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PubMedDate not supplied

Vaginal tampon model for toxic shock syndrome.

The effects of tampon composition, inoculum size, and simulated menses on production of toxic shock syndrome toxin 1 (TSST-1) and toxic shock syndrome (TSS) were evaluated in a rabbit model that simulates tampon use in humans. Three small generic compressed-fiber tampons were successively inserted vaginally (remained in place 4.5 hours x 2; overnight x 1). Tampon no. 1 was inoculated with live TSST-1-positive staphylococci plus 5 mL of saline or simulated menses (defibrinated rabbit blood plus 2.5 g of bovine serum albumin/dL) immediately after insertion; saline or simulated menses alone were used with tampons no. 2 and 3. The vagina was washed after removal of tampon no. 3. TSS-like illness was produced consistently in animals with carboxymethyl cellulose/polyester foam tampons, which supported higher organism counts and greater TSST-1 production in association with subsequent tampons. Cotton and rayon tampons were not associated with as much clinical illness, organism growth, or TSST-1 production. Simulated menses supported toxin production and clinical illness when the inoculum was one-tenth that required for controls. Sham tampon insertion was associated with TSS-like illness in two of 10 rabbits; thus, other factors may promote TSS in the absence of vaginal tampons. This model reliability reproduces menstrual TSS, since one-time vaginal inoculation with TSST-1-positive staphylococci in the presence of blood and certain tampons leads to TSS, and may be useful in evaluating catamenial products and in understanding other factors important in TSST-1 production in vivo and the development of TSS.

Animals↗
PubMed1998

Another toxic shock syndrome. Streptococcal infection is even more dangerous than the staphylococcal form.

In the battery of diseases caused by group A streptococci, streptococcal toxic shock syndrome is among the most severe. Its nonspecific presentation and rapid progression require that the treating physician be both knowledgeable and vigilant. Certain signs and symptoms suggest that caution is in order: Pain out of proportion to physical findings may herald deep tissue involvement in a patient who at first glance appears to have cellulitis. Streptococcal infection accompanied by hypotension, confusion, or unexplained acute renal insufficiency is a clue to streptococcal toxic shock syndrome. Treatment consists of antibiotic and supportive care, with aggressive surgical debridement of soft-tissue foci of infection when necessary. Anecdotal evidence suggests that intravenous immunoglobulin may have a place in neutralizing the secreted streptococcal toxins that are thought to mediate features of the disease. At present, even with aggressive therapy, the mortality rate of streptococcal toxic shock syndrome can exceed 50%. Understanding of its pathogenesis is progressing. However, until effective interventions are developed, early detection appears to be the best weapon.

Humans↗
PubMed1989

Toxic shock syndrome toxin 1 binds to major histocompatibility complex class II molecules.

Toxic shock syndrome toxin 1 (TSST-1) is a 22-kDa exotoxin produced by strains of Staphylococcus aureus and implicated in the pathogenesis of toxic shock syndrome. In common with other staphylococcal exotoxins, TSST-1 has diverse immunological effects. These include the induction of interleukin 2 receptor expression, interleukin 2 synthesis, proliferation of human T lymphocytes, and stimulation of interleukin 1 synthesis by human monocytes. In the present study, we demonstrate that TSST-1 binds with saturation kinetics and with a dissociation constant of 17-43 nM to a single class of binding sites on human mononuclear cells. There was a strong correlation between the number of TSST-1 binding sites and the expression of major histocompatibility complex class II molecules, and interferon-gamma induced the expression of class II molecules as well as TSST-1 binding sites on human skin-derived fibroblasts. Monoclonal antibodies to HLA-DR, but not to HLA-DP or HLA-DQ, strongly inhibited TSST-1 binding. Affinity chromatography of 125I-labeled cell membranes over TSST-1-agarose resulted in the recovery of two bands of 35 kDa and 31 kDa that comigrated, respectively, with the alpha and beta chains of HLA-DR and that could be immunoprecipitated with anti-HLA-DR monoclonal antibodies. Binding of TSST-1 was demonstrated to HLA-DR and HLA-DQ L-cell transfectants. These results indicate that major histocompatibility complex class II molecules represent the major binding site for TSST-1 on human cells.

Animals↗
PubMed1990

Mutants of staphylococcal toxic shock syndrome toxin 1: mitogenicity and recognition by a neutralizing monoclonal antibody.

