title: High prevalence of genetically-determined mannose binding lectin deficiency in young children with invasive pneumococcal disease.
abstract: Susceptibility to invasive pneumococcal disease (IPD) correlates with age, younger children being the group with the highest burden of disease. The relevance of the innate immune response and particularly the role of mannose-binding lectin (MBL) in combating IPD is not well known. This is a 2-year prospective study (February 2011 to March 2013) including patients with IPD who attended two hospitals from Catalonia, Spain. Variables including attack rate of pneumococcal serotype (high or low invasive potential serotypes) and genotypes associated with low serum MBL levels were recorded. One hundred and forty-seven patients were included in the study. One hundred and two (69.4%) patients were children or adolescents <18 years and 45 (30.6%) were adults. Overall, low-MBL genotypes (O/O; XA/O) were detected in 23 (15.6%) patients. Children <2 years showed a higher frequency of low-MBL genotypes compared with other patients (31.0% vs. 11.9%; p = 0.031). Further sub-analysis revealed a higher proportion of low-MBL genotypes in children <2 years with IPD caused by opportunistic or low-attack-rate serotypes when compared with older patients (46.2% vs. 13.2%; p = 0.02). However, no statistically significant differences between the two groups were observed when including patients infected with invasive or high-attack-rate serotypes (18.8% vs. 10.0%; p = 0.59). Our data suggest that young children with a genetically determined low-MBL production are at a higher risk of developing IPD, particularly that caused by opportunistic or low-attack-rate pneumococcal serotypes.
authors.affiliation: Molecular Microbiology Department, Hospital Universitari Sant Joan de Deu and University of Barcelona, Esplugues, Spain.
authors.forename: C
authors.initials: C
authors.lastname: Muñoz-Almagro
authors.forename: C
authors.initials: C
authors.lastname: Bautista
authors.forename: M T
authors.initials: MT
authors.lastname: Arias
authors.forename: R
authors.initials: R
authors.lastname: Boixeda
authors.forename: E
authors.initials: E
authors.lastname: Del Amo
authors.forename: C
authors.initials: C
authors.lastname: Borrás
authors.forename: N
authors.initials: N
authors.lastname: Armiger
authors.forename: L
authors.initials: L
authors.lastname: Garcia
authors.forename: G
authors.initials: G
authors.lastname: Sauca
authors.forename: L
authors.initials: L
authors.lastname: Selva
authors.forename: M F
authors.initials: MF
authors.lastname: de Sevilla
authors.forename: P
authors.initials: P
authors.lastname: Ciruela
authors.forename: J C
authors.initials: JC
authors.lastname: Yebenes
authors.forename: R
authors.initials: R
authors.lastname: Pallares
authors.forename: F
authors.initials: F
authors.lastname: Lozano
mesh_terms: D000368:Aged; D002648:Child; D002675:Child, Preschool; D020022:Genetic Predisposition to Disease; D006801:Humans; D007223:Infant; D037601:Mannose-Binding Lectin / Q000097:blood / Q000172:deficiency / Q000235:genetics*; D008875:Middle Aged; D009894:Opportunistic Infections / Q000453:epidemiology / Q000235:genetics* / Q000382:microbiology; D011008:Pneumococcal Infections / Q000453:epidemiology / Q000235:genetics* / Q000382:microbiology; D020641:Polymorphism, Single Nucleotide; D015995:Prevalence; D011446:Prospective Studies; D065288:Serogroup; D013030:Spain / Q000453:epidemiology; D013296:Streptococcus pneumoniae / Q000302:isolation & purification*
chemical_list: C445619:MBL2 protein, human; D037601:Mannose-Binding Lectin
keywords: Streptococcus pneumoniae; molecular methods; paediatrics; pneumococcal disease