• Infectious Disease Medicine
• Paediatrics
• Sepsis

It is now nearly 50 years since the description of staphylococcal toxic shock syndrome (TSS) in children by James Todd in 1978.1 Streptococcal TSS-like syndrome was first reported in 1987.2

TSS is now known to be caused by toxin-producing strains of Staphylococcus aureus and Groups A, C and G Streptococci, although several other organisms have also been associated with TSS.

It has subsequently become clear that this rare syndrome with high morbidity and mortality is due to a superantigen (SAg)-mediated process causing massive lymphocyte activation with uncontrolled cytokine release causing the clinical features which are well described.

SAgs produced by these organisms bind to major histocompatability complex (MHC) class II receptors on antigen presenting cells and interact with T cells via the T-cell receptor Vβ chain, inducing MHC-unrestricted T-cell activation and proliferation. The released cytokines, including interferon-γ, rapidly induce the release of tumour necrosis factor (TNF) and interleukin 1 (IL1), resulting in a cytokine storm, which leads to multiorgan dysfunction and shock.3

Intravenous immunoglobulin (IVIG) is a blood-derived product made from thousands of healthy blood samples. It contains mainly monomeric, purified, multispecific immunoglobulin G and smaller fractions containing other immunoglobulin isotypes and immune components. A dose of 2 g/kg of IVIG has hypothetical anti-inflammatory and immunomodulatory effects in the treatment of TSS, mainly including promoting antigen recognition and activating innate immune recognition. Additionally, IVIG has been shown to block the activity of …