The etiologic diagnosis of community-acquired pneumonia (CAP) remains challenging in children because blood cultures have low sensitivity. Novel approaches are needed to confirm the role of Streptococcus pneumoniae.
In this study, pneumococcal etiology was determined by serology using a subset of blood samples collected during a prospective multicentre observational study of children <15 years of age hospitalized in Belgium with radiogram-confirmed CAP. Blood samples were collected at admission and 3–4 weeks later. Pneumococcal (P)-CAP was defined in the presence of a positive blood or pleural fluid culture. Serotyping of S. pneumoniae isolates was done with the Quellung reaction. Serological diagnosis was assessed for 9 serotypes using World Health Organization–validated IgG and IgA serotype-specific enzyme-linked immunosorbent assays (ELISAs).
Paired admission/convalescent sera from 163 children were evaluated by ELISA (35 with proven P-CAP and 128 with nonproven P-CAP). ELISA detected pneumococci in 82.8% of patients with proven P-CAP. The serotypes identified were the same as with the Quellung reaction in 82% and 59% of cases by IgG ELISA and IgA ELISA, respectively. Overall, ELISA identified a pneumococcal etiology in 55% of patients with nonproven P-CAP. Serotypes 1 (51.6%), 7F (19%) and 5 (15.7%) were the most frequent according to IgG ELISA.
In conclusion, the serological assay allows recognition of pneumococcal origin in 55% of CAP patients with negative culture. This assay should improve the diagnosis of P-CAP in children and could be a useful tool for future epidemiological studies on childhood CAP etiology.
From the *Department of Pediatrics, Université Catholique Louvain, University Hospital Mont-Godinne, Yvoir; †Immunobiology Clinic, Hôpital Erasme; ‡Laboratory of Vaccinology and Mucosal Immunity, Université Libre de Bruxelles; §Department of Pediatric Pulmonology, Cystic Fibrosis Clinic and Pediatric Infectious Diseases, Universitair Ziekenhuis Brussel (UZ Brussel), Brussels; ¶Unité de Biostatistique et Documentation Médicale, Université Catholique Louvain, University Hospital Mont-Godinne, Yvoir; ‖Pediatric Infectious Disease Department, Infection Control and Hospital Epidemiology Unit, Université Libre de Bruxelles-Hôpital Universitaire des Enfants Reine Fabiola, Brussels; **Department of Pediatrics, Jessa Hospital, Hasselt; ††Bacterial Genetics and Physiology Laboratory, Université Libre de Bruxelles, Gosselies; ‡‡Department of Laboratory Medicine-Microbiology, Pneumococcal Reference Laboratory, Universitair Ziekenhuis Katholieke Universiteit Leuven, Leuven; and §§Pfizer, Inc., Brussels, Belgium.
D.T. and J.S. contributed equally to this work.
This study was presented in part at the 28th and 29th annual meetings of the European Society for Paediatric Infectious Diseases in Nice, France, in May 2010 and in The Hague, The Netherlands, in June 2011.
This work was supported by Pfizer, Inc. D.T. has received advisory board honoraria from GlaxoSmithKline Biologicals and Pfizer in the last 3 years. I.D.S. has been an invited speaker for Pfizer and has participated in advisory boards from GlaxoSmithKline Biologicals and Pfizer in the last 3 years. A.V. has received speaker and advisory board honoraria from GlaxoSmithKline Biologicals, MSD and Pfizer in the last 3 years. P.R.S. has received research funding from Pfizer. F.S. is a full-time employee of Pfizer. A.M. has received speaker and advisory board honoraria from GlaxoSmithKline Biologicals and Pfizer (including coordinating the advisory scientific board) in the last 3 years. F.M. has received advisory board honoraria from Pfizer in the last 3 years. The authors have no other funding or conflicts of interest to disclose.
Address for correspondence: David Tuerlinckx, MD, Cliniques Universitaires de Mont-Godinne, Département de pédiatrie, Avenue G. Thérasse 1, 5530 Yvoir, Belgium. E-mail: email@example.com.