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Review
. 2018 Sep 17;8(1):88.
doi: 10.1186/s13613-018-0438-y.

Streptococcal toxic shock syndrome in the intensive care unit

Affiliations
Review

Streptococcal toxic shock syndrome in the intensive care unit

Marylin Schmitz et al. Ann Intensive Care. .

Abstract

The streptococcal toxic shock syndrome is a severe complication associated with invasive infections by group A streptococci. In spite of medical progresses in the care of patients with septic shock during the last decades, this condition has remained associated with a high mortality. Early recognition and multidisciplinary management are key to the care of patients with streptococcal toxic shock syndrome, with intensive and appropriate intensive support of failing organs, rapid diagnosis of infectious source(s), and surgical management. The epidemiology and risk factors for streptococcal toxic shock syndrome remain to be better studied, including the possible causal role of exposure to nonsteroidal anti-inflammatory drugs. In this review article, the authors review the current knowledge of streptococcal toxic shock syndrome and discuss the pathophysiology as well as its supportive and specific treatment.

Keywords: Bacterial toxins; Group A streptococcus; Necrotizing fasciitis; Sepsis; Streptococcal toxic shock syndrome.

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Figures

Fig. 1
Fig. 1
Palmar desquamation occurring a few days after STSS
Fig. 2
Fig. 2
Muscle necrosis (black) of a thigh during surgical debridement in a patient with toxic streptococcal toxic shock syndrome due to S. pyogenes necrotizing fasciitis
Fig. 3
Fig. 3
Schematic representation of T cell activation by a conventional peptide antigen (orange) and by a superantigen, binding unspecifically MHCII and T cell receptor, resulting to a massive, multiclonal release of T cell mediators and pro-inflammatory cytokines, in contrast to regulated, antigen-dependent inflammatory response during a conventional T cell activation, with activation of a single T cell clone. APC antigen-presenting cell, TcR T cell receptor, MHCII major histocompatibility class II molecule, TNF-α tumor necrosis factor alpha, IFN-γ interferon gamma, IL interleukin

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