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A case of toxic shock syndrome presenting with macular erythema and subepidermal bullae is described. The patient meets the Centers for Disease Control criteria for toxic shock syndrome. A biopsy of the bullae and macular erythema revealed, respectively, subepidermal bullae and superficial perivascular infiltration. This case demonstrates the potential difficulty in differentiating between toxic shock syndrome and toxic epidermal necrolysis.
Toxic shock syndrome toxin-1 (TSST-1), isolated from Staphylococcus aureus strains associated with toxic shock syndrome (TSS), is known as a potent mitogen and interleukin-1 inducer. The potential of TSST-1 as an interleukin-2 (IL-2) inducer was tested on human peripheral blood lymphocytes (HPBL) and murine spleen lymphocytes (MSL). These cells were incubated with TSST-1 and the supernatants analysed for IL-2 production. Preincubation of IL-2-dependent indicator cells (IC) with a monoclonal antibody specific for murine IL-2 receptors inhibited their proliferation by supernatants of TSST-1-treated MSL, thus strongly suggesting that they contain IL-2. The concentrations of TSST-1 required for HPBL or MSL to produce IL-2 ranged between 10(-1) and 10(-4) micrograms/ml. The amount of IL-2 units/ml varied little from one experiment to another. In contrast, IL-2 production by PHA-stimulated HPBL or Con A-stimulated MSL showed great variability and dependence on mitogen concentration. T-cell depleted MSL exposed to TSST-1 produced less IL-2. Experiments with germ-free mice and TSST-1-primed mice demonstrated that IL-2 production is not related to TSST-1 antigenicity.
Toxic shock syndrome toxin-1 (TSST-1), the potent staphylococcal exoprotein linked to most cases of the toxic shock syndrome, is a V beta-restricted T-cell mitogen (a so-called "superantigen"). TSST-ovine (TSST-O) is a natural variant of TSST-1, and is produced by certain ovine mastitis-associated strains of Staphylococcus aureus. Compared to TSST-1, TSST-O is only weakly mitogenic for leporine or murine splenocytes. It differs from TSST-1 at 7 amino acid residues over its 194 amino acid length. Terminus shuffling between the two proteins has suggested that their C-terminal differences (T69, Y80, E132, and I140 in TSST-1; 169, W80, K132, and T140 in TSST-O) are in part responsible for their discrepant mitogenic properties. In order to explore further the functional consequences of altering TSST-1 at residues 132 and 140, we engineered point mutants of TSST-1 at those positions. The mutant proteins were purified to homogeneity from culture supernants of a nontoxigenic strain of S. aureus using a combination of ultrafiltration, liquid-phase isoelectric focusing, and ion-exchange chromatography. The mutants retained global structural integrity as evidenced by circular dichroism spectroscopy, their preserved resistance to trypsin digestion, and their preserved binding to a neutralizing murine monoclonal antibody. The mutants were then tested for mitogenicity for human T-cells: The mutant I140T was approximately as active as wild-type TSST-1, while the mutant E132D was about 10-fold attenuated. On the other hand, the mutants E132A or E132K were each at least 1000-fold attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)
Toxic shock syndrome toxin 1 (TSST-1) is a potent immunomodulating substance isolated from Staphylococcus aureus strains associated with toxic shock syndrome (TSS). Flow cytometric analysis was used to compare scatter changes in several cell-surface phenotype markers on human mononuclear cells exposed in vitro to TSST-1 or to phytohemagglutinin, a lectin with similar effects on the immune response. The results showed differences between PHA and TSST-1 in the appearance of the tested T cell subset markers and of interleukin 2 receptors. In general, the stimulation of mononuclear cells by TSST-1 was slower than that by phytohemagglutinin. TSST-1 induced the production of interferon in cultures of murine spleen cells. By means of inhibition studies with specific antibodies to interferon, the interferon produced was characterized as the gamma type. Human mononuclear cells exposed to the toxin also produced gamma interferon, with levels similar to those induced by staphylococcal enterotoxin A, a known potent interferon inducer. The induction of gamma interferon by TSST-1 may play a role in the immunosuppression caused by TSST-1.
