Abstract

Toxic shock syndrome (TSS) is an uncommon complication of infection caused by streptococci and staphylococci. It is associated with a high mortality rate. When evaluating patients with shock symptoms from skin or soft tissue sources, a high index of suspicion for TSS must be maintained. Prompt diagnosis and integrative management with surgical intervention, antibiotics, hemodynamic stabilization, and adjuvants like intravenous immunoglobulins improve survival.

Highlights

  • BackgroundToxic shock syndrome (TSS) is a toxin-mediated disease, most commonly caused by invasive Group A streptococcal (GAS) and staphylococcal infections leading to immune activation and massive cytokine release

  • While streptococci are well known to cause a range of infections from benign pharyngitis to more serious conditions like endocarditis, scarlet fever, pneumonia, meningitis, osteomyelitis, rheumatic fever; skin infections like cellulitis, necrotizing fasciitis, myositis, and bacteremia; and septic shock [1], Streptococcal TSS may result from any condition caused by the streptococci

  • The superantigen binds and forms the superantigen-major histocompatibility (MHC) class-II complex with the MHC class-II, which binds to T cell receptors, leading to non-specific activation of T cells, leading to a massive release of pro-inflammatory cytokines, which are responsible for the systemic toxicity

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Summary

Introduction

Toxic shock syndrome (TSS) is a toxin-mediated disease, most commonly caused by invasive Group A streptococcal (GAS) and staphylococcal infections leading to immune activation and massive cytokine release. TSS's exact pathogenesis is unclear, but studies have shown a complex interplay between bacterial toxins and the body's response to the infection as the cause of the severity of the clinical manifestations seen [1]. The toxins that cause TSS are referred to as superantigen and include staphylococcal enterotoxins, toxic shock syndrome toxin-1 (TSST-1), and streptococcal pyrogenic exotoxins [4]. They are generated by toxigenic strains of Streptococcus pyogenes and Staphylococcus aureus that have acquired an underlying genetic material needed to transcribe the toxins from a plasmid or a bacteriophage. We aim to shed light on IVIG's use in its treatment, as it remains a serious and life-threatening condition

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