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PubMed1989

Binding of type-I and type-II collagens to Staphylococcus aureus strains isolated from patients with toxic shock syndrome compared to other staphylococcal infections.

Toxic shock syndrome toxin-1 (TSST-1) producing strains of Staphylococcus aureus isolated from 18 patients with toxic shock syndrome (TSS) and from 56 patients with other diagnoses were compared for capacity to interact with various serum and connective tissue proteins. TSS associated isolates showed significantly stronger binding of Type-I collagen (Cn-I) and Cn-II than non-TSS strains, in a particle agglutination assay (PAA) as well as in 125I labelled Cn uptake experiments. 125I Cn-IV binding, was similar between the two groups, whereas in PAA, a stronger interaction was observed for non-TSS than TSS associated strains. The median binding of 125I Cn to TSS-associated strains were 52.2 (Cn-I), 30.6 (Cn-II) and 20.0 (Cn-IV) compared to 20.0 (Cn-I), 14.4 (Cn-II) and 24.4 (Cn-IV) values of non-TSS strains. A saturation with 125I Cn-I and Cn-II binding was established for TSS (30 min) and non-TSS (15 min) strains. 125I Cn-IV binding reached a saturation in 10 min and 90 min with TSS and non-TSS strains respectively. Finally, the binding profiles of TSS associated and non-TSS strains to fibronectin, fibrinogen, laminin and IgG did not differ in both PAA and radioisotope assays. In scanning electron microscopy, cells of TSS associated strains bound to the reprecipitated native Cn-I fibrils. In contrast, most cells of non-TSS strains were localized to the distal end or were trapped between the Cn fibrils.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Toxins↗

PubMed1993

Toxic shock syndrome complicating influenza A in a child: case report and review.

Despite extensive literature on toxic shock syndrome, reports of its manifestations in children remain relatively uncommon. Similarly, toxic shock syndrome in association with influenza B or influenza-like illness has been reported in 12 patients, but it has been reported to occur following influenza A in only two patients to date. We report a third case of toxic shock syndrome in a child with influenza A and review the association between epidemic influenza and toxic shock syndrome ("the Thucydides syndrome").

Child↗

PubMed1984

Analysis of the mitogenic effects of toxic shock toxin on human peripheral blood mononuclear cells in vitro.

It has been shown previously that the staphylococcal enterotoxins A and B are T-cell mitogens and also cause inhibition of murine plaque-forming cells generated in vitro. Similarly, toxic shock toxin, a 24,000-MW protein produced by toxic shock-associated strains of Staphylococcus aureus, is mitogenic and inhibits the generation of both murine and rabbit plaque-forming cells. In this study, an analysis of the T-cell response to toxic shock toxin was performed. Human peripheral blood mononuclear cells responded to toxic shock toxin over a broad dosage range (1 ng/ml to 5 micrograms/ml) with maximum proliferation at day 4 (96 hr) of culture. Heat treatment (100 degrees C for 60 min) of toxic shock toxin attenuated its mitogenic effects by only a small amount, and this attenuation could be reversed with increasing concentration of the toxin. By cytofluorography, both untreated and toxic shock toxin-treated small lymphocytes manifested normal percentages of OKT3+, OKT11+, OKT4+, OKT8+, HLA/DR+, and Leu-7+ cells. However, toxic shock toxin-induced blasts were 99% OKT11+ and expressed the receptor for interleukin 2 (89%-100% TAC+). Approximately 85% of the blasts were OKT4+, and 25% of the blasts were OKT8+. Proliferation of purified, double-rosetted T cells was enhanced monotonically by the addition of irradiated "non-T" cells. Irradiated, monocyte-enriched non-T cells were 2.5 times more potent than unfractionated non-T cells in producing quantitatively similar proliferation by toxic shock toxin-stimulated, autologous T cells. In addition, preincubation of non-T cells for 24 hr with toxic shock toxin, followed by extensive washing and irradiation, induced substantial proliferation by unexposed, autologous T cells. These data show that toxic shock toxin is mitogenic for T cells and requires accessory cells for maximal activity. Further, this substance appears to induce both a subset of OKT4+ (Class II MHC-restricted) and OKT8+ (Class I MHC-restricted) blasts.

Antigen-Presenting Cells↗

PubMed1993

Toxic shock syndrome associated with vulvar necrotizing fasciitis.