Toxic shock syndrome toxin-1 (TSST-1), an extra-cellular 22 kDa single chain protein produced by most Staphylococcus aureus strains isolated from patients with toxic shock syndrome (TSS), induces modifications of blood cell values similar to those observed during TSS. We therefore analyzed the effects of TSST-1 on the proliferation and differentiation of murine granulocyte-macrophage progenitor cells (CFU-culture) and the eventual role of endotoxin in this response. TSST-1 had no direct effect on the proliferation of CFU-culture and was unable to influence the CSF-induced proliferation and differentiation of these progenitors. In contrast, TSST-1 was a potent inducer in spleen cell cultures of a factor with an ability to induce both colony formation by bone marrow cells and proliferation of an IL-3-dependent cell line. Nanogram amounts of TSST-1 were able to induce the release of CSF activity in spleen cell cultures from both normal and LPS-hyporesponsive mice. Cells from C3H/HeJ mice were as responsive as cells from C3H/He Pas mice. Furthermore, in spleen cell cultures from normal mice, TSST-1 and LPS did not act synergistically to induce CSF activity. Nanogram amounts of TSST-1 were also able to induce CSF activity in vivo but failed to induce IL-3 activity in the serum and organ-conditioned media from TSST-1-treated mice.
Toxic shock syndrome toxin-1 (TSST1) is a superantigenic exotoxin produced by certain strains of Staphylococcus aureus Structurally, TSST1 is composed of two domains: residues determined by crystallography to directly interact with MHC II molecules reside within the N-terminal domain, while TSST1 residues critical for superantigenicity are within the C-terminal domain. In this study, we expressed the individual N- and C-terminal domains of TSST1 in Escherichia coli and studied their biologic activities. The TSST1 N-terminal domain (TSST(1-87)) did not induce proliferation of human PBLs or release of TNF-beta, but did induce TNF-alpha release. However, TSST1-elicited proliferation and release of both TNF isoforms were inhibited by a molar excess of TSST(1-87). The TSST1 C-terminal domain (TSST(88-194)) did not bind MHC II molecules, yet it elicited production of TNF-alpha and TNF-beta, and induced TCR Vbeta-specific proliferation similarly to intact TSST1. When covalently cross-linked to tumor cells, TSST(88-194) elicited a local in vivo antitumor response indistinguishable from TSST1. Although intact TSST1 causes lethal shock in vivo, the individual domains of this molecule may have therapeutic potential: the N-terminal domain to antagonize lymphocyte activation and TNF release during acute TSST1-precipitated toxic shock syndrome, and the C-terminal domain to stimulate antitumor responses without MHC II binding.
The toxic shock syndrome (TSS) is a newly-recognized entity caused by a Staphylococcal exotoxin and associated with the use of tampons for menstrual protection. Two cases are presented which demonstrate the spectrum of severity of the disease. The common nature of its early symptoms necessitates a high index of suspicion to preclude a progression to the later stages of the disease, thereby reducing morbidity and mortality.
Toxic-shock syndrome (TSS) is believed to be caused by a toxin produced by Staphylococcus aureus. An exotoxin has been identified that is associated with strains of S. aureus isolated from patients with TSS. Coded strains of S. aureus were tested for the presence of the exotoxin by polyacrylamide gel isoelectric focusing. Sixty isolates of S. aureus were tested; 28 (100%) of 28 isolates from patients with TSS but only five (16%) of 32 control isolates produced the toxin (P much less than 0.001). This protein exotoxin, which was purified by differential precipitation with ethanol and thin-layer isoelectric focusing, had an isoelectric point of 7.2. When tested by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the toxin migrated as a homogeneous protein with a molecular weight of 22,000. The exotoxin produced fever in rabbits and enhanced susceptibility to lethal shock caused by endotoxin. Other biologic properties of the exotoxin included lymphocyte mitogenicity and the capacity to suppress synthesis of IgM antibody to sheep erythrocytes.
The toxicity of toxic shock syndrome (TSS) toxin-1 (TSST-1) was evaluated in female, specific pathogen-free rabbits and conventional rabbits. Results after intravenous injections of TSST-1 given to both types of rabbits indicated that specific pathogen-free rabbits were resistant to the lethal effects observed in conventional rabbits. Lethality could be prevented by simultaneous administration of polymyxin B, and analysis of serum before and after dosing confirmed that dosing with TSST-1 resulted in circulating endotoxin. Analysis of sera from humans with TSS showed that endotoxin was present in acute-phase sera but not in convalescent-phase sera. These observations suggest that endogenous endotoxin contributes to rabbit susceptibility to TSST-1 and may play a role in human TSS.
