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Related Experiment Videos

Primary immunodeficiencies associated with pneumococcal disease.

Capucine Picard1, Anne Puel, Jacinta Bustamante

  • 1Pediatric Immunology-Hematology Unit, Necker-Enfants Malades Hospital, University of Paris René Descartes, Paris, France, EU. picardc@necker.fr

Current Opinion in Allergy and Clinical Immunology
|November 13, 2003
PubMed
Summary
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Certain primary immunodeficiencies, especially B-cell defects and complement deficiencies, significantly increase the risk of pneumococcal disease. Understanding these predispositions aids in diagnosing and managing infections in vulnerable patients.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Genetics

Background:

  • Primary immunodeficiencies (PIDs) encompass over 100 distinct conditions.
  • Streptococcus pneumoniae infections, particularly invasive pneumococcal disease, pose a significant threat to individuals with PIDs.
  • Previous reviews have not specifically detailed which PIDs confer the highest risk for pneumococcal infections.

Purpose of the Study:

  • To identify and review primary immunodeficiencies that predispose individuals to Streptococcus pneumoniae infections.
  • To emphasize the association between specific PIDs and invasive pneumococcal disease.
  • To synthesize current knowledge on the immunological mechanisms underlying pneumococcal susceptibility in PIDs.

Main Methods:

  • Systematic review of medical literature.

Related Experiment Videos

  • Analysis of case studies detailing S. pneumoniae infections in patients with PIDs.
  • Focus on identifying patterns of increased risk for invasive pneumococcal disease.

    • Main Results:

    • High-risk PIDs include most B-cell defects, classical complement pathway deficiencies, C3 deficiency, congenital asplenia, anhidrotic ectodermal dysplasia with immunodeficiency (NF-kappaB pathway), and interleukin-1 receptor associated kinase-4 deficiency.
    • Patients with alternative/third pathway complement deficiencies and hyperimmunoglobulin E syndrome have a lower risk.
    • Phagocytic disorders do not appear to confer a particular vulnerability to S. pneumoniae.

    Conclusions:

    • Protective immunity against S. pneumoniae relies on antibody and complement-mediated opsonization, splenic macrophages, and IL-1R-associated kinase-4 and NF-kappaB signaling pathways.
    • Identifying high-risk PIDs is crucial for the diagnostic workup of patients presenting with pneumococcal disease.
    • This review enhances understanding of human immunity to S. pneumoniae and informs clinical practice.