Mannose-binding lectin-deficient genotypes as a risk factor of pneumococcal meningitis in infants.
Carles Bautista-Rodriguez, Cristian Launes, Iolanda Jordan, Maria Andres, Maria Teresa Arias, Francisco Lozano, Juan Jose Garcia-Garcia, Carmen Muñoz-Almagro
Author Information
Carles Bautista-Rodriguez: Pediatrics Department, University Hospital Sant Joan de Deu, Barcelona, Spain.
Cristian Launes: Pediatrics Department, University Hospital Sant Joan de Deu, Barcelona, Spain.
Iolanda Jordan: CIBER de Epidemiologia y Salud Publica (CIBERESP), Instituto de Salud Carlos III, Madrid, Spain.
Maria Andres: CIBER de Epidemiologia y Salud Publica (CIBERESP), Instituto de Salud Carlos III, Madrid, Spain.
Maria Teresa Arias: Department of Immunology, Centre de Diagnostic Biomedic, Hospital Clinic of Barcelona, Barcelona, Spain.
Francisco Lozano: School of Medicine, University of Barcelona, Barcelona, Spain.
Juan Jose Garcia-Garcia: Pediatrics Department, University Hospital Sant Joan de Deu, Barcelona, Spain.
Carmen Muñoz-Almagro: CIBER de Epidemiologia y Salud Publica (CIBERESP), Instituto de Salud Carlos III, Madrid, Spain. ORCID
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.
