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At least 19 recordsLinked to original sources
PubMed1989

[Streptococcus-induced syndrome of toxic shock (streptococcal toxic shock syndrome)].

Report on the first case of streptococcal toxic shock syndrome in the GDR. The patient was a 54-year-old female. One week before admission to the hospital she cut her finger. The day before admission to the hospital she presented with a painful left shoulder. Demarcation followed, and Streptococcus pyogenes (group A streptococci) was isolated from this area. The temperature rose to more than 40 degrees C and she became confused, hypotensive and anuric. There was evidence for disseminated intravascular coagulation. She died 23 h after admission. Clinical course and laboratory parameters resembles staphylococcal toxic shock syndrome, except a diarrhoea. The streptococcal strain produced a large amount of erythrogenic toxin type B (more than 20 ng/ml), but not erythrogenic toxins A or C. Erythrogenic toxins of Streptococcus pyogenes seem to play the same role in the development of streptococcal toxic shock syndrome as the toxic shock syndrome 1 (TSST-1) in staphylococcal toxic shock syndrome.

Animals↗
PubMed1989

Relative strength of the mitogenic and interleukin-2-production-inducing activities of staphylococcal exotoxins presumed to be causative exotoxins of toxic shock syndrome: toxic shock syndrome toxin-1 and enterotoxins A, B and C to murine and human T cells.

Several observations suggest that staphylococcal enterotoxins A, B and C (SEA, SEB and SEC, respectively), in addition to toxic shock syndrome toxin-1 (TSST-1), are causative exotoxins of toxic shock syndrome (TSS). Based on the view that polyclonal T cell activation with the causative exotoxins, resulting in over-production of lymphokines, is involved in the development of the pathological changes observed in TSS, we investigated the activities of these four exotoxins to induce proliferation and interleukin 2 production in murine and human lymphocytes by using in vitro culture systems. The results showed that all these exotoxins are strong polyclonal inducers of proliferation and interleukin 2 production in human T cells, whereas TSST-1 and SEA are strong and SEB and SEC are weak polyclonal inducers in murine T cells. These results suggest that SEA, SEB and SEC, in addition to TSST-1, are possibly involved as causative exotoxins in the development of the pathological changes observed in TSS.

Adult↗
PubMed1984

Presence of toxic shock toxin in toxic shock and other clinical strains of Staphylococcus aureus.

Toxic shock toxin (TST), also known as pyrogenic exotoxin C (Schlievert et al., J. Infect. Dis. 143:509-516, 1981) and staphylococcal enterotoxin F (Bergdoll et al., Lancet i:1017-1021, 1981), was purified from toxic shock strains of Staphylococcus aureus by preparative isoelectric focusing and by chromatofocusing. Neither method produced an absolutely pure protein as determined by silver staining of sodium dodecyl sulfate-acrylamide gels, although chromatofocusing was the better method of the two. Three molecular weight variants of the protein were found in the two toxic shock syndrome strains that were studied, regardless of the purification method that was used. An isoelectric point of 7.15 and molecular weights of 21,400, 22,100, and 23,200 were determined for the different forms of the protein from electrophoresis data. A sedimentation coefficient of 2.3S was determined by sucrose gradient centrifugation, and a Stokes radius of 2 X 10(-7) cm was determined by gel filtration. An average molecular weight of 18,900 for all of the TST forms was calculated from these data by the Stokes-Einstein equation. A survey for TST in 32 control and 46 toxic shock strains of S. aureus by isoelectric focusing and by agarose gel double immunodiffusion with specific rabbit antiserum revealed that the isoelectric focusing method tends to overestimate the number of TST-positive strains because of the detection of non-TST, neutral staphylococcal proteins. Based on immunodiffusion data, the association of TST with toxic shock strains was found to be 100% in vaginal isolates and 62% in non-vaginal isolates. In the control strains, TST was found in 16% of the vaginal strains and 23% of the non-vaginal strains. The value of this toxin as a marker for toxic shock and its relationship to the pathogenesis of this disease are discussed.