BACKGROUND: Fifty percent of toxic shock syndrome is associated with nonmenstrual etiologies such as postoperative wound infection. CASE: A 44-year-old woman developed necrotizing vulvar fasciitis that was successfully treated with surgical debridement and broad-spectrum antibiotics. However, after improving for 3 days postoperatively, she developed fever, a generalized maculopapular rash, and renal and liver abnormalities. As her condition worsened, she developed hypotension and respiratory distress. After 5 days in the intensive care unit, she gradually improved. Her wound culture from admission grew multiple organisms, including Staphylococcus aureus that produced toxic shock syndrome toxin-1. CONCLUSION: Toxic shock may occur in varied gynecologic settings, including pelvic and perineal infection. Successful management requires a prompt and aggressive response to multi-organ system failure.

Adult↗

PubMed2000

Toxic shock syndrome after suction lipectomy.

We present a case of toxic shock syndrome with necrotizing fasciitis after suction lipectomy. The patient underwent aesthetic suction lipectomy of the abdomen, buttocks, and thighs during an office procedure by a cosmetic surgeon. On postoperative day 2, the patient was referred to the emergency department of our hospital because of pain. On admission, the patient was in toxic shock. She required intensive medical treatment for about 1 month, along with psychiatric help to adapt after the illness. Although toxic shock syndrome is a rare postoperative complication, every plastic surgeon should be acquainted with it. A combination of early recognition, diagnosis, and aggressive supportive therapy is the only successful treatment.

Adult↗

PubMed1982

Genetic studies on Staphylococcal strains from patients with toxic shock syndrome.

Thirteen isolates of Staphylococcus aureus that produce the toxic shock syndrome exotoxin were screened to identify and characterize this specific determinant and understand its role in pathogenicity. These stains belong to phage group I, are sensitive to phage 29, and are similar with respect to their resistance to cadmium, arsenate, and penicillin. These three resistances, commonly found on plasmids in many strains of S. aureus, were not plasmid-associated in 13 toxic shock strains. The cadmium and arsenate resistances were cotransferred both in transduction and in protoplast fusion; penicillin resistance was unlinked. The toxic syndrome exotoxin gene was not linked to any of these three traits. We suggest that the trait is borne by a special genetic element that acts as a heterologous chromosomal insertion and is independent of the cadmium-arsenate linkage group or the penicillinase-determinant. The genetic properties of extracellular proteins in S. aureus are reviewed as possible models for the acquisition or expression of this toxic shock antigen.

Arsenates↗

PubMed1996

The refined crystal structure of toxic shock syndrome toxin-1 at 2.07 A resolution.

The pyrogenic toxin toxic shock syndrome toxin-1 from Staphylococcus aureus is a causative agent of the toxic shock syndrome disease. It belongs to a family of proteins known as superantigens that cross-link major histocompatibility class II molecules and T-cell receptors leading to the activation of a substantial number of T cells. The crystal structure of this protein has been refined to 2.07 A with an Rcryst value of 20.4% for 51,240 reflections. The final model contains three molecules in the asymmetric unit with good stereochemistry and a root-mean-square deviation of 0.009 A and 1.63 from ideality for bond lengths and bond angles, respectively. The overall fold is considerably similar to that of other known microbial superantigens (staphylococcal enterotoxins). However, a detailed structural analysis shows that toxic shock syndrome toxin-1 lacks several structural features that affect its specificity for V beta elements of the T-cell receptor and also its recognition by major histocompatibility class II molecules.

Amino Acid Sequence↗

PubMed1985

Toxic shock syndrome. II. Estimated occurrence in Colorado as influenced by case ascertainment methods.

Medical records for hospitalized patients between 30 days and 30 years of age at two hospitals, one in each of two Colorado counties, were reviewed for possible cases of toxic shock syndrome conforming to one or both of two clinical case definitions. Patients with toxic shock syndrome were detected in each year from 1970 through 1982. Fifty patients with possible toxic shock syndrome were identified; 14 were males, five were premenarchal females, and the remaining 31 were females of menstrual age of whom 21 (42% overall) were menstruating at the time of illness. The combined annual toxic shock syndrome incidence rate ranged between 0.8/100,000 population less than or equal to 30 years of age (1974) and 9.1/100,000 (1980) with a maximum of 15.8/100,000 (1980) in females between the ages of 10 and 30. Incidence curves for males, females less than or equal to 30 years of age, and females of menstrual age (10-30 years) fluctuated in a statistically (p less than 0.02) nonrandom fashion, each peaking in 1979-1980 and declining in 1981. In a separate statewide voluntary case reporting system, 103 cases of toxic shock syndrome of all ages were reported by health care providers with onset from 1970-1982. A minimum estimate of 26 (26%) of these were not menstrually-associated, occurring in five females prior to menarche, three following menopause, three postpartum, and 15 males. Total cases reached an annual peak in 1980, declined somewhat in 1981, and increased during 1982 to levels comparable to 1980. Less than half (46%) of the strictly defined cases actively ascertained in the retrospective hospitalized population study had been reported voluntarily to the statewide system. Jurisdictions depending primarily on passive toxic shock syndrome case ascertainment techniques, even with periodic active solicitations, may not be reliably detecting the majority of cases, and those cases which are so reported may be limited by physician perception of syndrome spectrum.

