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. 2022 Sep 10;75(4):719-722.
doi: 10.1093/cid/ciac079.

Endocarditis Caused by Nontypeable Streptococcus pneumoniae

Stefanie S V Henriet  1 , Jeroen D Langereis  2 , Stephanie W Lo  3 , Stephen Bentley  3 , Rob J Mesman  4 , Zina Fejzic  5 , Laura van Niftrik  4 , Nina M van Sorge  6 , Heiman F L Wertheim  7 , Marien I de Jonge  2 , Amelieke J H Cremers  7
Affiliations

Endocarditis Caused by Nontypeable Streptococcus pneumoniae

Stefanie S V Henriet et al. Clin Infect Dis. .

Abstract

The Streptococcus pneumoniae capsule is regarded as indispensable in bacteremia. We report an infant with a ventricular septal defect and infective endocarditis caused by nontypeable S. pneumoniae. In-depth investigation confirmed a deficient capsule yet favored pneumococcal fitness for causing infective endocarditis, rather than a host immune disorder, as the cause of infective endocarditis in this case.

Keywords: Streptococcus pneumoniae; bacterial polysaccharide capsule; infective endocarditis; pathogenesis.

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Conflict of interest statement

Potential conflicts of interest. N. M. v. S. reports that patent WO 2013/020090 A3 has been licensed by the company Vaxcyte, generating royalties when milestones are reached and royalties from a patent on vaccine development against Streptococcus pyogenes, not part of the work submitted here (licensee University of California San Diego inventors, N. M. v. S. and Victor Nizet). N. M. v. S. also reports consulting fees from MSD (fee for service paid directly to the institution, related to pneumococcal invasive disease, and consulting fee for an expert panel) and GlaxoSmithKline (fee for service paid directly to the institution, related to pneumococcal invasive disease); payment or honoraria from MSD for expert meeting contribution on pneumococcal disease); and personal stocks from GenMab, Bank of America, and exchange-traded funds. All other authors report no potential conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.

Figures

Figure 1.
Figure 1.
Experimental examination of the pneumococcal endocarditis isolate compared with 2 Streptococcus pneumoniae serotype 38 wcyV wild-type blood isolates. A, Pneumococcal capsule encoding sequence. Capsular biosynthesis genes of the pneumococcal study isolates compared with the S. pneumoniae serotype 38 cps reference sequence. Genes are represented as arrows on the forward and reverse strands, with functional annotation indicated above. Gray blocks indicate regions of sequence similarity, and the white gap (ie, no similarity) within wcyV indicates a 92–base pair deletion in the wcyV gene of the endocarditis isolate compared with the wild-type wcyV sequence present in the 2 selected comparator blood isolates. B–G, Pneumococcal capsular phenotype. Polysaccharide capsule surrounding the cells of the pneumococcal study isolate as visualized by transmission electron microscopy of ultrathin sections of chemically fixed and resin-embedded cells; scale bars represent 200 nm. The endocarditis isolate (D, G) demonstrates loss of capsule compared with wild-type isolates 1 (B, E) and 2 (C, F). H–J, Host-pathogen interaction ex vivo. H, Immunoglobulin G (IgG) deposition to the bacterial surface determined by flow cytometry. I, Percentage survival of the S. pneumoniae isolates in whole blood. J, Adhesion of S. pneumoniae isolates to human umbilical vein endothelial cells (HUVECs) (n = 8). Closed circles represent plasma specimens from healthy controls; open circles, plasma from the patient with endocarditis. For each plasma sample, the average of 4 experiments was used to determine statistical significance. Abbreviations: AU, arbitrary units; NS, not significant. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001 (1-way analysis of variance with Tukey post hoc test).
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