Bacterial Toxins↗
PubMedDate not supplied

Ecology of toxic shock syndrome: amplification of toxic shock syndrome toxin 1 by materials of medical interest.

Historically, the literature suggests that staphylococcal exoproteins, including enterotoxins, are stimulated by various physicochemical ecologic factors, many of which have been shown to stimulate production of toxic shock syndrome toxin 1 (TSST-1). The propensity of different fibers and other substances to amplify TSST-1 production in toxic shock syndrome-associated strains of Staphylococcus aureus, as well as a comparative analysis of the underlying mechanisms of TSST-1 production, are reported. Two hundred twenty intravaginal devices or other products and materials and 60 experimental controls were examined for their propensity to induce TSST-1 production. Certain materials are superior to unaltered cotton in providing a more absorbent fiber--nutrients are efficiently drawn in, concentrating protein between fibers, and thereby creating an ideal physicochemical environment for the amplification of TSST-1 and other toxins. The greatest stimulation of TSST-1 was observed with (in decreasing order): polyester and carboxymethyl cellulose, polyacrylates, viscose rayon, gelatin foam, polyurethane, and cotton. No toxin was found with nasal tampons (polymer of polyvinyl acetal) or with vaginal cups (an elastomeric polymer). Results are discussed in terms of specific ecologic parameters from historical as well as recent perspectives.

Bacterial Toxins↗
PubMedDate not supplied

Distribution and expression of toxic shock syndrome toxin 1 gene among Staphylococcus aureus isolates of toxic shock syndrome and non-toxic shock syndrome origin.

Toxic shock syndrome toxin 1 (TSST-1), plays a significant role in the pathogenesis of TSS. TSST-1 production is subject to physiologic and environmental constraints. Thus, DNA probes that detect the chromosomal gene encoding the toxin are of value diagnostically, epidemiologically, and for studies of gene expression. Several synthetic oligonucleotide probes complementary to two regions of the TSST-1 gene were used to ascertain the presence of this gene in the chromosomal DNA of 261 strains of S. aureus from various TSS-related and non-TSS-related sources. Isolates were from clinically confirmed menstrual and nonmenstrual cases of TSS and from healthy vaginal carriers of S. aureus. Other strains tested included clinical non-TSS isolates and food poisoning-associated staphylococcal isolates. Detection of the TSST-1 gene by the labeled gene probes correlated in all but two cases with production of TSST-1. Ten Centers for Disease Control (CDC) strains that were isolated from TSS patients and did not produce TSST-1 were also examined, as were several strains of Staphylococcus epidermidis isolated from patients with suspected TSS. Neither group of strains possessed the TSST-1 gene. Finally, a 7-kilobase DNA restriction fragment of S. aureus containing the entire TSST-1 gene was transformed into Escherichia coli strains HB101 and DH5 alpha via a plasmid vector.

Bacterial Toxins↗
PubMedDate not supplied

Risk of developing toxic shock syndrome associated with toxic shock syndrome toxin 1 following nongenital staphylococcal infection.

Few risk factors for nonmenstrual toxic shock syndrome (TSS) have been identified. This study sought to determine at what rate and under what circumstances nongenital toxigenic Staphylococcus aureus infections led to TSS. Clinical isolates of S. aureus were examined for the production of TSS toxin 1 (TSST-1), and available sera from infected patients were tested for antibody to this toxin. Twenty-six percent of 810 isolates produced TSST-1. Isolates from children were more likely to be positive for TSST-1 than were those from adults. None of 57 patients with TSST-1-positive staphylococcal infection and a TSST-1 antibody titer of greater than or equal to 1:100 developed TSS. Eight of 65 tested patients with TSST-1-positive isolates had antibody below the presumably protective level of 1:100. Two of these patients had definite TSS, three had probable or possible TSS, and three probably did not have TSS. In patients lacking protective antibody to TSST-1, the interval between acquisition and infection with staphylococci, the type and amount of toxins produced, the site of infection, and still-unclarified aspects of host susceptibility may all affect the rate and severity of TSS.

Adult↗
PubMed1985

Development of serum antibody to toxic shock toxin among individuals with toxic shock syndrome in Wisconsin.