Adolescent↗

PubMed2005

The mechanism of superantigen-mediated toxic shock: not a simple Th1 cytokine storm.

The profound clinical consequences of Gram-positive toxic shock are hypothesized to stem from excessive Th1 responses to superantigens. We used a new superantigen-sensitive transgenic model to explore the role of TCRalphabeta T cells in responses to staphylococcal enterotoxin B (SEB) in vitro and in two different in vivo models. The proliferative and cytokine responses of HLA-DR1 spleen cells were 100-fold more sensitive than controls and were entirely dependent on TCRalphabeta T cells. HLA-DR1 mice showed greater sensitivity in vivo to two doses of SEB with higher mortality and serum cytokines than controls. When d-galactosamine was used as a sensitizing agent with a single dose of SEB, HLA-DR1 mice died of toxic shock whereas controls did not. In this sensitized model of toxic shock there was a biphasic release of cytokines, including TNF-alpha, at 2 h and before death at 7 h. In both models, mortality and cytokine release at both time points were dependent on TCRalphabeta T cells. Anti-TNF-alpha pretreatment was protective against shock whereas anti-IFN gamma pretreatment and delayed anti-TNF-alpha treatment were not. Importantly, anti-TNF-alpha pretreatment inhibited the early TNF-alpha response but did not inhibit the later TNF-alpha burst, to which mortality has previously been attributed. Splenic T cells were shown definitively to be the major source of TNF-alpha during the acute cytokine response. Our results demonstrate unequivocally that TCRalphabeta T cells are critical for lethality in toxic shock but it is the early TNF-alpha response and not the later cytokine surge that mediates lethal shock.

Animals↗

PubMed1994

Postoperative toxic shock syndrome after lumbar laminectomy in a male patient.

OBJECTIVES: Postoperative toxic shock syndrome in a male patient who underwent a lumbar laminectomy has not been reported. This case report identifies a rare, and potentially fatal, postoperative complication. RESULTS: Early diagnosis and aggressive medical management were successful in this patient and are the cornerstone of treatment in toxic shock syndrome. CONCLUSION: Spine surgeons should consider postoperative toxic shock syndrome as a diagnosis in a patient with fever, gastrointestinal symptoms, and hypotension in the presence of a benign-appearing lumbar laminectomy wound.

Diskectomy↗

PubMedDate not supplied

Direct effects of purified staphylococcal toxic shock syndrome toxin 1 on myocardial function of isolated rabbit atria.

Toxic shock syndrome is associated with reversible cardiomyopathy. The cardiac dysfunction may be mediated by toxic shock syndrome toxin 1 (TSST-1), an exotoxin generated by Staphylococcus aureus. However, the effects of purified TSST-1 on cardiac function are unknown. In a study of the toxin's effect on myocardial function, TSST-1 (200 ng/mL) was added to muscle baths containing isolated rabbit atria. TSST-1 caused time-dependent inhibition of developed force (systolic function) but did not alter resting force (an index of muscle stiffness or cardiac compliance). These data show that TSST-1 can directly inhibit myocardial function, but the significance of this effect in patients with toxic shock syndrome remains to be determined.

Animals↗

PubMed1982

Toxic shock syndrome: a critique of the 1980 Wisconsin case-control study.

Seven cases of toxic shock syndrome has been reported to the Wisconsin Division of Health by 6 January 1980; all seven cases were in female patients, six of whom had onset of illness during active menstruation. Through passive reporting of cases by physicians and patients themselves, a total of 38 patients with confirmed cases of toxic shock syndrome had been identified by the Division of Health by 30 June 1980. Thirty-five patients with menstrual toxic shock syndrome were each age-matched to three menstruating control subjects as part of a case-control study to identify potential risk factors associated with menstrual toxic shock syndrome. Statistically significant findings included increased tampon usage by patients as compared with controls, and fewer patients than controls were using any method of birth control. Numerous other health and hygiene variables were examined and found not to be statistically significant. We critically review the potential biases inherent to the study design. The conclusions and experience gained in this study were crucial to the designing of later case-control studies.

Adolescent↗

PubMed1983

Postoperative toxic shock syndrome.

Previously, most cases of the toxic shock syndrome (TSS) have been described in a menses-related clinical setting. Recently, however, cases have been described in nonmenses-related clinical settings, in particular, in association with postoperative wound infections. Three cases of TSS occurred as a complication of surgical procedures. Toxic shock syndrome complicated the postoperative course of one patient undergoing routine inguinal herniorrhaphy, to our knowledge the first reported case of this syndrome directly resulting in the patient's death in the postoperative setting. In another case, TSS, with recurrence, resulted from a Staphylococcus aureus wound infection after unilateral salpingo-oophorectomy, to our knowledge the first reported case of recurrence in a nonmenses-related setting.

