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Mannose-binding lectin-deficient genotypes as a risk factor of pneumococcal meningitis in infants
Carles Bautista-Rodriguez1, Cristian Launes1,2, Iolanda Jordan2,3,4
1Pediatrics Department, University Hospital Sant Joan de Deu, Barcelona, Spain.
Insights
Mannose-binding-lectin deficient genotypes increase the risk of pneumococcal meningitis in infants under 12 months. These genetic variations are linked to severe cases, particularly those caused by less invasive pneumococcal serotypes.
Area of Science:
- Immunogenetics
- Pediatric Infectious Diseases
- Microbial Pathogenesis
Background:
- Pneumococcal meningitis (PM) remains a significant cause of childhood morbidity and mortality.
- Mannose-binding lectin (MBL) plays a crucial role in innate immunity against bacterial pathogens like Streptococcus pneumoniae.
- MBL deficiency, often due to MBL2 gene polymorphisms, can impair immune responses.
Purpose of the Study:
- To investigate the association between MBL2 genotypes and the susceptibility to pneumococcal meningitis in pediatric patients.
- To determine if MBL deficiency influences the clinical presentation and outcomes of pneumococcal meningitis in children.
Main Methods:
- A 16-year retrospective study (2001-2016) of pediatric patients (≤18 years) diagnosed with pneumococcal meningitis.
- Analysis of pneumococcal serotype invasiveness and MBL2 genotypes associated with low serum MBL levels.
- Comparison of MBL2 genotype frequencies between age groups and clinical subgroups.
Main Results:
- Of 48 patients, 18.8% carried MBL2 deficient genotypes.
- Children ≤12 months old had a 7-fold increased risk of carrying MBL2 deficient genotypes compared to older children (p < 0.01).
- MBL2 deficient genotypes were more prevalent in infants ≤12 months with PM caused by opportunistic serotypes (54.5%) and those admitted to the Pediatric Intensive Care Unit (46.7%).
Conclusions:
- MBL2 genotype variations significantly impact susceptibility to pneumococcal meningitis in children under 12 months.
- MBL deficiency may play a role in the pathogenesis of PM, especially when caused by less invasive pneumococcal serotypes.
Objectives:
The objective of this study was to evaluate to evaluate the role of mannose-binding-lectin deficient genotypes in pneumococcal meningitis (PM) in children.
Methods:
We performed a 16-year retrospective study (January 2001 to March 2016) including patients ≤ 18 years with PM. Variables including attack rate of pneumococcal serotype (high or low invasive capacity) and MBL2 genotypes associated with low serum MBL levels were recorded.
Results:
Forty-eight patients were included in the study. Median age was 18.5 months and 17/48 episodes (35.4%) occurred in children ≤ 12 months old. Serotypes with high-invasive disease potential were identified in 15/48 episodes (31.2%). MBL2 deficient genotypes accounted for 18.8% (9/48). Children ≤ 12 months old had a 7-fold risk (95% CI: 1.6-29.9; p < 0.01) of having a MBL2 deficient genotype in comparison to those > 12 months old. A sub-analysis of patients by age group revealed significant proportions of carriers of MBL2 deficient genotypes among those ≤ 12 months old with PM caused by opportunistic serotypes (54.5%), admitted to the PICU (Pediatric Intensive Care Unit) (46.7%) and of White ethnicity (35.7%). These proportions were significantly higher than in older children (all p<0.05).
Conclusions:
Our results suggest that differences in MBL2 genotype in children ≤12 months old affects susceptibility to PM, and it may have an important role in the episodes caused by non-high invasive disease potential serotypes.