Toxic shock syndrome toxin 1 (TSST-1), a 22-kilodalton protein made by strains of Staphylococcus aureus harboring the chromosomal toxin gene, may elicit toxic shock syndrome in humans. In vitro, TSST-1 induces T cells to proliferate and macrophages to secrete interleukin-1. To conduct a structure-function analysis, point mutations on the TSST-1 gene were generated by site-directed mutagenesis to identify amino acids critical for activity of the toxin. Specific tyrosine and histidine residues were replaced by alanines. Wild-type and mutant TSST-1 gene constructs were expressed in Escherichia coli, and the products were tested for their mitogenic potential and reactivity with a TSST-1 neutralizing monoclonal antibody (MAb 8-5-7). Four of the mutants were similar to the wild type; i.e., the mutant toxins stimulated murine T cells and reacted with MAb 8-5-7 equally as well as the wild type. Two mutants exhibited a decrease in mitogenic activity, but one of these retained the capacity to bind with MAb 8-5-7 while the other was no longer recognized by the same antibody. One double mutant demonstrated minimal mitogenic activity and did not react in enzyme-linked immunosorbent and immunoblot assays with MAb 8-5-7. The data show that specific residues near the carboxy terminus of TSST-1 are essential for mitogenic activity and in forming the epitope recognized by neutralizing MAb 8-5-7.

Animals↗
PubMed1983

Toxic shock syndrome in a patient with systemic lupus erythematosus.

A case is presented of toxic shock syndrome in a patient with systemic lupus erythematosus. Toxic shock syndrome is rarely reported in patients who are immunosuppressed, perhaps because such patients are often treated vigorously with antibiotics at the earliest sign of infection. The association in this case may have been coincidental.

Adult↗
PubMed1989

Crystal violet binding, cell surface properties and extracellular enzyme profiles of Staphylococcus aureus producing toxic shock syndrome toxin-1.

Staphylococcus aureus isolated from clinically diagnosed cases of toxic shock syndrome (TSS) showed susceptibility to phage types belonging to both I and III groups (90.5%). Phage typing patterns showed a wide diversity among 87 toxic shock syndrome toxin-1 (TSST-1) positive strains isolated from different non TSS clinical sources. Toxin producing strains isolated from both TSS and non TSS showed a remarkable ability to bind to crystal violet (pattern C/D, 97.2%) incorporated into brain heart infusion agar media at subinhibitory concentrations and these isolates were traced to biotype var. hominis. The cellular fatty acid compositions of TSS and non-TSS strains belonging to the three biotypes S. aureus var. hominis, S. aureus var. bovis and S. aureus var. canis did not differ. TSST-1 producing strains demonstrated a high salt aggregation test value (above 1.5) indicating a low cell surface hydrophobicity. Both TSS and non TSS strains demonstrated a high lipolytic activity. TSST-1 positive strains in general, showed significantly higher lipase activity than strains isolated from septicemia (p less than 0.0001) and superficial (p less than 0.0001) infections. The proteolytic activity is higher among TSS (median value 0.075 U/ml) than to non TSS (median value 0.045 U/ml) strains. There was no correlation with the quantity of toxin production in vitro and to the properties described.

Bacterial Toxins↗
PubMed1984

Diagnostic bias and toxic shock syndrome.

Diagnostic bias could have occurred in the tampon/toxic shock syndrome association if the original diagnostic judgments by physicians or the subsequent diagnostic selections by investigators were influenced by knowledge of the patient's gender, menstrual history, or catamenial product. To determine whether such diagnostic bias can occur, a set of descriptive vignettes was prepared for six cases (Series X) having diverse resemblances to toxic shock syndrome or Kawasaki's disease. For each vignette in Series X, a paired case in a complementary Series Y was described in identical text except for different information about gender, menstrual history, or tampon use. Either Series X or Series Y was sent to a randomly selected sample of internists, family practitioners, and infectious disease subspecialists. The physicians were asked to provide a diagnosis for each case, using their own nomenclature or choosing from a list of 22 diagnostic possibilities. Six weeks later, respondents were asked to provide diagnoses for the complementary series of cases. Regardless of medical specialty or type of series received first, the 368 responding physicians were more likely to diagnose toxic shock for menstruating tampon-users or menstruating women than for non-menstruating women or men. In the most striking difference, toxic shock was diagnosed in 85 percent of instances when the case was described in a menstruating tampon-user, but in 23 percent of instances when the same case was described in a man (odds ratio = 18.8). Since the current epidemiologic data may be seriously distorted by diagnostic bias, the results indicate the need for scientifically valid investigations of the toxic shock syndrome/tampon relationship.

