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24009156
Intraclonal variations among Streptococcus pneumoniae isolates influence the likelihood of invasive disease in children.

J Infect Dis, 2014/2/01;209(3):377-88.

Browall S[1], Norman M, Tångrot J, Galanis I, Sjöström K, Dagerhamn J, Hellberg C, Pathak A, Spadafina T, Sandgren A, Bättig P, Franzén O, Andersson B, Örtqvist Å, Normark S, Henriques-Normark B

Affiliations

PMID: 24009156DOI: 10.1093/infdis/jit481

Impact factor: 7.759

Abstract
background: Pneumococcal serotypes are represented by a varying number of clonal lineages with different genetic contents, potentially affecting invasiveness. However, genetic variation within the same genetic lineage may be larger than anticipated.
methods: A total of 715 invasive and carriage isolates from children in the same region and during the same period were compared using pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing. Bacterial genome sequencing, functional assays, and in vivo virulence mice studies were performed.
results: Clonal types of the same serotype but also intraclonal variants within clonal complexes (CCs) showed differences in invasive-disease potential. CC138, a common CC, was divided into several PFGE patterns, partly explained by number, location, and type of temperate bacteriophages. Whole-genome sequencing of 4 CC138 isolates representing PFGE clones with different invasive-disease potentials revealed intraclonal sequence variations of the virulence-associated proteins pneumococcal surface protein A (PspA) and pneumococcal choline-binding protein C (PspC). A carrier isolate lacking PcpA exhibited decreased virulence in mice, and there was a differential binding of human factor H, depending on invasiveness.
conclusions: Pneumococcal clonal types but also intraclonal variants exhibited different invasive-disease potentials in children. Intraclonal variants, reflecting different prophage contents, showed differences in major surface antigens. This suggests ongoing immune selection, such as that due to PspC-mediated complement resistance through varied human factor H binding, that may affect invasiveness in children.

Keywords: PcpA; PspA; PspC; Streptococcus pneumoniae; bacteriophages; factor H binding; intraclonal variation; invasive disease potential; pneumococcal infections; surface proteins

MeSH terms
Adolescent; Animals; Antigens, Bacterial; Carrier State; Child; Child, Preschool; Disease Models, Animal; Electrophoresis, Gel, Pulsed-Field; Female; Genetic Variation; Genome, Bacterial; Genotype; Humans; Infant; Male; Membrane Proteins; Mice; Mice, Inbred C57BL; Molecular Typing; Pneumococcal Infections; Prophages; Sequence Analysis, DNA; Streptococcus Phages; Streptococcus pneumoniae; Virulence
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