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PubMed1995

A toxic shock syndrome toxin 1 mutant that defines a functional site critical for T-cell activation.

Toxic shock syndrome toxin 1 (TSST-1), a superantigen produced by Staphylococcus aureus, is a causative agent of toxic shock syndrome (TSS). This superantigen is a potent stimulator of T cells and macrophages/monocytes, resulting in the release of cytokines that are implicated in the pathogenesis of TSS. This study characterizes a mutant TSST-1, derived by site-directed mutagenesis, that has an alanine substitution at histidine 135 (mutant 135). This single-amino-acid change results in a mutant toxin that has lost mitogenic activity for T cells. In contrast to wild-type TSST-1, this mutant does not induce T cells to express interleukin-2, gamma interferon, or tumor necrosis factor beta (TNF-beta). The inability of mutant 135 to activate T cells is not due to a lack of binding to the class II major histocompatibility complex receptor. In addition, the mutant TSST-1 does not induce expression of TNF-alpha, which plays a role in the development of lethal shock. The lack of TNF-alpha induction by mutant 135 is likely due to its inability to activate T cells. These data suggest that the mutation at histidine 135 in TSST-1 affects toxin interactions with the T-cell receptor rather than the class II major histocompatibility complex receptor.

Animals↗

PubMed1986

Antibodies to staphylococcal enterotoxins and toxic shock syndrome toxin 1 in sera of patients and healthy people in Rio de Janeiro, Brazil.

Sera from 33 persons with staphylococcal infections and from 37 healthy persons were surveyed for the presence of antibody to staphylococcal enterotoxins A, B, C, D, and E and toxic shock syndrome toxin 1. Thirty-one (93.9%) of the patients and 35 (94.6%) of the control group had antibodies to one or more of the enterotoxins. The numbers of patients with antibody to the enterotoxins were as follows: A, 8; B, 9; C, 7; D, 17; E, 21; and toxic shock syndrome toxin 1, 11. The numbers of healthy individuals with antibody to the enterotoxins were as follows: A, 6; B, 12; C, 8; D, 27; E, 21; and toxic shock syndrome toxin 1, 9.

Antitoxins↗

PubMed1999

[Toxic shock syndrome related to the operation of nose].

OBJECTIVE: To study the clinical features of Toxic shock syndrome. METHOD: The clinical information of two cases was analysed. RESULT: It indicates that this disease is caused by TSST-1 which is created by staphylococcus-aureus. The clinical features are acute toxic-shock syndrome with many complications and high mortality. CONCLUSION: More attention should be payed for it.

Adolescent↗

PubMed1983

Purification and some physicochemical properties of toxic-shock toxin.

A procedure for the purification of a protein marker for the staphylococci isolated from toxic-shock syndrome patients has been developed. The purification procedure involves the removal of the toxic protein from culture supernatant fluids of toxic-shock syndrome associated Staphylococcus aureus strains FRI-1169 and FRI-1183 by batch absorption with CG-50 resin, ion-exchange chromatography on CM-Sepharose CL-6B, and gel permeation chromatography on Sephacryl S-200. The purified toxin is a simple protein with a molecular weight of 24 000 +/- 500 as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The isoelectric point of the major band is 7.0 as determined by isoelectric focusing in polyacrylamide gels. The TS-toxin's reactivity with its specific antibody is not affected by tryptic digestion at pH 8.0 but is slowly reduced by treatment with pepsin at pH 4.5. The TS-toxin consists of 188 amino acid residues. Serine was shown to be the NH2-terminal amino acid residue by end-group analysis. Initial studies indicated the protein was emetic; thus tentatively it was called staphylococcal enterotoxin F. In this paper it is called TS-toxin because the emetic action in monkeys has not been confirmed.

Amino Acids↗

PubMed1987

Detection and quantitation of toxic shock syndrome toxin 1 in vitro and in vivo by noncompetitive enzyme-linked immunosorbent assay.