The toxic shock syndrome (TSS) most often is seen in young, healthy women who become symptomatic during menstruation. The association between TSS and the use of tampons is strong. The symptoms usually begin suddenly and are often nonspecific. Prostration and hypotensive shock can occur within 24 hours. Milder forms of the disease also may be seen. The overall mortality rate is approximately 8 percent. This report describes a mild case of TSS in a young, healthy, 16-year-old female who developed symptoms during menstruation. She had been using regular-size tampons, which were changed frequently, but she did not change tampons during the night. A positive cervical culture for Staphylococcus aureus confirmed the diagnosis. The patient responded to supportive care and intravenous oxacillin. Her generalized maculopapular rash disappeared within 24 hours of admission, and her hands began to desquamate by the time of discharge. The patient was urged to avoid the use of tampons for four months subsequent to discharge.
Streptococcal toxic shock syndrome(STSS) is known to progress rapidly into septic shock and multiple organ failure with frequently necrotizing fasciitis, and high mortality (approximately 40%). The diagnosis of STSS is confirmed based on the diagnosis criteria induced by the working group of the United State. Several extracellular products such as SPE A, B, and C having pyrogenic and superantigenic activity as well as SPE F, SPE G, H, J, SME Z, SME Z2, SSA are likely to involved in the pathogenesis of STSS. Recent studies have demonstrated an important role of certain cytokines, such as TNF-alpha, in laboratory animals. The exact role of such products in the pathogenesis of STSS, however, is currently unknown. The role of several virulence factors of group A streptococci in the pathogenesis of STSS was discussed in this review.
Streptococcal toxic shock syndrome (STSS) which is the most severe form of invasive infection caused by group A streptococci has made a global resurgence. To establish the presence of STSS, hypotension and multiorgan failure must accompany evidence of Streptococcal pyogenes infection. We report a case of STSS in a 61 year old diabetic man. The patient presented with septicaemia and septic arthritis of the right knee joint. Group A streptococci were cultured from both blood and pus aspirate from knee joint. The patient had signs of STSS. Early radical drainage debridement plus appropriate antibiotic therapy altered the usual devastating outcome. A wider recognition of the diverse clinical manifestations of group A streptococci is emphasized for early diagnosis, better treatment and possibly improved outcome.
Toxic shock syndrome (TSS) is reported in 2 children. TSS occurred 10 days after an accidental injury of the fore foot in one case and 5 days following surgery for severe uretero-vesical reflux in the other. The clinical illness was defined by the case definition formulated for epidemiologic studies (CDC, 1982). The diagnosis was confirmed by isolation of a Staphylococcus aureus strain producing TSST, at the infected site. Toxin-induced mediators such as interleukin I and Tumor Necrosis Factor have been incriminated in septic shock with multivisceral involvement. As in our 2 cases, the syndrome may be delayed or even absent.
Toxic shock syndrome is associated with burn injuries in children and is a cause of significant morbidity in this group. Despite multiple cases of toxic shock syndrome in adults being reported since its original description it has not been reported in adult burn patients. We report a case of toxic shock syndrome in an adult following 25% flame burns.
Toxic shock syndrome is a recently discovered and widely publicized disease found to occur in young menstruating women and thought to be associated with the use of vaginal tampons. To this date, there has been no known report of a similar disease being caused by nasal or sinus packing. The following is a discussion of the toxic shock syndrome (TSS) and a presentation of two cases that demonstrated a striking similarity to that disease.
Staphylococcal toxic shock syndrome toxin 1 (TSST1) induced the release of tumour necrosis factor (TNF) from human and rabbit monocytes in vitro. Nanogram amounts of TSST1 were sufficient to induce TNF release. There was considerable variation in response between cells from different rabbits and different donors. Rabbit monocytes were slightly more sensitive to TSST1 than were human monocytes. Release of TNF in vivo could explain many of the symptoms of toxic shock syndrome.
Toxic shock syndrome is frequently complicated by renal dysfunction. The mechanism of this functional disturbance is unclear. The present report concerns a 33-year-old woman with reversible renal failure in the course of toxic shock syndrome owing to rhabdomyolysis. It is suspected that the renal consequences of muscle injury play a pathophysiological role in the acute renal failure of toxic shock syndrome.
Toxic shock syndrome is a rapidly developing disease which may be lethal if not recognized and treated early. While this disease is usually associated with menstruating females, it is being seen in both male and female patients following clean, elective surgery. Toxic shock syndrome has been reported following surgical procedures which normally have a very low incidence of postoperative wound infections. Toxic shock syndrome is associated with Staphylococcus aureus bacteria which produce the toxic shock syndrome toxin 1. Three patients with postoperative toxic shock syndrome, of varying degrees of severity, are presented. Prompt institution of resuscitative and therapeutic measures can prevent the potentially fatal outcome of this postoperative complication.