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PubMed2000

Streptococcal toxic shock syndrome associated with necrotizing fasciitis.

Streptococcal toxic shock syndrome (strep TSS) with associated necrotizing fasciitis is a rapidly progressive process that kills 30-60% of patients in 72-96 h. Violaceous bullae, hypotension, fever, and evidence of organ failure are late clinical manifestations. Thus, the challenge to clinicians is to make an early diagnosis and to intervene with aggressive fluid replacement, emergent surgical debridement, and general supportive measures. Superantigens such as pyrogenic exotoxin A interact with monocytes and T lymphocytes in unique ways, resulting in T-cell proliferation and watershed production of monokines (e.g. tumor necrosis factor alpha, interleukin 1, interleukin 6), and lymphokines (e.g. tumor necrosis factor beta, interleukin 2, and gamma-interferon). Penicillin, though efficacious in mild Streptococcus pyogenes infection, is less effective in severe infections because of its short postantibiotic effect, inoculum effect, and reduced activity against stationary-phase organisms. Emerging treatments for strep TSS include clindamycin and intravenous gamma-globulin.

Diagnosis, Differential↗

PubMed2001

Toxic shock syndrome and bacterial superantigens: an update.

Toxic shock syndrome (TSS) is an acute onset illness characterized by fever, rash formation, and hypotension that can lead to multiple organ failure and lethal shock, as well as desquamation in patients that recover. The disease is caused by bacterial superantigens (SAGs) secreted from Staphylococcus aureus and group A streptococci. SAGs bypass normal antigen presentation by binding to class II major histocompatibility complex molecules on antigen-presenting cells and to specific variable regions on the beta-chain of the T-cell antigen receptor. Through this interaction, SAGs activate T cells at orders of magnitude above antigen-specific activation, resulting in massive cytokine release that is believed to be responsible for the most severe features of TSS. This review focuses on clinical and epidemiological aspects of TSS, as well as important developments in the genetics, biochemistry, immunology, and structural biology of SAGs. From the evolutionary relationships between these important toxins, we propose that there are five distinct groups of SAGs.

Amino Acid Sequence↗

PubMed1997

Toxic shock syndrome after burn injuries in children.

Toxic shock syndrome is a life-threatening exotoxin mediated disease caused by Staphylococcus aureus, which was originally described as affecting menstruating women, but has lately been reported after surgical procedures and burns. The high mortality emphasises the importance of early diagnosis. In most cases there is a prodromal period with fever (> 38.9 degrees C), myalgia, headache, and vomiting before the onset of hypotension and multiorgan failure. We present two cases in children with minor burns, and review current recommendations for treatment.

Bandages↗

PubMed1994

Recent advances in toxic shock syndrome.

The pathogenesis and treatment of toxic shock has become clearer even as its epidemiology has evolved. Nonmenstrual cases due to Staphylococcus aureus can be difficult to diagnose and treat. Invasive Streptococcus pyogenes infections are life threatening.

Humans↗

PubMed2003

[Menstrual staphylococcal toxic shock is still a reality].

INTRODUCTION: Staphylococcal toxic shock replies to precise clinical-biological criteria; but can be difficult to diagnose. Today, the nonmenstrual form of shock is the most frequent. The incidence of menstrual shock is low but their potential severity must be recalled. OBSERVATIONS: A young 14 year-old girl and a 33 year-old woman presented with menstrual shock that was treated successfully. A relapse in the form of staphylococcal scarlet fever occurred in the second patient. In both cases, the strain Staphylococcus aureus, which produces the TSST-1 toxin, had been identified. CONCLUSION: The possibility of the occurrence of a menstrual staphylococcal shock in the year 2002 must be known. The polymorphism of the clinical and biological manifestations must be underlined. The search for a toxin can be conducted in an appropriate centre.

Adolescent↗

PubMedDate not supplied

Toxic shock syndrome in patients with external fixators.