Toxic shock syndrome toxin 1 (TSST-1), an exotoxin produced by many Staphylococcus aureus strains, is implicated as the prime causal agent of toxic shock syndrome (TSS). A sensitive and specific noncompetitive enzyme-linked immunosorbent assay (ELISA) capable of detecting TSST-1 at concentrations from 0.5 to 16 ng/ml was developed. This assay did not detect other staphylococcal enterotoxins including A, B, C1, C2, C3, D, and E. Possible interactions with protein A were readily eliminated by pretreatment of test samples with 10% normal rabbit serum. The assay was adapted for rapid screening of TSST-1 production by S. aureus isolates in culture supernatants in vitro and for detection of TSST-1 in vaginal washings of TSS patients and healthy controls in vivo. All 35 S. aureus isolates confirmed to be TSST positive by Ouchterlony immunodiffusion and 59 of 60 isolates confirmed to be TSST-1 negative gave concordant results by ELISA. Interestingly, toxigenic S. aureus strains isolated from TSS patients quantitatively produced significantly more TSST-1 in vitro compared with toxigenic control strains (P less than 0.05, Mann-Whitney rank sum test). TSST-1 could be detected by ELISA in three of four vaginal washings collected within 3 days of hospitalization from three women with acute menstrual TSS, compared with 0 of 17 washings from nine TSS patients hospitalized longer than 3 days (P = 0.003, Fisher's exact test) and 1 of 15 washings from 14 healthy control women (P = 0.016). This noncompetitive ELISA should be particularly useful for rapid screening of TSST-1 production by S. aureus isolates, for the purification and biochemical characterization of TSST-1, and for human and animal studies of the pathogenesis of TSS.

Bacterial Toxins↗

PubMed1993

Menstrual toxic shock syndrome complicated by persistent bacteremia: case report and review.

An unusual case of menstrual toxic shock syndrome (TSS) is described in which the patient had persistent Staphylococcus aureus bacteremia despite therapy with iv cloxacillin. There was no demonstrable evidence of endocarditis or an abscess as a focus for persisting bacteremia. The strain of S. aureus isolated from the blood and vagina produced toxic shock syndrome toxin 1 (TSST-1) and enterotoxin A. Bacteremia occurs uncommonly in association with TSS; however, aggressive high-dose antistaphylococcal therapy should be instituted for treating this possible complication.

Adult↗

PubMed2005

Prevalence of toxic shock syndrome toxin 1-producing Staphylococcus aureus and the presence of antibodies to this superantigen in menstruating women.

Menstrual toxic shock syndrome (mTSS) is thought to be associated with colonization with toxic shock syndrome toxin 1 (TSST-1)-producing Staphylococcus aureus in women with insufficient antibody titers. mTSS has been associated with menstruation and tampon use, and although it is rare, the effects can be life threatening. It remains of interest because of the widespread use of tampons, reported to be about 70% of women in the United States, Canada, and much of Western Europe. This comprehensive study was designed to determine S. aureus colonization and TSST-1 serum antibody titers in 3,012 menstruating women in North America between the ages of 13 and 40, particularly among age and racial groups that could not be assessed reliably in previous small studies. One out of every four subjects was found to be colonized with S. aureus in at least one of three body sites (nose, vagina, or anus), with approximately 9% colonized vaginally. Eighty-five percent of subjects had antibody titers (> or =1:32) to TSST-1, and the vast majority (81%) of teenaged subjects (13 to 18 years) had already developed antibody titers. Among carriers of toxigenic S. aureus, a significantly lower percentage of black women than of white or Hispanic women were found to have antibody titers (> or =1:32) to TSST-1 (89% versus 98% and 100%). These findings demonstrate that the majority of teenagers have antibody titers (> or =1:32) to TSST-1 and are presumed to be protected from mTSS. These findings also suggest that black women may be more susceptible to mTSS than previously thought.

Adolescent↗

PubMed1982

Toxic shock syndrome: an ecologic imbalance within the genital microflora of women?

Epidemiologic data suggested that toxic shock syndrome (TSS) may be caused by an imbalance among the flora of the female genital tract. Since natural defense mechanisms often involve antagonistic interactions between the flora and potential pathogens, the ability of genital lactobacilli to inhibit Staphylococcus aureus was determined in agar overlay assays. Lactobacilli were chosen for study because previous investigations had suggested an important role for this genus in maintenance of health of the female genital tract. Fourteen of 50 strains of lactobacilli and Lactinex inhibited the growth of certain staphylococci, including strains from cases of TSS. The inhibitory activity of some lactobacilli was variable and could be enhanced by exogenously supplied substrates. Growth of one consistently inhibitory lactobacillus was inhibited by Staphylococcus aureus. A model for the etiology of toxic shock syndrome in menstruating women is proposed. The model includes antagonistic interactions between lactobacilli and staphylococci and the influence of tampons on these interactions to favor the staphylococcus.

