Bordetella pertussis: Morphology and Identification, Antigenic Structure, Pathogenesis and Pathology, Clinical Findings, Diagnostic Laboratory Tests, Immunity, Treatment, Flashcards
(9 cards)
Bordetella pertussis: morphology and identification
Bordetella pertussis is a small, encapsulated, Gram-negative coccobacillus. It is strictly aerobic and non-motile. It grows on Bordet-Gengou agar or Regan-Lowe charcoal agar. Colonies appear small, smooth, and silver on specialized media. It does not ferment carbohydrates and is oxidase and catalase positive.
Bordetella pertussis: antigenic structure
The bacterium expresses several important antigens: pertussis toxin (PT), filamentous hemagglutinin (FHA), pertactin, fimbriae, adenylate cyclase toxin, and tracheal cytotoxin. These surface and secreted proteins are virulence factors and targets of immune responses. PT is an A-B toxin and key immunogen in vaccines.
Bordetella pertussis: pathogenesis and pathology
B. pertussis attaches to the ciliated respiratory epithelium via adhesins (FHA, fimbriae, pertactin). Pertussis toxin inhibits G-proteins, impairing immune cell function and causing lymphocytosis. Adenylate cyclase toxin increases cAMP, impairing phagocytes. Tracheal cytotoxin kills ciliated cells. The result is mucociliary clearance disruption, inflammation, and persistent cough.
Bordetella pertussis: clinical findings
Pertussis progresses through 3 stages: 1) Catarrhal stage – mild cough, runny nose, highly contagious; 2) Paroxysmal stage – severe spasmodic coughing fits with inspiratory whoop, vomiting, and lymphocytosis; 3) Convalescent stage – gradual recovery over weeks. Infants may develop apnea or severe complications like pneumonia, seizures, and encephalopathy.
Bordetella pertussis: diagnostic laboratory tests
Nasopharyngeal swab or aspirate is collected. Culture on Regan-Lowe or Bordet-Gengou medium is diagnostic but slow (3–7 days). PCR is rapid and sensitive. Direct fluorescent antibody staining and serology can also be used. Leukocytosis with lymphocyte predominance is characteristic.
Bordetella pertussis: immunity
Infection induces incomplete immunity that wanes over time. Vaccination induces antibody and memory response, especially against pertussis toxin, FHA, and pertactin. Neither natural infection nor vaccination provides lifelong protection. Booster doses are required.
Bordetella pertussis: treatment
Macrolides (azithromycin, clarithromycin, or erythromycin) are effective, especially during the catarrhal stage. Antibiotics reduce transmission but do not affect symptoms during the paroxysmal stage. Supportive care (e.g., oxygen, hydration) is critical in infants.
Bordetella pertussis: prevention
Vaccination is the primary prevention method. The acellular pertussis vaccine (DTaP or Tdap) contains inactivated pertussis toxin, FHA, pertactin, and fimbriae. DTaP is given to children; Tdap booster is for adolescents and adults. Cocooning (vaccinating close contacts) protects infants. Pregnant women should receive Tdap during each pregnancy.
Bordetella parapertussis: characteristics and clinical relevance
Bordetella parapertussis is similar in morphology to B. pertussis but causes a milder form of whooping cough. It lacks pertussis toxin but produces similar adhesins. It is less virulent and less contagious. It can be identified by PCR or culture. Immunity from pertussis vaccine does not reliably protect against B. parapertussis.