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Pathology 2 - Second Year BHMS

Contents

Pathology 2 - Second Year BHMS

Contents

CoursesBHMSPathology 2 - Second Year BHMSBORDETELLA PERTUSSIS

BORDETELLA PERTUSSIS

Content

BORDETELLA PERTUSSIS

  • Bordetella pertussis – gram‑negative, aerobic, non‑motile coccobacillus, 0.5‑1.5 µm, grows on Bordet‑Gengou or Regan‑Lowe medium with heated blood.

  • Causative agent of whooping cough (pertussis), highly contagious droplet infection.

  • Types of disease presentation

    • Classic (paroxysmal cough with whoop)
    • Atypical (mild, prolonged cough, often in adolescents)
  • Transmission → inhalation of droplets → bacteria reach ciliated epithelium of trachea/bronchi.

  • Pathogenesis (step‑wise)

    1. Adhesion → filamentous hemagglutinin (FHA) and pertactin bind to ciliary receptors.
    2. Colonization → microcolonies form on respiratory epithelium.
    3. Toxin production → pertussis toxin (PT), tracheal cytotoxin (TCT), adenylate cyclase toxin (ACT), dermonecrotic toxin.
    4. PT action → ADP‑ribosylates Gi proteins → ↑cAMP → lymphocytosis, systemic effects.
    5. TCT → destroys cilia → ciliostasis → impaired mucociliary clearance.
    6. ACT → inhibits phagocytosis, induces apoptosis of immune cells.
    7. Result → intense coughing, vomiting, possible hypoxia.
  • Memory trick for pathogenesis: “FAT‑CAT” → FHA/pertactin, Adhesion, Toxins, Cilia loss, ACT, Toxin effects.

  • Clinical manifestations

    • Incubation 7‑10 days (up to 21 days).
    • Catarrhal stage – mild rhinorrhea, low‑grade fever, occasional cough.
    • Paroxysmal stage – sudden bursts of cough → high‑pitched “whoop” on inspiration, post‑tussive vomiting, apnea in infants.
    • Convalescent stage – cough persists weeks‑months, may be triggered by cold air.
    • Complications – pneumonia, rib fractures, pulmonary hemorrhage, encephalopathy, seizures, secondary bacterial infection, death in infants.
  • Laboratory diagnosis

    • Culture → Bordet‑Gengou or Regan‑Lowe agar, 37 °C, 5‑7 days → tiny dew‑drop colonies.
    • PCR → detection of IS481, pertussis toxin gene from nasopharyngeal swab/aspirate; rapid, high sensitivity.
    • Serology → ELISA for anti‑pertussis toxin IgG (single high titre or four‑fold rise) – useful after 3 weeks of illness.
    • Peripheral blood smear → marked lymphocytosis (especially in infants) – supportive clue.
  • Management

    • Early macrolides – erythromycin 40 mg/kg/day in 4 doses for 14 days or azithromycin 10 mg/kg day 1 then 5 mg/kg daily for 4 days → reduces transmission, may shorten cough if given ≤3 weeks.
    • Trimethoprim‑sulfamethoxazole – alternative for macrolide‑resistant strains.
    • Supportive care – hydration, antipyretics, monitor infant apnea, oxygen if needed.
    • Vaccination – whole‑cell (wP) and acellular (aP) vaccines; aP contains detoxified PT, FHA, pertactin, fimbriae. Primary series at 6, 10, 14 weeks; boosters at 18 months, 5 years; Tdap in adolescents/adults.
  • Prevention

    • High vaccine coverage → herd immunity.
    • Chemoprophylaxis for close contacts – single dose azithromycin or erythromycin.
  • Key exam points from textbooks

    • Robbins – PT mechanism (ADP‑ribosylation of Gi) → lymphocytosis.
    • Harsh Mohan – description of catarrhal, paroxysmal, convalescent stages.
    • Ananthanarayan & Paniker – culture media, characteristic colony morphology.
    • Chatterjee – role of FHA and pertactin in adhesion.
    • NCH – vaccination schedule, management of infant apnea.