Ecology↗

PubMedDate not supplied

On the pathogenesis of toxic shock syndrome.

Understanding of the pathogenesis of toxic shock syndrome (TSS) has come from the juxtaposition of epidemiologic, clinical, immunologic, and physiologic studies. A hypothesis has been developed for the pathogenesis of menstrually related TSS. Certain tampon fibers that are highly absorbent for water are also ion exchangers for magnesium ions. The latter ions uniquely affect the production of TSS toxin 1 (TSST-1) by appropriate strains of Staphylococcus aureus, with a marked increase in the amount of toxin when magnesium concentrations are limiting and suppression of toxin production when magnesium is in excess. Many epidemiologic features of TSS could be explained by this hypothesis. The absorbability of highly absorptive fibers is not affected by the addition of small amounts of magnesium sufficient to suppress production of TSST-1; thus absorption is distinguishable from toxin production in vitro. TSST-1 stimulates production of interleukin 1 and of tumor necrosis factor and is highly toxic when absorbed slowly. Like TSST-1, staphylococcal enterotoxins are lethal to rabbits when given by slow injection, and some enterotoxins may be more lethal than TSST-1.

Bacterial Toxins↗

PubMed1996

[Toxic shock syndrome due to Streptococcus pyogenes: a case report].

An increasing number of severe invasive Group A streptococcal infections have recently been reported. A new syndrome similar to the staphylococcal toxic shock syndrome, defined "streptococcal toxic shock-like syndrome" is also described. We report a case of streptococcal toxic shock-like syndrome with atypical clinical onset. A 67 years old man was admitted on the emergency department because of pain in the scapular area without fever. The patient developed irreversible shock and died after 36 hours. Diagnosis was made with autopsy. We stress the possibility of infectious cause in presence of severe multi organ failure with rapid clinical exacerbation.

English Abstract↗

PubMed2003

Neonatal toxic shock syndrome-like exanthematous disease (NTED).

The author and colleagues recently discovered an emerging neonatal infectious disease: neonatal toxic shock syndrome-like exanthematous disease (NTED), which is induced by the superantigen toxic shock syndrome toxin-1 (TSST-1), produced by methicillin-resistant Staphylococcus aureus (MRSA). The massively expanded Vbeta2+ T cells were rapidly deleted in the peripheral blood of patients with NTED. A marked depletion of Vbeta2+ T cells was also observed in the peripheral blood before the expansion of these T cells. Anergy is specifically induced in the TSST-1 reactive T cells of patients with NTED. Rapid recovery from NTED without complications is expected to be related to the induction of immunologic tolerance in neonatal patients. Anti-TSST-1 IgG antibody of maternal origin was found to play a protective role in preventing the development of NTED. The number of hospitals that have experience caring for patients with NTED has increased threefold in the past 5 years. Most MRSA isolates from neonatal intensive care units in Japan were found to be a single clone of coagulase type II and to possess TSST-1 and staphylococcal enterotoxin C genes. The timing and increased incidence of NTED suggest the emergence of a new MRSA clone. By recognizing that TSST-1 can induce NTED, healthcare providers may give increased attention to this disease in neonatal wards.

Antilymphocyte Serum↗

PubMed1983

Toxic shock syndrome related to nasal packing.

While toxic shock syndrome (TSS) is generally considered to be a tampon-related illness, an increasing number of reported cases have been related to surgical wounds. At least one case has been reported following nasal surgery with nasal packing. We report two additional cases of TSS associated with nasal packing. Because nasal packing is in some ways analogous to the use of tampons for menstrual hygiene, and nasal carriage of Staphylococcus aureus is frequent, the scarcity of TSS cases reported to occur following nasal packing is surprising. Otorhinolaryngologists are urged to report TSS cases associated with nasal packing to their state and local health departments or the Centers for Disease Control to aid in the understanding of the pathogenesis of this disease.

Adult↗

PubMedDate not supplied

Toxic shock syndrome following submandibular gland excision.

