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Familial late complement component (C6, C7) deficiency with chronic meningococcemia

J D Clough, M L Clough, A Weinstein

    Archives of Internal Medicine
    |July 1, 1980
    PubMed
    Summary

    Two patients with chronic meningococcemia lacked hemolytic complement due to C6 or C7 deficiency. These autosomal co-dominant traits did not affect their recovery after antibiotic treatment.

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    Area of Science:

    • Immunology
    • Complement System Biology
    • Molecular Immunology

    Background:

    • Chronic meningococcemia is a rare but serious bacterial infection.
    • The complement system plays a crucial role in host defense against Neisseria meningitidis.
    • Deficiencies in terminal complement components are associated with increased susceptibility to meningococcal disease.

    Observation:

    • Two patients with chronic meningococcemia presented with a complete lack of hemolytic complement activity.
    • Genetic analysis revealed C6 deficiency in one patient and C7 deficiency in the other.
    • Family studies indicated autosomal co-dominant inheritance patterns for both C6 and C7 deficiencies, independent of HLA linkage.

    Findings:

    • Complement-deficient sera from these patients supported monocyte chemotaxis.

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  • However, these sera failed to mediate phagocytosis or lysis of meningococci.
  • Antibiotic treatment led to successful recovery in both individuals.

    • Implications:

    • This study highlights the critical role of terminal complement components (C6 and C7) in protecting against Neisseria meningitidis infections.
    • Understanding the genetic basis and functional consequences of complement deficiencies is vital for managing recurrent meningococcal disease.
    • Despite complement deficiencies, effective antibiotic therapy can resolve chronic meningococcemia, suggesting a multifaceted approach to treatment.