Usefulness of analysis of the Vbeta repertoire of T cells for the early diagnosis of staphylococcal and streptococcal toxic shock syndrome
Abstract number: 1732_65
Guillaume C., Thomas D., Ferry T., Perpoint T., Richard J.C., Allaouchiche B., Vandenesch F., Peyramond D., Etienne J.
Objectives: Staphylococcal and streptococcal toxic-shock syndrome (TSS) are severe illnesses associated with the production of superantigenic toxins, which activate specific fractions of the T-cell population by linking the Vbeta domain of the T-cell receptor. Each superantigenic toxin is associated with a characteristic Vbeta ``signature'' in vitro. We postulate that an early analysis of the Vbeta repertoire of T cells in vivo during TSS may facilitate the diagnosis and the introduction of antitoxinic agents.
Methods: We have prospectively included in 2005 and 2006 patients with streptococcal or staphylococcal TSS according to case definition. The Vbeta repertoire of T cells (24 Vbeta segments) was analysed by flow cytometry with fresh PBMC obtained in the first 48 hours of admission. The presence of each superantigenic toxin gene in S. aureus and S. pyogenes isolates were detected by PCR.
Results: Four patients with staphylococcal (three menstrual and one non-menstrual) and two patients with streptococcal TSS (one postpartal and another associated with S. pyogenes bloodstream infection) were included in the study.
In cases of menstrual S. aureus TSS, a Vbeta 2 expansion corresponding to the signature of TSST-1, was detected at admission. Corresponding isolates were positive for the gene encoding TSST-1. A Vbeta amplification corresponding to the signature of SEB was detected in the patient with staphylococcal non-menstrual TSS. The corresponding isolate was positive for the gene encoding SEB but also genes encoding SEA and SED. All patients received clindamycin, when cultures detected S. aureus (none received linezolid as all isolates were susceptible to methicillin), and the latter received intravenous immunoglobulins (IVIg).
In cases of S. pyogenes TSS, a Vbeta signature of SPEB was detected in the patient with the postpartal TSS. No Vbeta signature was detected in the other patient who developped severe disseminated intravascular coagulation requiring limb amputations. The two corresponding isolates were positive for the gene encoding SPEB. All patients with streptococcal TSS received clindamycin and IVIg when cultures detected S. pyogenes.
Conclusion: The analysis of the Vbeta repertoire in patients with staphylococcal and streptococcal TSS may be a useful tool for the early diagnosis, apart in the case of associated severe bloodstream infection. Such analysis may facilitate the early introduction of anti-toxinic agents such as clindamycin, linezolid or IVIg.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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