Acute toxic shock syndrome (TSS), initially described in association with the use of super absorbent tampons in menstruating women, has complicated a variety of surgical procedures. Recent attention in head and neck surgery has focused on absorbent packing materials, such as those used in postoperative nasal care. It is important to maintain a high index of suspicion in all postoperative patients to fever, hypotension, and erythroderma. We report TSS following submandibular gland excision.

Dermatitis, Exfoliative↗

PubMed2005

Diffuse venous thromboemboli associated with IVIg therapy in the treatment of streptococcal toxic shock syndrome: case report and review.

Streptococcal toxic shock syndrome (STSS) is a severe invasive disease with a 40-80% mortality rate. Inflammatory cytokines induced by streptococcal pyrogenic exotoxins (SPEs) produce the clinical manifestations of a flu-like syndrome, followed by high fevers and multiorgan failure. Previously published reports have described the use of intravenous immunoglobulin (IVIg) as adjunctive treatment for STSS. However, concerns have been raised about the thromboembolic complications of this therapy. We report a severe case of STSS treated with two adjunctive courses of IVIg complicated by severe bilateral pulmonary thromboemboli. To our knowledge, this is the only reported case of thromboemboli associated with IVIg for STSS. The results of this case support the cautious use of IVIg for STSS and demonstrate the need for controlled trials to determine the appropriate timing, dosage, and course of treatment.

Adult↗

PubMed2005

[Toxic shock syndrome associated with nasal packing].

Staphiloccocal Toxic Shock Syndrome is a potentially fatal multisystem disease associated to nasal packing, catheter insertion, retention of foreign materials and uneffective sterile techniques. It is usually developed in the immediate postoperative period (first 48 hours) with hypotension, skin rash, fever, multisystemic failure and shock. We report a case in a 24-year-old man secondary to nasal surgery.

Adult↗

PubMed2000

A survey into toxic shock syndrome (TSS) in UK burns units.

Toxic shock syndrome (TSS) is a rare complication of a Staphylococcus aureus infection and is primarily seen in children with small burns. The true incidence of TSS in burns patients is not known and the number of presumptive cases rarely reported. This survey was undertaken to determine if the incidence of TSS in children with burns could be related to the type of dressing used to cover the wound. A questionnaire was compiled and sent to the Senior Nurse in charge of each of the UK burns units. General information on the number of admissions, age of the patient, cause of injury and burn wound management was sought. An 81% response was obtained after two mailshots and follow up telephone calls. Seventy percent (23/33) of units which answered the survey nursed children. Of these, eight units had either not encountered TSS previously or not had a case within the past two years. These units were small, admitting a maximum of 50 patients each year. Of the units where TSS was encountered, approximately 2.5% of children admitted showed symptoms of TSS. Of the units who nursed both adults and children, seven units had seen TSS in burned adult patients which has not been reported in the literature. Of the eight units where TSS had not been recently encountered, four routinely administered prophylactic antibiotics to prevent infection whereas routine administration of antibiotics occurred in only two of the 15 units where TSS was seen. Although wound management procedures differed slightly there were many similarities. These included wound cleaning with normal saline, covering with either silver sulphadiazine (1%) or povidone iodine (10%), depending upon the infection status, and dressing with a paraffin tulle, gauze and crepe bandages. No association between the management of the burn wound and subsequent development of TSS could be established.

Adult↗

PubMed1982

[Toxic shock syndrome].

Since the description of the toxic shock syndrome as a disease entity approximately 700 cases have been reported, mainly in young women during their period using tampons. The cause is thought to be toxins of Staph. aureus. The disease was now observed in a 13-year-old girl, presenting as severe acute septicaemia. The aetiopathogenetic connection with use of tampons could only be established during a second, entirely identical, illness, occurring again precisely 3 days after the onset of the following period.

Adolescent↗

PubMed1988

Characterization of staphylococci from patients with toxic shock syndrome.

Fifty staphylococcal strains that produced toxic shock syndrome (TSS) toxin 1 and that were isolated from patients with TSS were characterized. One strain had more properties that were characteristic of Staphylococcus hyicus than of Staphylococcus aureus. Forty-four strains had the same properties or differed in only one property. Thirty-five of the 50 strains produced either enterotoxin A or C or both in addition to TSS toxin 1.

Humans↗