Intravenous Immunoglobulin Therapy for Streptococcal Toxic Shock Syndrome—A Comparative Observational Study

Abstract

Twenty-one consecutive patients with streptococcal toxic shock syndrome (TSS) between December 1994 and April 1995 were treated with a median dose of 2 g of intravenous immunoglobulin (IVIG)/kg (cases) and were compared with 32 patients with streptococcal TSS between 1992 and 1995 who did not receive IVIG therapy (controls). The outcome measure was 30-day survival. Patient plasma was tested for its ability to inhibit T cell activation induced by the infecting strain. The proportion of cases with 30-day survival was higher than that of the controls with 30-day survival (67% vs. 34%, respectively; P Å .02). Multivariate analysis revealed that IVIG administration and a lower Acute Physiology and Chronic Health Evaluation II score were associated with survival; the odds ratio for survival associated with IVIG therapy was 8.1 (95% confidence interval, 1.6 -45; P Å .009). IVIG therapy enhanced the ability of patient plasma to neutralize bacterial mitogenicity and reduced T cell production of interleukin-6 and tumor necrosis factor a. IVIG may be an effective adjunctive therapy for streptococcal TSS, possibly because of its ability to neutralize bacterial exotoxins.Streptococcal toxic shock syndrome (TSS) is the most severe tion and cytokine production [7]. Administration of intravenous immunoglobulin (IVIG) can block in vitro T cell activation by manifestation of invasive disease due to group A streptococcus (GAS); the case-fatality rate associated with streptococcal TSS staphylococcal and streptococcal superantigens [8 -10]. Several case reports have been published in which IVIG adminisis as high as 81% [1 -6]. The mechanism whereby gram-positive organisms cause shock is as yet not determined, but there tration in the setting of streptococcal TSS appeared to correlate with clinical improvement [11 -15], and there is evidence that is increasing evidence that it is the result of cytokine induction by exotoxins(s) belonging to the family of gram-positive bacte-IVIG contains superantigen-neutralizing antibodies [16]. The Ontario Streptococcal Study Group has conducted popurial superantigens. This family includes the enterotoxins and TSS toxin-1 produced by Staphylococcus aureus and the streplation-based surveillance for all invasive GAS disease in Ontario, Canada, since 1 January 1992 [6]. The case-fatality rate tococcal pyrogenic exotoxins of Streptococcus pyogenes [7,8].Superantigens bind to cells expressing major histocompatiassociated with streptococcal TSS has been ú65% and has remained stable over time [6,17]. In the winter of 1994, noting bility complex class II molecules and interact directly with the b chain of the T cell receptor to cause massive T cell proliferaan increase in rates of streptococcal TSS [17] and recognizing the potential for IVIG to decrease the high case-fatality rates associated with this disease, we initiated an observational study of the use of IVIG to treat patients with GAS TSS.

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“…Wheras a number of adjuvant therapies have been proposed-including specific therapies targeting bacterial toxins such as intravenous gamma globulin [7,8], plasmapheresis [9], and activated protein C [10,11] and the more generalized therapy of hyperbaric oxygen therapy (HBOT) [12,13]-there have been no universally accepted changes in the management of NSTI over the last three decades. Consequently, NSTI mortality has remained approximately 10-43% [14][15][16][17][18][19][20], and early diagnosis and aggressive site debridement remain the standard of care.…”

Human Leukocyte Antigen Class II Transgenic Mouse Model Unmasks the Significant Extrahepatic Pathology in Toxic Shock Syndrome

“…However, intravenously administered immunoglobulins are effective in treating streptococcal TSS, 25 and recently, antibiotics such as linezolid have been effective in treatment of staphylococcal TSS in some patients. 26 Nevertheless, the lack of effective therapies could be attributed to incomplete understanding of the immunopathogenesis of TSS.…”

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“…Finally, antibodies obtained from volunteers immunized with protective antigen may have the capacity to neutralize anthrax toxin (12). Similarly, polyclonal (commercially available intravenous immunoglobulin) and monoclonal antibody preparations against superantigens have the capacity to neutralize the immunostimulatory activity of superantigens (TSST-1, SEs, and SPEs) (13)(14)(15)(16)(17)(18).…”