Bordetella pertussis

Bordetella pertussis is a small, aerobic, gram-negative coccobacillus transmitted person to person by respiratory droplets. Humans are its only reservoir. It is fastidious in the laboratory and traditionally grown on Bordet-Gengou or Regan-Lowe media, although nucleic acid amplification testing has largely replaced culture for diagnosis. The organism does not invade the bloodstream; it colonizes ciliated respiratory epithelium and causes disease through its toxins.

Two virulence factors dominate exam questions. Pertussis toxin is an AB-type exotoxin that ADP-ribosylates the inhibitory G protein (Gi), disabling it and thereby leaving adenylate cyclase unopposed. The resulting rise in cyclic AMP contributes to the striking lymphocytosis seen in infected children and impairs immune cell function. A separate adenylate cyclase toxin enters host cells and generates cAMP directly, while tracheal cytotoxin destroys ciliated cells, crippling mucociliary clearance and driving the persistent cough. Filamentous hemagglutinin and pertactin mediate adherence.

The illness classically runs three stages. The catarrhal stage resembles a common cold and is the most contagious. The paroxysmal stage brings violent coughing fits followed by an inspiratory "whoop" and often post-tussive vomiting, with a characteristic lymphocyte-predominant leukocytosis. The convalescent stage involves a gradually waning cough that can persist for weeks, earning pertussis the name "the hundred-day cough." Infants are at highest risk of severe complications such as apnea and pneumonia. Macrolides are the treatment of choice and are most useful early, since much of the later illness is toxin-mediated. Prevention relies on the acellular DTaP and Tdap vaccines.

USMLE Step 1 tests Bordetella pertussis within bacteriology, most often through a vignette featuring an unvaccinated child with paroxysmal cough and lymphocytosis, or through a direct question about the mechanism of pertussis toxin on Gi signaling.