Toxic shock syndrome (TSS), first described by Todd et al. in 1978, can be a life-threatening entity. Familiarity with the pathogenesis and clinical presentation of TSS may help achieve early diagnosis and prompt appropriate intervention. TSS is not a septicemia, but a toxemia. The most extensively described pathogenesis involves a focus of specific Staphylococcus aureus strains capable of producing an exotoxin (TSST-1). We report two patients who developed TSS while in external fixators and describe their initial symptoms, management, and subsequent problems. This report will serve to alert pediatric orthopaedic surgeons to this entity and enable them to recognize its rather precipitous presentation and initiate appropriate treatment.

Bone Nails↗

PubMed1992

Role of protein tyrosine phosphorylation in monokine induction by the staphylococcal superantigen toxic shock syndrome toxin-1.

The staphylococcal superantigen toxic shock syndrome toxin-1 (TSST-1) is a potent inducer of IL-1 beta and TNF-alpha synthesis in human monocytes. As superantigens are high affinity ligands for MHC class II molecules, the induction of monokines by TSST-1 provides a biologically relevant model of MHC class II-mediated transmembrane signaling. In this study, we show that TSST-1 induces cytoplasmic protein tyrosine phosphorylation in the human monocytic cell line THP-1. This induction was greatly enhanced by cross-linking TSST-1 with biotin-avidin. The functional relevance of tyrosine phosphorylation induced by TSST-1 was demonstrated by the finding that three specific inhibitors of protein tyrosine kinases strongly inhibited the induction of IL-1 beta mRNA by TSST-1. These data suggest that protein tyrosine kinase activation plays a critical role in MHC class II-mediated transmembrane signalling by staphylococcal superantigens.

Antigens, Bacterial↗

PubMed1986

Enhancement of endotoxin-induced isolated renal tubular cell injury by toxic shock syndrome toxin 1.

The pathogenesis of toxic shock syndrome (TSS) remains unknown. On the basis of experimental data, it has been hypothesized that staphylococcal TSS Toxin 1 (TSST-1) may interact synergistically with low levels of endotoxin and give rise to many of the clinical findings. We have demonstrated previously that lipid A, the biologically active component of lipopolysaccharide (LPS), or endotoxin, induces dose-dependent necrosis of isolated rat renal tubular cells (RTCs). In the present studies, the authors investigated whether this injury could be augmented by TSST-1. The viability of RTCs was assessed by vital dye exclusion. Incubation of freshly isolated rat RTCs with either 1 ng/ml of TSST-1 or 0.1 ng/ml LPS or lipid A had minimal cytotoxicity (less than 6%). Exposure of RTCs to 1 ng/ml TSST-1 for 20 minutes, followed by washing, resulted in a significant enhancement of cytotoxicity when RTCs were exposed to 0.1 ng/ml LPS or lipid A. The sensitization of RTCs by TSST-1 to LPS- or lipid-A-induced injury was prevented by methylamine and chloroquine, two inhibitors of receptor-mediated endocytosis (RME). Chelation of extracellular calcium by 2 mM EGTA also blocked the TSST-1-induced sensitization of RTCs to LPS or lipid A. Inhibition of RTC arachidonic acid metabolism by methylprednisolone, indomethacin, ibuprofen, and piriprost significantly inhibited RTC necrosis induced by TSST-1 and LPS or lipid A by 33-62%. Thiourea and deferoxamine, agents which ameliorate oxidant injury, also inhibited this synergistic injury by 34-67%. Thus, TSST-1 enhanced the cytotoxic effects of LPS/lipid A, and the sensitization of RTCs appeared to involve RME or TSST-1. Oxidative metabolism of arachidonic acid and generation of reactive oxygen species appeared to participate in LPS/lipid-A-mediated RTC death.

Animals↗

PubMed1981

Acute cholestasis in patients with toxic- shock syndrome.

Serum liver function tests were performed in 22 females fulfilling the criteria for toxic-shock syndrome. All patients showed evidence of hepatic dysfunction during their hospital course. These findings included hyperbilirubinemia in the absence of laboratory evidence for significant hemolysis, mold elevation of the transaminases, threefold increase in their serum bile salt concentration, and hypoalbuminemia. These findings are best explained by hypoperfusion of the liver and a canalicular injury secondary to staphylococcal exotoxin. Cholestasis appears to be a universal finding in toxic-shock syndrome.

Alanine Transaminase↗

PubMedDate not supplied

Streptococcal toxic shock syndrome from a puncture wound to the foot.