Adolescent↗
PubMed1988

Association of toxic shock toxin-1 determinant with a heterologous insertion at multiple loci in the Staphylococcus aureus chromosome.

Most Staphylococcus aureus strains associated with toxic shock syndrome and producing toxic shock syndrome toxin 1 (TSST-1) require tryptophan because of a genetic defect in tryptophan biosynthesis. The association between TSST-1 production and tryptophan auxotrophy was not correlated with the phage type, the colonization site, or the disease status of the patient from whom the isolate came. Protoplast fusion and transformation mapping located the genetic determinant of TSST-1 production (tst) very close to the trp operon in such strains and very close to tyrB in a Trp+ TSST-1+ strain. Southern blot hybridization of ClaI-restricted chromosomal DNA with a tst-specific probe revealed a common homologous segment in all of the Trp+ strains with tst linked to tyrB. These results confirmed that the tst determinant in Trp- strains is located at one site, whereas in Trp+ TSST-1+ strains the determinant is located elsewhere on the S. aureus chromosome. It is suggested that the TSST-1 determinant is associated with the insertion of a transposonlike segment into several sites on the S. aureus chromosome.

Bacterial Toxins↗
PubMed1997

Refined structures of three crystal forms of toxic shock syndrome toxin-1 and of a tetramutant with reduced activity.

The structure of toxic shock syndrome toxin-1 (TSST-1), the causative agent in toxic shock syndrome, has been determined in three crystal forms. The three structural models have been refined to R-factors of 0.154, 0.150, and 0.198 at resolutions of 2.05 A, 2.90 A, and 2.75 A, respectively. One crystal form of TSST-1 contains a zinc ion bound between two symmetry-related molecules. Although not required for biological activity, zinc dramatically potentiates the mitogenicity of TSST-1 at very low concentrations. In addition, the structure of the tetramutant TSST-1H [T69I, Y80W, E132K, I140T], which is nonmitogenic and does not amplify endotoxin shock, has been determined and refined in a fourth crystal form (R-factor = 0.173 to 1.9 A resolution).

Bacterial Toxins↗
PubMed1981

Toxic shock in the teenage patient.

The toxic shock syndrome (TSS) is a newly described syndrome. It affects predominantly teenage girls and young women at or around the time of their menstrual period. There is fever, diarrhea, vomiting, and profound shock with mental confusion, decreased renal function, and a scarlatiniform rash that later desquamates. Rapid recognition and vigorous fluid therapy is essential. There is a relationship of menses, Staphylococcus aureus, and the use of tampons in the etiology of this new syndrome.

Adolescent↗
PubMed1999

Comparison of pathogenic factors expressed by group A Streptococci isolated from patients with streptococcal toxic shock syndrome and scarlet fever.

Streptococcal toxic shock syndrome (STSS) is an illness with high mortality. To obtain clues to understanding the pathogenesis of STSS, we investigated the expression of several pathogenic factors in ten group A streptococcus (GAS) isolates from ten patients with STSS in Japan, in comparison with ten GAS isolates from children with scarlet fever. The ten scarlet fever-derived GAS isolates were equally low in lethality and anti-phagocytic activity in mice and in the production of streptolysin O (SLO), and equally high in production of superantigenic exotoxins (SAGTs) and cysteine proteinase. By comparison, the ten STSS-derived GAS isolates were heterogeneous in the expression of the above pathogenic factors, which ranged from low to high values. Most of the ten STSS-derived isolates were higher in lethality and anti-phagocytic activity and production of SLO, and lower in the production of SAGTs and cysteine proteinase than the ten scarlet fever-derived isolates. The results suggest that the lethality and anti-phagocytic activity examined in mice and SLO may be involved mainly in the development of most of the ten STSS cases.

Animals↗
PubMed1994

Bacterial laryngotracheitis associated with toxic shock syndrome in an adult.

