Pertussis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [2]

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Overview

Pertussis is primarily a toxin-mediated disease. Bordetella pertussis attaches to the cilia of the respiratory epithelial cells, proliferates and produces virulence factors that paralyze the cilia, and causes inflammation of the respiratory tract, which interferes with the clearing of pulmonary secretions.

Pathophysiology

Pathogenesis

• Bordetella pertussis has tropism for pulmonary tissue and rarely disseminates to other organs.
• The steps involved in the pathogenesis of pertussis include the following:

• Inoculation
• Attachment to the respiratory epithelium
• Proliferation
• Production of virulence factors (toxins)
• Evasion of host immune cells
• Tissue destruction

Virulence Factors

Bordetella pertussis produces multiple antigenic and biologically active virulence factors responsible for the clinical manifestations of pertussis. These virulence factors include:

• Pertussis toxin (PT)

• PT undergoes ADP-ribosylation of G proteins to disrupt signal transduction in host cells.

• Filamentous hemagglutinin (FHA)

• Suface protein responsible for the interaction and adhesion between host cells and Bordetella pertussis.
• FHA is a component of the acellular DTaP vaccine.

• Agglutinogens
• Adenylate cyclase toxin (ACT)

• ACT delivers an adenylate cyclase domain into the host cell and increases the intracellular cAMP concentration.
• Following cAMP delivery, phagocyte activity is inhibited, and phagocytes undergo apoptosis.

• Pertactin (PRN)

• PRN defends Bordetella pertussis against the host neutrophil (immunomodulation).
• PRN is a component of the acellular DTaP vaccine.

• Tracheal cytotoxin

• TCT is responsible for the death of host respiratory cells using intracellular IL-1 and nitric oxide.

• Lipooligoosaccharide (LOS)
• Dermonecrotic toxin (DNT)

• DNT de-aminates signaling proteins (similar mechanism to Pasteurella multicida leukotoxin).
• Unique outer membrane component that is thought to play a role in clinical manifestations of pertussis.
• Unknown virulence mechanism.

• Fimbriae (FIM)

• Surface appendages to adhere to host cells and avoid host immune cells (immunomodulation).
• FIM is a component of the acellular DTaP vaccine.