What are the clinical stages of pertussis?

Pertussis progresses through three distinct clinical stages. First is the incubation period, lasting about 7–10 days. Second is the catarrhal stage, characterized by mild upper respiratory symptoms, sneezing, and low-grade fever; patients are most contagious during this phase. Third is the paroxysmal stage, featuring severe paroxysms of coughing followed by a characteristic inspiratory "whoop," often complicated by hypoxia, post-tussive vomiting, and exhaustion.

Which specific antigens are included in the acellular pertussis vaccine?

The acellular pertussis vaccine typically contains up to five purified components derived from Bordetella pertussis: pertussis toxoid, filamentous hemagglutinin (FHA), pertactin, and type 2 and type 3 fimbriae.

What laboratory diagnostic methods are used to detect pertussis?

Laboratory confirmation utilizes culture isolation via nasopharyngeal swab plated onto selective media (e.g., Bordet-Gengou or charcoal agar). Rapid diagnostics include direct fluorescent antibody (DFA) staining or PCR detection of B. pertussis DNA in nasopharyngeal secretions. Retrospective diagnosis in later stages relies on serology (ELISA, agglutination tests).

How do the growth requirements of B. pertussis and B. parapertussis differ?

Bordetella pertussis grows only on complex media containing adsorbents (Bordet-Gengou agar, charcoal agar). Bordetella parapertussis is less fastidious and can grow on simple laboratory media such as nutrient agar.

What is the significance of phase variation in Bordetella?

When cultured in vitro, Bordetella species can undergo smooth-to-rough (S-to-R) phase variation from the virulent Phase I (expressing toxins and surface antigens) to the avirulent Phase IV due to the loss of surface virulence factors.

How does pertussis toxin exert its cellular effect?

The A-B toxin enters the host cell and catalyzes ADP-ribosylation of the inhibitory $G_i$ regulatory protein, preventing its normal function. This results in unchecked activation of adenylate cyclase, massive accumulation of intracellular cAMP, and disrupted cellular signaling.

Home › Microbiology › Bordetella pertussis and Bordetella parapertussis

Bordetella pertussis and Bordetella parapertussis

Bordetella pertussis, Bordetella parapertussis

For medical students2 min readUpdated 2026-10-10

Bordetella pertussis and Bordetella parapertussis are small, Gram-negative coccobacilli of the genus Bordetella that cause acute respiratory infections characterized by paroxysmal coughing. Bordetella pertussis is the primary human pathogen responsible for whooping cough.

FamilyAlcaligenaceae, genus Bordetella

TropismRespiratory ciliated epithelium

MorphologySmall Gram-negative coccobacilli

RespirationObligate aerobes

General Characteristics and Morphology

Bordetella pertussis (the causative agent of pertussis) and Bordetella parapertussis are bacteria that cause respiratory tract infections in humans. Historically, the organism was first isolated by J. Bordet and O. Gengou in 1906. These bacteria belong to the family Alcaligenaceae.

morphologically, they are very small Gram-negative rods (coccobacilli). They are non-motile and possess a microcapsule. When stained with toluidine blue, bipolar granules (accumulations of lipids that stain metachromatically) may be observed.

Culture Characteristics

Bordetellae are obligate aerobes. Bordetella pertussis is notoriously fastidious. Its growth requires complex media supplemented with adsorbents (blood, charcoal) because the bacterium produces toxic metabolites that inhibit its own growth. Classic media include:

Bordet-Gengou agar (containing blood, potato extract, and glycerol).
Charcoal-blood agar (CBA).

On Bordet-Gengou medium, B. pertussis colonies appear small, shiny, resembling "droplets of mercury" or "pearls." Bordetella parapertussis and other related species are less fastidious, grow faster, and can be cultured on simple media (such as nutrient agar).

Virulence Factors

The pathogenicity of Bordetella species is driven by adhesion factors and toxin production:

Adhesins: The key factor is filamentous hemagglutinin (FHA), which binds to glycolipid receptors on epithelial cilia. Pili, pertactin, and capsule agglutinogens also play a role.
Pertussis toxin (PT): Specific to B. pertussis. It ADP-ribosylates the inhibitory G-protein ($G_i$), leading to uncontrolled cAMP synthesis and causing systemic effects (lymphocytosis, histamine sensitization).
Tracheal cytotoxin: Damages ciliated cells, causing ciliostasis (cessation of ciliary movement) and epithelial necrosis.
Adenylate cyclase toxin: Increases intracellular cAMP and protects the bacteria from phagocytosis.

Epidemiology and Prevention

Pertussis is a strict human anthropanthroponosis. Transmission occurs via respiratory droplets. The infection is highly contagious (secondary attack rate of 0.75–0.9), particularly during the catarrhal stage. The disease poses the highest risk to infants under one year of age.

Prevention relies on the DTaP/DTwP vaccine, which contains killed B. pertussis cells (whole-cell) or purified acellular antigens. Acellular vaccines are less reactogenic but confer a less durable immunity.

Frequently asked questions

What are the clinical stages of pertussis?: Pertussis progresses through three distinct clinical stages. First is the incubation period, lasting about 7–10 days. Second is the catarrhal stage, characterized by mild upper respiratory symptoms, sneezing, and low-grade fever; patients are most contagious during this phase. Third is the paroxysmal stage, featuring severe paroxysms of coughing followed by a characteristic inspiratory "whoop," often complicated by hypoxia, post-tussive vomiting, and exhaustion.
Which specific antigens are included in the acellular pertussis vaccine?: The acellular pertussis vaccine typically contains up to five purified components derived from Bordetella pertussis: pertussis toxoid, filamentous hemagglutinin (FHA), pertactin, and type 2 and type 3 fimbriae.
What laboratory diagnostic methods are used to detect pertussis?: Laboratory confirmation utilizes culture isolation via nasopharyngeal swab plated onto selective media (e.g., Bordet-Gengou or charcoal agar). Rapid diagnostics include direct fluorescent antibody (DFA) staining or PCR detection of B. pertussis DNA in nasopharyngeal secretions. Retrospective diagnosis in later stages relies on serology (ELISA, agglutination tests).
How do the growth requirements of B. pertussis and B. parapertussis differ?: Bordetella pertussis grows only on complex media containing adsorbents (Bordet-Gengou agar, charcoal agar). Bordetella parapertussis is less fastidious and can grow on simple laboratory media such as nutrient agar.
What is the significance of phase variation in Bordetella?: When cultured in vitro, Bordetella species can undergo smooth-to-rough (S-to-R) phase variation from the virulent Phase I (expressing toxins and surface antigens) to the avirulent Phase IV due to the loss of surface virulence factors.
How does pertussis toxin exert its cellular effect?: The A-B toxin enters the host cell and catalyzes ADP-ribosylation of the inhibitory $G_i$ regulatory protein, preventing its normal function. This results in unchecked activation of adenylate cyclase, massive accumulation of intracellular cAMP, and disrupted cellular signaling.

Go deeper

Biochemical activity and differential species diagnosis
Mechanisms of genotypic and phenotypic variation
Pathogenesis of pertussis and disease stages
Mechanisms of specific immunity
Microbiological diagnostic methods for pertussis