of adenylate cyclase toxin in Bordetella pertussis pathogenesis, and how does it synergize with other virulence factors to promote infection?

<p>It blocks phagocyte activity, preventing bacterial clearance, and works with tracheal cytotoxin to damage ciliated cells. (D)</p> Signup and view all the answers

How does Bordetella pertussis evade host defenses to establish infection?

<p>By inhibiting phagocyte activity and damaging ciliated cells. (C)</p> Signup and view all the answers

While acellular vaccines have significantly reduced the incidence of whooping cough, why does Bordetella pertussis remain a public health concern?

<p>Acellular vaccines offer limited duration of protection and do not prevent asymptomatic carriage and transmission. (D)</p> Signup and view all the answers

A research team is investigating the genetic diversity of Bordetella pertussis strains circulating in a population with high vaccination coverage. What evolutionary trend would they MOST likely observe?

<p>Antigenic drift in surface proteins, such as pertactin and fimbriae, to evade vaccine-induced immunity. (D)</p> Signup and view all the answers

Flashcards

Bordetella pertussis

A gram-negative, coccobacillus, aerobic bacteria that causes whooping cough.

Pertussis toxin

Attaches to cilia, impairs function, leading to mucus production and severe coughing. AB5 exotoxin increases cAMP and causes edema.

Tracheal cytotoxin (TCT)

Fragment released from the peptidoglycan of the B. pertussis cell wall that paralyzes cilia and causes necrosis.

Adenylate cyclase toxin

Blocks phagocytes from getting to the infection site and prevents them from killing bacteria; works with tracheal cytotoxin to damage ciliated cells.

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Catarrhal stage of Whooping Cough

1-2 weeks, resembles common cold with rhinorrhea, sneezing, malaise, low-grade fever and poses highest risk to contacts

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Paroxysmal stage of Whooping Cough

2-4 weeks, ciliated epithelial cells are extruded, impaired mucus clearance, classic whooping cough paroxysms, vomiting and exhaustion. Possible decreased oxygen levels, seizures, encephalopathy, and death. Risk of pneumonia.

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Convalescent stage of Whooping Cough

Paroxysms diminish in number and severity, secondary complications can occur.

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Filamentous hemagglutinin, pertacin, and agglutinogens (fimbriae)

Pili-like adhesion proteins that help the bacteria attach to ciliated epithelial cells.

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Treatment/Prevention of Whooping Cough

Azithromycin (limited effect on cough) and supportive care (oxygen, suction). Prevention with acellular vaccine (DPT).

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Study Notes

  • Bordetella pertussis causes whooping cough, a severe and uncontrollable coughing illness.
  • Bordetella parapertussis causes a milder form of the illness.
  • Bordetella is a gram-negative, coccobacillus, aerobic bacteria.
  • Bordetella has a worldwide distribution that primarily infects infants and young children.
  • Cases have declined in the U.S. due to vaccination.
  • Incubation period of 7 - 10 days.
  • The cough has three stages: catarrhal, paroxysmal, and convalescent.

Catarrhal Stage

  • Resembles the common cold with rhinorrhea, sneezing, malaise, and low-grade fever.
  • Lasts for 1 - 2 weeks.
  • Poses the highest risk to contacts.

Paroxysmal Stage

  • Ciliated epithelial cells are extruded from the respiratory tract.
  • Clearance of mucus is impaired.
  • Classic "whooping" cough paroxysms occur, frequently terminated with vomiting and exhaustion.
  • Lasts 2 - 4 weeks.
  • Decreased oxygen levels can cause seizures, encephalopathy, and even death.
  • Risk of pneumonia caused by other pathogens.

Convalescent Stage

  • Paroxysms diminish in number and severity.
  • Secondary complications can occur.
  • Whooping sound with cough following by vomiting.
  • Best diagnosed during the catarrhal phase via nasopharyngeal swab.
  • Difficult to culture, but Bordet-Gengou medium can be used.
  • ELISA can detect antibodies to pertussis toxin, filamentous hemagglutinin, pertactin, and fimbriae antigens.
  • Fluorescent antibody staining and PCR are effective for bacterial DNA detection.
  • Azithromycin has little effect on the prolonged cough stage.
  • Supportive care, including oxygen therapy and suction of mucus, is crucial during the paroxysmal stage.
  • Preventative acellular vaccine (DPT vaccine) contains 5 antigens purified from the organism, as well as a killed vaccine.
  • Pili-like adhesion proteins such as filamentous hemagglutinin, pertactin, and agglutinogens (fimbriae) help the bacteria attach to ciliated epithelial cells.
  • Once B. pertussis attaches, it immobilizes the cilia, preventing mucus clearance, and releases toxins like pertussis toxin, adenylate cyclase toxin, and tracheal cytotoxin.
  • These virulent factors cause severe coughing fits.

Virulent Factors:

  • Tracheal cytotoxin
  • Pertussis toxin
  • Adenylate cyclase toxin
  • Pili-like adhesion proteins
  • Whooping cough is caused by pertussis toxin, produced by the small, encapsulated Bordetella bacteria
  • Pertussis toxin is an AB5 exotoxin

Pertussis Toxin:

  • Attaches to cilia, impairing their function and leading to mucus production.
  • Causes ADP-ribosylation, increased cAMP, and edema of the respiratory mucosa, resulting in severe cough.
  • Bacteria spread through air droplets and contaminated surfaces.

Adenylate Cyclase Toxin:

  • Blocks phagocytes from reaching the infection site and prevents them from killing bacteria.
  • Works in conjunction with tracheal cytotoxin, which damages ciliated cells.

Tracheal Cytotoxin:

  • A fragment released from the peptidoglycan of the B. pertussis cell wall.
  • Increases the production of nitric oxide and IL-1alpha, causing cytopathology.
  • Directly inhibits cilia movement, disrupting normal clearance mechanisms in the respiratory tree and leading to the characteristic pertussis cough.
  • Paralyzes cilia on tracheal epithelial cells, causing blebbing and necrosis of ciliated epithelia.

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