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Pathology and pathogenesis of fatal Bordetella pertussis infection in infants

Christopher D Paddock1, Gary N Sanden, James D Cherry

  • 1Infectious Disease Pathology Branch, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA. cpaddock@cdc.gov

Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America
|June 19, 2008
PubMed

Insights

Bordetella pertussis pneumonia in infants causes severe pulmonary hypertension through airway inflammation and increased leukocytes. This study details the pathology, offering insights into infant deaths from pertussis.

Area of Science:

  • Pediatric Pathology
  • Infectious Diseases
  • Pulmonary Medicine

Background:

  • Bordetella pertussis infection causes significant infant mortality worldwide.
  • Pulmonary hypertension is a common, severe complication in infants with pertussis, but its mechanisms are poorly understood.
  • Previous pathological descriptions of pertussis in infants are outdated.

Purpose of the Study:

  • To characterize the pulmonary pathology in infants who died from Bordetella pertussis pneumonia.
  • To elucidate the pathophysiological mechanisms underlying pulmonary hypertension in these cases.

Main Methods:

  • Autopsy respiratory tissue samples from 15 infants (
  • Histochemical stains, immunohistochemical evaluation, and electron microscopy were employed.
  • A novel immunohistochemical stain for B. pertussis was utilized.

Main Results:

  • Pulmonary findings included necrotizing bronchiolitis, intra-alveolar hemorrhage, and fibrinous edema.
  • Marked leukocytosis and leukocyte aggregates in pulmonary vasculature were observed.
  • Extracellular and intracellular B. pertussis bacteria and antigens were identified in respiratory tissues and macrophages.

Conclusions:

  • Pertussis should be considered in infant deaths with leukocytosis, bronchopneumonia, or pulmonary hypertension.
  • B. pertussis pneumonia likely triggers pulmonary vasoconstriction and increased leukocyte mass via pertussis toxin.
  • These events compromise pulmonary blood flow, worsen hypoxemia, and drive refractory pulmonary hypertension.
Abstract

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