Epidemiology


Etiology


  • Pathogen: Bordetella pertussis is a gram‑negative, obligate aerobic coccobacillus.

Pathophysiology


  • Proliferation of Bordetella pertussis on ciliated epithelial cells of the respiratory mucosa → production of virulence factors (e.g., tracheal cytotoxin) → paralysis of respiratory epithelium cilia and inflammation → secretion of inflammatory exudate into respiratory tract → compromise of small airways → cough, pneumonia, cyanosis
  • Bordetella pertussis produces pertussis toxin → ADP-ribosylation of the α subunit of Gi protein → inhibition of Gi protein → adenylate cyclase disinhibition → cAMP accumulation → impaired cell signaling pathways → systemic manifestations associated with whooping cough (e.g., hypoglycemia, lymphocytosis, modulation of host immune response)

Clinical features


  • Catarrhal (1-2 weeks): mild cough, rhinitis
  • Paroxysmal (2-6 weeks): severe coughing spells with inspiratory whoop, posttussive emesis (risk of dehydration); ± apnea/cyanosis (infants)
    • Lungs are usually clear to auscultation
  • Convalescent (weeks to months): gradual resolution

Diagnostics


  • Diagnosis is primarily clinical, supported by lab findings.
  • PCR of a nasopharyngeal swab is the gold standard for confirmation.
  • Culture on specialized media like Bordet-Gengou or Regan-Lowe agar is possible but less sensitive.
  • CBC often shows a marked lymphocytosis, which is unusual for a bacterial infection.
    • Pertussis toxin causes lymphocytosis by preventing lymphocytes from entering lymphoid tissues.
  • Serology can be useful later in the disease course (>4 weeks).

Differential diagnostics

  • Viral URIs: Pertussis cough progressively worsens instead of improving.
  • Mycoplasma pneumoniae: Also causes a persistent cough but typically without the “whoop” or post-tussive emesis.

Treatment

  • First-Line Antibiotic Therapy:
    • MacrolidesAzithromycin (5 days), Clarithromycin, or Erythromycin.
    • Infants < 1 monthAzithromycin is required (Erythromycin is contraindicated due to increased risk of hypertrophic pyloric stenosis).
    • Clinical Note: Antibiotics eradicate the organism and prevent transmission; they do not alter the clinical course if started during the paroxysmal phase.
  • Alternative Therapy:
    • Trimethoprim-sulfamethoxazole (TMP-SMX) if macrolide-allergic (contraindicated in infants < 2 months).
  • Post-Exposure Prophylaxis (PEP):
    • Macrolide for ALL close contacts regardless of vaccination status. c
      • Adult family members can act as asymptomatic reservoirs and infect others
  • Prevention:
    • DTaP series: 5 doses in infancy/childhood (2, 4, 6, 15-18 months, 4-6 years).
    • Tdap booster: At age 11-12 years, then every 10 years (Td or Tdap). c
    • Pregnancy: Tdap administered during every pregnancy (preferably 27-36 weeks GA) to confer passive immunity to the newborn.