Nonmenstrual toxic shock syndrome (TSS) in adults has been associated with various staphylococcal respiratory tract infections, including pharyngitis, tonsillitis, pneumonia, and postinfluenza respiratory tract infections. In children, nonmenstrual TSS has also been described as a complication of bacterial tracheitis. We describe the case of a 40-year-old woman who presented with laryngotracheitis as well as clinical and laboratory evidence of TSS. Culture of her sputum samples yielded pure growth of Staphylococcus aureus, which was shown to produce TSS toxin 1 (TSST-1). The patient responded promptly to therapy with iv clindamycin. We discuss the association of TSS with staphylococcal laryngotracheitis and the role of clindamycin in the treatment of TSS. To our knowledge, there are no previous reports of TSS complicating laryngotracheitis in adults.

Adult↗
PubMed1990

Staphylococcal and streptococcal pyrogenic toxins involved in toxic shock syndrome and related illnesses.

Toxic-shock syndrome (TSS) is an acute onset, multiorgan illness which resembles severe scarlet fever. The illness is caused by Staphylococcus aureus strains that express TSS toxin-1 (TSST-1), enterotoxin B, or enterotoxin C. TSST-1 is associated with menstrual TSS and approximately one-half of nonmenstrual cases; the other two toxins cause nonmenstrual cases, 47% and 3%, respectively. The three toxins are expressed in culture media under similar environmental conditions. These conditions may explain the association of certain tampons with menstrual TSS. Biochemically, the toxins are all relatively low molecular weight and fairly heat and protease stable. Enterotoxins B and C, share nearly 50% sequence homology with streptococcal scarlet fever toxin A; they share no homology with TSST-1 despite sharing numerous biological properties. Numerous animal models for development of TSS have suggested mechanisms of toxin action, though the exact molecular action is not known. The toxins are all potent pyrogens, induce T lymphocyte proliferation, requiring interleukin 1 release from macrophages, suppress immunoglobulin production, enhance endotoxin shock, and enhance hypersensitivity skin reactions. The genetic control of the toxins has been studied and suggests the exotoxins are variable traits. Some additional properties of TSS S. aureus which facilitate disease causation have been clarified.

Amino Acid Sequence↗
PubMed2003

[Streptococcal toxic shock syndrome: a case report].

Streptococcal toxic shock syndrome (STSS) is the most severe form of invasive infections caused by group A streptococci. In this report, a 36-years-old man who was admitted to our clinic with the complaints of fever, rash, skin lesions, abdominal pain, weakness and anuria for 2 days, has been presented. His body temperature was 39.5 degrees C and blood pressure was 50/20 mmHg. In physical examination, diffuse erythematous rash on the body, cellulitis on left leg and foot, fungal lesions on the toes, and abdominal tenderness were noted. Laboratory results revealed a dramatic increase in leukocyte count, increased sedimentation rate, elevated blood urea nitrogen, cretinine, liver enzymes and bilirubin levels. Group A streptococci were isolated from the blood culture of the patient. Despite supportive (intravenous saline, dopamine) and antibiotic (clindamycin-ceftriaxone combination) therapies, adult respiratory distress syndrome has developed in two days, and he died on the third day. This case was presented to draw attention to STSS, which was a rare clinical entity with rapid progression to mortality despite aggressive medical therapy.

Adult↗
PubMed2004

[Staphylococcal toxic shock syndrome].

[A case of menstrual toxic shock syndrome (TSS) in a woman aged 21 is reported. Diagnosis was made on clinical basis and was followed by successful treatment]

Adult↗
PubMed1991

Toxic shock syndrome and its potential complications.

Toxic shock syndrome is a potentially lethal disease since the infective process established in the body can lead to multisystem involvement. The critical care nurse's understanding of this pathologic process and its potential complications will help in prevention, early diagnosis and treatment.

Adult↗
PubMed1990

[Cavitated pneumonia and toxic shock syndrome: presentation of a case].

Toxic shock syndrome (TSS) is a potentially fatal acute disease preferentially affecting menstruating women and is related to the use of vaginal tampons seems to be due to an specific exotoxin produced by some Staphylococcus aureus strains. We present here the case of a male patients suffering cavitated pneumonia who developed a systemic clinical picture comparable to TSS. This unusual form of presentation is discussed as well as the diagnostic criteria which define this entity.

Adult↗