The presence of Staphylococcus aureus producing toxic shock toxin (TST) and the absence of antibody to TST (anti-TST) in acute-phase sera are markers for toxic shock syndrome (TSS). We used radioimmunoassay methods to examine 133 acute-phase and 277 convalescent-phase serum specimens from 181 patients with TSS for anti-TST. Among confirmed menstrual cases, nine (9.5%) of 95 patients had demonstrable anti-TST in acute-phase sera obtained during the first seven days of illness; patients with probable or non-menstrual TSS had a higher prevalence of anti-TST in acute-phase sera. Five (33.3%) of 15 individuals with confirmed menstrual TSS developed anti-TST as early as seven to nine days after TSS onset; 32 (62.7%) of 51 patients had demonstrable anti-TST in sera obtained more than one year after their episode of TSS. This study demonstrates a gradual rate and low magnitude of development of anti-TST after TSS and supports the diagnostic usefulness of measuring anti-TST levels in sera from patients suspected of having TSS.

Acute Disease↗
PubMed1982

Toxic shock syndrome or toxic epidermal necrolysis? Case reports showing clinical similarity and histologic separation.

A case of toxic shock syndrome and a case of drug-induced toxic epidermal necrolysis with renal involvement are described. The two patients had similar early clinical manifestations and therefore posed a difficult differential diagnosis. Diagnostic distinction is important because therapy differs considerably. A skin biopsy in each case proved helpful in establishing the correct diagnosis, since there appears to be a different histologic pattern for each condition: superficial perivascular dermatitis for toxic shock syndrome and an interface dermatitis for toxic epidermal necrolysis.

Adult↗
PubMed1984

Association of high levels of serum antibody to staphylococcal toxic shock antigen with nasal carriage of toxic shock antigen-producing strains of Staphylococcus aureus.

Forty-four asymptomatic male subjects were examined for their nasal carriage of strains of Staphylococcus aureus capable of producing staphylococcal toxic shock antigen (TSA), an exotoxin implicated in the pathogenesis of toxic shock syndrome. In addition, the levels of antibody to TSA in sera from these subjects were determined by an enzyme-linked immunosorbent assay. S. aureus was isolated from the anterior nares of 23 subjects. Of those 23 isolates of S. aureus, 9 were found to produce TSA. All individuals carrying strains of S. aureus capable of producing TSA had high to moderate levels of antibody to TSA. In contrast, those individuals carrying strains not producing TSA had levels of antibody to TSA ranging from high to nondetectable. A second examination of nasal samples from 42 of these subjects revealed that 86% of those carrying S. aureus initially still carried S. aureus after a period of 3 months; all subjects found to carry TSA-producing strains initially and that were examined a second time yielded TSA-producing strains once again.

Adult↗
PubMed2003

Effects of total body irradiation and cyclosporin a on the lethality of toxic shock syndrome toxin-1 in a rabbit model of toxic shock syndrome.

Toxic shock syndrome (TSS) may be mediated by superantigen-activated T cells, a theory we tested in rabbits, which are more susceptible to the lethal effects of superantigens, such as TSS toxin-1 (TSST-1), than are mice. Rabbits exposed to 10 cGy of total body irradiation exhibited T cell deficiency, with profound depletion of splenic lymphocytes and circulating CD4(+) lymphocytes, as well as an inability to manifest delayed-type hypersensitivity. Nevertheless, these rabbits remained completely susceptible to TSST-1, indicating that TSS can occur in the setting of marked immunosuppression.

Animals↗
PubMed1985

Animal studies of toxic shock syndrome.

Toxic shock syndrome (TSS) was first described in 1978 and since that year over 2990 cases have been reported to the Communicable Disease Center. The estimated case-fatality rate is 5.6%. The disease is characterized by fever, hypotension, rash, desquamation, and involvement of at least three other organ systems. Approximately 85% of the cases are menstrually related and tampon use has been identified as a risk factor. The remaining 15% of the cases occur in both sexes and are not specifically related to age or geographic location. In all cases where sought there is evidence for infection by Staphylococcus aureus. Nearly all S. aureus isolates are phage type 52/29 and elaborate a unique exotoxin (toxic shock toxin). This review explores both the successful and unsuccessful attempts to induce toxic shock or a TSS-like syndrome in animals other than man. The review identifies the baboon as an animal model of TSS and discusses the clinical and pathologic sequellae, in this species, after exposure to purified toxic shock toxin.