Puncture wounds to the foot are a common occurrence. If treated properly, the majority will be resolved without major complications. Toxic shock syndrome and streptococcal toxic shock-like syndrome are devastating complications of some staphylococcal and streptococcal infections. This paper discusses the similarities and differences between the two toxic states, reviews the pathophysiology, and presents a case report of near-fatal streptococcal toxic shock-like syndrome secondary to a puncture wound of the foot.

Adult↗

PubMed1994

Apparent lower rates of streptococcal toxic shock syndrome and lower mortality in children with invasive group A streptococcal infections compared with adults.

Since 1985 there have been worldwide reports of increases in severe invasive Group A streptococcal (IGAS) infections. We reviewed the charts of all children with IGAS infections (defined as isolation of Group A streptococcus from a normally sterile site) presenting to our institution over a 7-year period (January, 1985, to December, 1991) and the literature. Streptococcal toxic shock syndrome required hypotension and multisystem organ involvement. Twenty-four patients (mean age, 4.96 +/- 4.4 years) were identified with IGAS infection. One patient (presenting in 1989) met the criteria for probable streptococcal toxic shock syndrome and none died. Eight of 19 Group A streptococcal isolates tested were streptococcal pyrogenic exotoxin (SPE) A producers, most (90%) had the speC gene and all had the speB gene and produced the toxin. No M or T type predominated. The low rates of streptococcal toxic shock syndrome and fatalities among children with IGAS infection are consistent with other pediatric but not with adult series. The apparent differences in outcome of IGAS between children and adults were not explained by the virulence factors we examined and may warrant further investigation.

Adolescent↗

PubMed1990

Toxic shock syndrome associated with use of latex nasal packing.

We treated a previously healthy young man who developed toxic shock syndrome 2 days after elective septoplasty with nonabsorbent latex packing. This case emphasizes that non-menstrual wound-associated toxic shock syndrome can occur after surgery that does not involve absorbent splinting or packing and should be considered in patients who present within a few days after surgery with fever, sunburnlike rash, hypotension, and multisystem complaints and laboratory abnormalities.

Adult↗

PubMed2004

Differences in potency of intravenous polyspecific immunoglobulin G against streptococcal and staphylococcal superantigens: implications for therapy of toxic shock syndrome.

Administration of intravenous polyspecific immunoglobulin G (IVIG) has been proposed as adjunctive therapy for toxic shock syndrome caused by Streptococcus pyogenes or Staphylococcus aureus. We investigated whether superantigen-containing culture supernatants prepared from streptococcal isolates (n=21) and staphylococcal isolates (n=20) from cases of severe sepsis were inhibited to an equal extent by IVIG in proliferation experiments that used human peripheral blood mononuclear cells. All 3 IVIG preparations tested were highly efficient in neutralizing the superantigens, and most supernatants were completely inhibited at concentrations ranging from 0.05 to 2.5 mg IVIG/mL. An important finding was that culture supernatants from S. pyogenes isolates were consistently inhibited to a greater extent than those of S. aureus isolates (P<.01). The findings demonstrate that staphylococcal superantigens are not inhibited as efficiently as streptococcal superantigens by IVIG, and, hence, a higher dose of IVIG may be required for therapy of staphylococcal toxic shock syndrome in order to achieve protective titers and clinical efficacy.

Humans↗

PubMed2005

Clostridium sordellii toxic shock syndrome after medical abortion with mifepristone and intravaginal misoprostol--United States and Canada, 2001-2005.

On July 19, 2005, the Food and Drug Administration (FDA) issued a public health advisory regarding the deaths of four women in the United States after medical abortions with Mifeprex (mifepristone, formerly RU-486; Danco Laboratories, New York, New York) and intravaginal misoprostol. Two of these deaths occurred in 2003, one in 2004, and one in 2005. Two of these U.S. cases had clinical illness consistent with toxic shock and had evidence of endometrial infection with Clostridium sordellii, a gram-positive, toxin-forming anaerobic bacteria. In addition, a fatal case of C. sordellii toxic shock syndrome after medical abortion with mifepristone and misoprostol was reported in 2001, in Canada. All three cases of C. sordellii infection were notable for lack of fever, and all had refractory hypotension, multiple effusions, hemoconcentration, and a profound leukocytosis. C. sordellii previously has been described as a cause of pregnancy-associated toxic shock syndrome.

