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[Recurring meningococcal meningitis in hereditary C 5 deficiency]
Abstract:
Inherited deficiency of the 5th complement component (C5) was the cause of recurrent meningococcal meningitis in a woman aged 20 years. Familial investigations confirmed an autosomal co-dominant type of inheritance for the defect. Whereas additional loss of chemotaxis only exists with a genetic defect in C5 complement, bacteriolytic activity of serum is lacking in all genetic defects of the terminal complement components C5 to C8. An intact bacteriolysis, however, is necessary for resistance against Neisseria meningitidis and Neisseria gonorrhoeae. Neisseria infections, particularly recurrent meningococcal meningitis or disseminated gonococcal infections, suggest the presence of a congenital or acquired deficiency in one of the complement components C5 to C8.
Insights
A 20-year-old woman
Area of Science:
- Immunology
- Genetics
Background:
- The complement system is crucial for innate immunity.
- Deficiencies in terminal complement components (C5-C8) impair bacteriolysis.
- Neisseria infections are associated with complement deficiencies.
Observation:
- A 20-year-old woman experienced recurrent meningococcal meningitis.
- Familial studies revealed an autosomal co-dominant inheritance pattern for C5 deficiency.
Findings:
- Inherited C5 deficiency was identified as the cause of recurrent meningococcal meningitis.
- Serum bacteriolytic activity is absent in deficiencies of C5 to C8.
- C5 deficiency specifically impacts chemotaxis in addition to bacteriolysis.
Implications:
- Recurrent Neisseria infections suggest terminal complement component deficiencies (C5-C8).
- Diagnosis of C5 deficiency is critical for managing recurrent meningococcal meningitis.
- Understanding complement pathways aids in predicting and treating Neisseria infections.