Adult↗

PubMed1986

Toxic shock syndrome and the vaginal contraceptive sponge.

Thirteen confirmed cases of toxic shock syndrome temporally related to use of the vaginal contraceptive sponge have been reported. The observed risk of toxic shock syndrome in sponge users may be elevated above estimated background rates, but this risk remains very low. Traumatic manipulation of the sponge, use during menstruation or the puerperium, and prolonged retention of the sponge may additionally increase toxic shock syndrome risk. As with all contraceptives, risks must be balanced against benefits.

Adolescent↗

PubMed1983

Toxic shock following staphylococcal peritonitis.

A case of toxic shock syndrome (TSS) in a male continuous ambulatory peritoneal dialysis (CAPD) patient is described. The prodromal phase started with staphylococcal peritonitis and deteriorated to the malignant phase of TSS approximately 48 hours from the time he presented to the local emergency room. Desquamation first affected the extremities and likely involved his gastrointestinal tract. His course of peritonitis involved unusual pain, with progression into toxic shock in spite of appropriate antibiotic coverage.

Adult↗

PubMedDate not supplied

Group A streptococcus and streptococcal toxic shock syndrome: a postpartum case report.

Streptococcal toxic shock syndrome from group A streptococcal disease is rare in the postpartum period, yet it is associated with high morbidity and mortality. Early diagnosis and treatment can lessen complications. Midwives can improve provision of postpartum care by being adequately educated about signs and symptoms of this disease, thereby enhancing their ability to recognize it and obtain the appropriate referral or collaborative medical care. A clinical presentation of postpartum streptococcal toxic shock syndrome, including provider follow-up, is presented.

Adult↗

PubMed2005

Streptococcal toxic shock syndrome in children without skin and soft tissue infection: report of four cases.

UNLABELLED: Streptococcal toxic shock syndrome is a fulminant, highly fatal disease characterized by evidence of group A beta-haemolytic streptococcus infection and early shock with consecutive organ failure. In adults, affected individuals usually have preceding skin or soft tissue infection. However, in paediatric patients, except for varicella, the background focus is usually respiratory tract infection, and early diagnosis of streptococcal toxic shock syndrome in such patients is difficult. We report four previously healthy children with streptococcal toxic shock syndrome. Pharyngitis was identified in three cases. All of them had constitutional symptoms such as fever, vomiting, diarrhoea, abdominal pain and physical findings of tachycardia and diffuse abdominal tenderness, but no concomitant skin infection. CONCLUSION: Streptococcal toxic shock syndrome should be considered in paediatric patients with fever, vomiting, diarrhoea, abdominal pain and early shock. Early diagnosis, prompt initiation of antibiotics and aggressive fluid therapy are lifesaving for such patients.

Adolescent↗

PubMed2000

Severe group A streptococcal infection and streptococcal toxic shock syndrome.

PURPOSE: To review the literature on group A streptococcal toxic shock syndrome, (STSS). DATA SOURCE: Medline and EMBASE searches were conducted using the key words group A streptococcal toxic shock syndrome, alone and in combination with anesthesia; and septic shock, combined with anesthesia. Medline was also searched using key words intravenous immunoglobulin, (IVIG) and group A streptococcus, (GAS); and group A streptococcus and antibiotic therapy. Other references were included in this review if they addressed the history, microbiology, pathophysiology, incidence, mortality, presentation and management of invasive GAS infections. Relevant references from the papers reviewed were also considered. Articles on the foregoing topics were included regardless of study design. Non-English language studies were excluded. Literature on the efficacy of IVIG and optimal antibiotic therapy was specifically searched. PRINCIPAL FINDINGS: Reports of invasive GAS infections have recently increased. Invasive GAS infection is associated with a toxic shock syndrome, (STSS), in 8-14% of cases. The STSS characteristically results in shock and multi-organ failure soon after the onset of symptoms, and is associated with a mortality of 33-81%. Many of these patients will require extensive soft tissue debridement or amputation in the operating room, on an emergency basis. The extent of tissue debridement required is often underestimated before skin incision. CONCLUSIONS: Management of STSS requires volume resuscitation, vasopressor/inotrope infusion, antibiotic therapy and supportive care in an intensive care unit, usually including mechanical ventilation. Intravenous immunoglobulin infusion has been recommended. Further studies are needed to define the role of IVIG in STSS management and to determine optimal anesthetic management of patients with septic shock.

Anesthesia↗