Abortifacient Agents↗

PubMed1985

Serological response to toxic shock syndrome toxin in Staphylococcus aureus infected patients and healthy controls.

The prevalence of antibodies to Toxic Shock Syndrome Toxin (TSST-1) in a Swedish healthy control population was investigated using an enzyme-linked immunosorbent assay (ELISA). 88% of the control group above the age of 10 showed positive antibody levels as compared to 31% of those who were under 10 years old. These results indicate a very common normal exposure to TSST-1 during early life and also identify the small risk-group of potential TSS-patients. Patients with S. aureus endocarditis and septicemia showed slightly higher antibody levels as compared to the controls (p less than 0.05). The difference was in part due to 3/4 septicemia patients, infected with TSST-1 producing strains, who showed very high antibody levels. None of these 4 patients developed any signs of TSS. 5/5 menstrual associated TSS-patients were negative in the ELISA in serial serum samples as were 3/5 non-menstrual associated TSS-patients. The TSST-1 ELISA is proposed for identifying chiefly young women at risk of acquiring menstrual related Toxic Shock Syndrome.

Antibodies, Bacterial↗

PubMed1988

Detection of staphylococcal toxic shock syndrome toxin 1 by a latex agglutination kit.

A commercial reversed passive latex agglutination kit (Oxoid), that detects toxic shock syndrome toxin 1 (TSST-1), was evaluated for its ability to support the clinical diagnosis of toxic shock syndrome (TSS) by detecting the presence of TSST-1 producing Staphylococcus aureus. 15/16 isolates from patients with TSS were positive, while 4/50 vaginal isolates from patients without TSS were positive. The kit can be recommended as it was easy to handle, and gave results identical with those obtained by a standard assay.

Bacterial Toxins↗

PubMedDate not supplied

[Bacterial toxic shock in urological diseases].

It is a review of present-day and historical aspects of bacterial toxic shock arising in urological setting. It is noted that conditions of its onset are changing, therapeutic approaches undergo revision, critical care facilities are updated. Among the causes of this complication the authors single out endoscopic procedures, transurethral interventions in the presence of infectious process, hospital infection, long stay at hospital. Forty-eight cases of bacterial toxic shock are reviewed in relation to classification, causes of development, treatment, bacteriological evaluation.

Bacterial Infections↗

PubMed1988

Toxic shock syndrome toxin-1 induces inositol phospholipid turnover, protein kinase C translocation, and calcium mobilization in human T cells.

Toxic shock syndrome toxin-1 (TSST-1) is a 22-kDa exotoxin produced by most Staphylococcus aureus strains responsible for toxic shock syndrome. TSST-1 is a mitogen for human T cells. The mechanism of T cell activation by TSST-1 was investigated. TSST-1 induced IL-2R expression, IL-2 synthesis, and proliferation in T cells in a monocyte-dependent fashion. Neither IL-1 nor IL-2, alone or in combination, substituted for monocytes in supporting TSST-1-induced mitogenesis. We investigated the mechanism by which TSST-1 induces initogenesis. TSST-1 failed to induce ADP-ribosylation of T cell membrane proteins. However, the toxin induced transient translocation of protein kinase C from cytosol to plasma membranes and also induced the mobilization of cellular Ca2+ stores in both PBMC and the Jurkat human tumor T cell line, suggesting that TSST-1 triggered inositol phospholipid turnover. This was directly demonstrated to be the case in both cellular preparations studied. TSST-1 induced the increased synthesis of the inositol phospholipid phosphatidyl inositol, phosphatidyl inositol-4 phosphate, and phosphoinositol inositol-4,5-bisphosphate, and induced the breakdown of inositol phospholipid as evidence by the accumulation of phosphatidic acid and inositol phosphates. We conclude that the action of TSST-1 involves the induction of inositol phospholipid turnover, protein kinase C activation, and mobilization of cellular Ca2+ stores. This effect is similar to that of mitogenic lectins and of anti-CD3 antibodies.

Adenosine Diphosphate Ribose↗