Similarities and Differences Between Staphylococcal and Streptococcal Toxic Shock Syndromes in Children: Results From a 30-Case Cohort.

Michèle Bes,Frédéric Laurent,Pierre-Adrien Bolze,Anne Tristan,Gerard Lina,Yves Gilletand,Cédric Badiou,François Vandenesch,Olivier Dauwalder,Etienne Javouhey,Claire Poyart,Aurelie Portefaix,Claire Jamen

doi:10.3389/fped.2018.00360

Abstract

Introduction: Toxic shock syndromes (TSS) are severe shocks due to staphylococcal or streptococcal infection that require specific treatments. The early recognition of these shocks is crucial to improve their outcomes.Objectives: The primary objective of this study was to compare characteristics and outcomes of staphylococcal and streptococcal TSS in children, in order to identify putative early clinical diagnostic criteria. Secondary objectives were to determine the toxin gene profiles of associated isolated strains and the relevance of measuring Vβ T-cell signatures to confirm the diagnosis.Study design: We performed a multicenter retrospective evaluation of clinical data, biological results, and treatment outcomes of children with a confirmed or probable case of staphylococcal or streptococcal TSS. Children were consecutively included if they were admitted to the pediatric intensive care units of Lyon (France), between January 2005 and July 2011.Results: Among the 30 analyzed children, 15 presented staphylococcal TSS and 15 streptococcal TSS. The most frequent origin of staphylococcal and streptococcal TSS was the lower respiratory tract (53%) and the genital tract (47%) respectively. Non-menstrual TSS syndrome cases presented more frequently with neurological alterations, and digestive signs were predominant in menstrual forms. Compared to Staphylococcal TSS, Streptococcal TSS presented with higher organ dysfunction scores (median Pediatric Index of Mortality 2 score 20.9 (4.1–100) vs. 1.7 (1.3–2.3), p = 0.001), required respiratory support more frequently (80 vs. 33%, p = 0.02), were intubated for a longer time (3 days (0.75–5) vs. 1 day (0–1.5), p = 0.006) and had a non-significant trend of higher, case-fatality rate (20 vs. 7%, p = 0.60). The lack of antitoxin therapy was associated with higher case-fatality rate (50 vs. 4%, p = 0.04). The Vβ repertoire measurements exhibited toxin dependent-alterations in accordance with the toxin gene profiles of isolated strains in both types of toxic shock syndromes. Regarding toxin gene profiles of isolated strains, 10/15 Staphylococcus aureus belonged to clonal complex (CC) 30 and 6/12 Streptococcus pyogenes were emm1 type suggesting clonal etiologies for both staphylococcal and streptococcal TSS.Conclusion: Despite the involvement of functionally similar toxins, staphylococcal and streptococcal TSS differed by their clinical signs, origin of infection and prognosis. The detection of Vβ profiles was useful to confirm the diagnosis of staphylococcal and streptococcal TSS and for the identification of involved toxins.

Highlights

Toxic shock syndromes (TSS) are severe shocks due to staphylococcal or streptococcal infection that require specific treatments
15 Str-TSS cases (11 confirmed and 4 probable cases according to the CDC criteria) and 15 Sta-TSS cases, 6 of which were menstrual Sta-TSS and 9 non-menstrual Sta-TSS (4 confirmed cases and 8 probable cases according to the CDC criteria) were included
We showed that the detection of Vβ profiles could confirm the diagnosis of Staphylococcal and Streptococcal TSS cases, signing a toxin involvement, correlated to the toxin gene profile of the isolated strains

Summary

Introduction

Toxic shock syndromes (TSS) are severe shocks due to staphylococcal or streptococcal infection that require specific treatments. Superantigens (SAg), in contrast with conventional antigens, do not need to be processed by antigen-presenting cells before being presented to T cells They instead directly stimulate T cells by cross-linking major histocompatibility complex class II molecules on the antigen-presenting cells with the variable portion of the T-cell antigen receptor chain (Vβ TCR), thereby inducing massive polyclonal cell proliferation [9, 10]. Due to their structural differences, each SAg links preferentially to one or several Vβ repertoire, inducing targeted T cell expansion and the massive pro-inflammatory response [11]. A transient depletion of targeted Vβ TCRs may be observed at the early phase of TSS due to the concomitant lymphopenia, to the mobilization/accumulation of T cells from peripheral blood to lymph nodes or to the spleen, and/or from downregulation of TCR molecules binding the toxin targeted Vβ repertoire(s) soon after T cell activation [12]

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