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Meningococcal disease associated with an acute post-streptococcal complement deficiency
Nikolaos Daskas1, Katie Farmer, Richard Coward
1Bristol Royal Hospital for Children, Bristol, UK.
Insights
Meningococcal disease typically results from chronic complement deficiencies. This study details a rare case in a child experiencing meningococcal disease due to a temporary complement deficiency linked to post-streptococcal glomerulonephritis.
Area of Science:
- Immunology
- Pediatrics
- Nephrology
Background:
- Complement pathway protein deficiencies increase meningococcal disease risk.
- Deficiencies are usually chronic, stemming from congenital issues or conditions like SLE and MPGN.
Observation:
- A child presented with meningococcal disease.
- The child had a transient complement deficiency.
Findings:
- The transient complement deficiency was caused by post-streptococcal glomerulonephritis (PSGN).
- This represents a novel cause of complement deficiency leading to meningococcal disease.
Implications:
- Highlights PSGN as a potential cause of transient complement deficiency.
- Suggests considering transient complement deficiencies in pediatric meningococcal disease cases.
- Expands understanding of complement deficiency in infectious disease susceptibility.
Abstract:
Chronic deficiencies in the complement pathway proteins are associated with an increased risk of meningococcal disease. Such deficiencies are caused by primary congenital immunodeficiency of a complement protein, properdin or mannose binding lectin, or are secondary to consumption of complement by systemic lupus erythematosus (SLE) or membranoproliferative glomerulonephritis (MPGN). Whatever the cause, the complement deficiency is always chronic. Here we report a case of meningococcal disease (MCD) in a child with a transient complement deficiency (CD), caused by post-streptococcal glomerulonephritis (PSGN).
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