Antigenic Structure, Pathogenesis, and Pathology of Bordetella pertussis
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p279
2025-09-09
336
B. pertussis produces a number of factors that are involved in the pathogenesis of disease. One locus on the B. pertussis chromosome acts as a central regulator of virulence genes. This locus has two Bordetella operons, bvgA and bvgS. The products of the A and S loci are similar to those of known two-component regulatory systems. bvgS responds to environmental signals, and bvgA is a transcriptional activator of the virulence genes. Filamentous hemagglutinin, a large surface protein, and fimbriae (surface appendages) mediate adhesion to ciliated epithelial cells and are essential for tracheal colonization. Pertussis toxin (a classic A/B structure toxin) promotes lymphocytosis, sensitization to histamine, and enhanced insulin secretion by means of adenosine diphosphate-ribosylating activity that disrupts function of signal transduction in many cell types. The filamentous hemagglutinin and pertussis toxin are secreted proteins and are found outside of the B. pertussis cells. Adenylate cyclase toxin (ACT), dermonecrotic toxin (DNT), and hemolysin also are regulated by the bvg system. ACT is an important virulence factor that inhibits phagocyte function but the role of DNT in pertussis is unknown. The tracheal cytotoxin is not regulated by bvg and kills respiratory epithelial cells in vitro. The lipooligosaccharide in the cell wall may also be important in causing damage to the epithelial cells of the upper respiratory tract.
B. pertussis survives for only brief periods outside the human host. There are no vectors. Transmission is largely by the respiratory route from early cases and possibly via carriers. The organism adheres to and multiplies rapidly on the epithelial surface of the trachea and bronchi and interferes with ciliary action. The blood is not invaded. The bacteria liberate the toxins and substances that irritate surface cells, causing coughing and marked lymphocytosis. Later, there may be necrosis of parts of the epithelium and polymorphonuclear infiltration, with peribronchial inflammation and interstitial pneumonia. Secondary invaders such as staphylococci or H. influenzae may give rise to bacterial pneumonia. Obstruction of the smaller bronchioles by mucous plugs results in atelectasis and diminished oxygenation of the blood. This probably contributes to the frequency of convulsions in infants with whooping cough.
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