Microbiology
Summary
Bordetella pertussis is the causative agent of whooping cough, a contagious respiratory disease. This bacterium employs a significant virulence factor called filamentous hemagglutinin (FHA) to adhere to the respiratory epithelium, aiding in colonization. Additionally, B. pertussis produces pertussis toxin, which disrupts the ADP-ribosylation of Gi protein and disables chemokine receptors on lymphocytes, contributing to lymphocytosis, a hallmark of the infection. Another notable toxin produced by B. pertussis is the adenylate cyclase toxin, responsible for elevating cAMP levels within host cells. Additionally, the bacterium produces the tracheal cytotoxin, which results in damage to the ciliated cells of the respiratory epithelium.
The progression of whooping cough is marked by distinct phases: the catarrhal stage, the paroxysmal stage (or whooping stage), and the convalescent stage. These three stages collectively span up to three months, often referred to as the "100-day cough." Effective elimination of B. pertussis from the respiratory tract is achieved using macrolides. Preventive measures involve administering the acellular vaccine for B. pertussis, a component of the DTaP vaccine that also includes antigens against diphtheria and tetanus toxoids.
Lesson Outline
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FAQs
B. pertussis is a gram-negative bacterium known to cause pertussis, commonly referred to as whooping cough. This highly contagious respiratory disease is characterized by severe coughing spells that can make it hard to breathe, often leading to the distinctive "whooping" sound.
The primary toxins produced by B. pertussis include pertussis toxin, adenylate cyclase toxin, and tracheal cytotoxin. Pertussis toxin ADP-ribosylates a host cell G protein, disrupting normal signaling and immune responses, contributing to pertussis symptoms. Additionally, PT increases mucus production and inhibits phagocytosis. Adenylate cyclase toxin disrupts host cell signaling by increasing cyclic AMP levels, inhibiting phagocytosis, and impairing immune responses. Tracheal cytotoxin damages ciliated epithelial cells lining the respiratory tract, contributing to inflammation and the characteristic "whooping" cough sound.
B. pertussis adheres to the ciliated epithelial cells in the upper respiratory tract and produces toxins that paralyze and destroy these cells. This damage prevents the cilia from effectively moving mucus and trapped particles, including the bacteria themselves, out of the respiratory tract, contributing to the characteristic severe cough of pertussis.
Increased counts of lymphocytes in the blood, known as lymphocytosis, is a common symptom in early stages of whooping cough, or pertussis. The pertussis toxin released by B. pertussis interferes with the lymphocyte recirculation, leading to their accumulation in the blood. This lymphocytosis is a unique feature of pertussis among respiratory infections.
Patients diagnosed with whooping cough are typically treated with macrolides, a type of antibiotic, to prevent the bacteria from multiplying further. Prophylactic antibiotics might also be given to those in close contact with the patient. The best prevention against B. pertussis is through vaccination. The acellular pertussis vaccine, often given in a combined form known as DTaP or Tdap (diphtheria, tetanus, and pertussis), is part of routine childhood immunizations and booster doses are recommended for adolescents and adults.
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