Animals↗
PubMed1990

Therapy of toxic shock syndrome.

Toxic shock syndrome (TSS) is an acute febrile, exanthematous illness associated with multisystem failure including shock, renal failure, myocardial failure and adult respiratory distress syndrome (ARDS). It usually presents with fever, pharyngitis, diarrhoea, vomiting, myalgia, and a scarlet fever-like rash, and may progress rapidly (within hours) to signs of hypovolaemic hypotension such as orthostatic dizziness or fainting. The signs and symptoms of toxic shock syndrome should be recognised early to permit successful therapy. Patients are usually suffering from hypovolaemia due to leaky capillaries and fluid loss into the interstitial space, and consequently large volumes of fluid, both crystalloid (e.g. saline, electrolyte-solutions) and colloid (e.g. albumin, intravenous gamma-globulin), may be necessary to maintain adequate venous return and cardiac output. Patients with toxic shock syndrome usually have a focus of staphylococcal infection such as a surgical wound infection or soft tissue abscess, or they may have TSS associated with menstruation and use of a vaginal device such as tampons. The site of infection should be adequately drained and treated with antimicrobial therapy. Subacute complications including ARDS and myocardial failure require a thorough understanding of the underlying pathophysiology to ensure appropriate treatment. Recurrences of TSS can be avoided by appropriate antimicrobial treatment and avoidance of recurrent conditions which might favour staphylococcal toxin production (e.g. use of tampons during menstruation). More than 95% of patients survive toxic shock syndrome if appropriate therapy is instituted early.

Humans↗
PubMed1994

Dual infections with Staphylococcus aureus and Streptococcus pyogenes causing toxic shock syndrome. Possible synergistic effects of toxic shock syndrome toxin 1 and streptococcal pyrogenic exotoxin C.

We describe a 35-year-old woman with clinical, microbiologic, and serologic findings suggesting that the patient developed toxic shock syndrome as a result of dual infections caused by toxin-producing strains of Staphylococcus aureus and Streptococcus pyogenes. Certain aspects of the pathogenesis of this toxin-related syndrome are reviewed.

Adult↗
PubMed1994

Advanced cervical carcinoma presenting with toxic shock syndrome.

Toxic shock syndrome is a multisystem disease which presents with a high fever, rash, gastrointestinal symptoms, and hypotension. A 58-year-old woman presented to the emergency room with these symptoms, hypotension and tachycardia. Because of vaginal spotting a pelvic examination was performed which demonstrated vulvo/vaginal erythema and a large vaginal mass consistent with an advanced cervical cancer with bilateral pelvic sidewall fixation. Cervical/vaginal biopsy demonstrated invasive squamous cell carcinoma and an initial chest X ray demonstrated multiple pulmonary metastases. After a total of 8 days of antibiotic therapy the patient received cis-platinum chemotherapy. The toxic shock syndrome was the presenting symptomatology in this patient with advanced cervical cancer. Toxic shock syndrome has been associated with the use of hyperabsorbent tampons as well as numerous other gynecologic procedures but has not been reported in patients with gynecologic cancer.

Anti-Bacterial Agents↗
PubMedDate not supplied

Hypercalcitoninemia, hypocalcemia, and toxic shock syndrome.

Toxic shock syndrome is a multisystem illness frequently complicated by hypocalcemia. The etiology of the hypocalcemia, which may be severe, is not well understood. We report two cases of fatal toxic shock syndrome accompanied by severe hypocalcemia; each patient also had an inappropriately elevated serum calcitonin level, which in one case was as high as 179,000 pg/mL. Hypercalcitoninemia may be a cause of the low serum calcium levels as well as of certain clinical manifestations of toxic shock syndrome.

Adolescent↗