†Deceased (see In Memoriam at the end of this document) *Representative of the Pediatric and Congenital Electrophysiology Society (PACES) ‡Representative of the European Heart Rhythm Association (EHRA) xRepresentative of the Society of Thoracic Surgeons (STS) {Representative of the American College of Cardiology (ACC) #Representative of the Latin American Heart Rhythm Society (LAHRS) **Representative of the Infectious Diseases Society of America (IDSA) ‡ ‡Representative of the American Heart Association (AHA) xxRepresentative of the American Society of Anesthesiologists (ASA) {{Representative of the Asia Pacific Heart Rhythm Society (APHRS)
Daptomycin (6 mg per kilogram daily) is not inferior to standard therapy for S. aureus bacteremia and right-sided endocarditis. (ClinicalTrials.gov number, NCT00093067 [ClinicalTrials.gov].).
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 (>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 (>1:32) to TSST-1 (89% versus 98% and 100%). These findings demonstrate that the majority of teenagers have antibody titers (>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.
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. Toxic shock syndrome is a severe and often fatal disorder consistently associated with Staphylococcus aureus infection and characterized by multiple organ dysfunction (1-3). The exotoxin toxic shock syndrome toxin 1 (TSST-1) is a 22-kDa protein (4) produced by most strains of S. aureus isolated from patients with toxic shock syndrome (5, 6) and capable of inducing the disease in animal models (7). TSST-1 induces interleukin 1 synthesis by human monocytes (8, 9), accessory-cell-dependent proliferation of human T lymphocytes (10, 11), and the suppression of pokeweed mitogeninduced immunoglobulin synthesis by human lymphocytes (12). All three activities appear to reside in a 14-kDa internal toxin fragment and could not be dissected with multiple monoclonal antibodies (mAbs) (13,14). The identification of a cellular receptor for TSST-1 is important for the understanding of the mechanism of action of this toxin. TSST-1 has been reported to bind to cultured epithelial cells (15) and to T cells but not to monocytes or B cells (16). To the best of our knowledge, the nature of the binding site has not been described. In the present study we demonstrate that TSST-1 binds to human major histocompatibility complex (MHC) class II molecules.MATERIALS AND METHODS Cell Preparations. Peripheral blood mononuclear cells (PBMCs) were isolated by standard methods (11). Highly purified populations of T lymphocytes and monocytes were prepared as described (11,17). The preparation of B cells (18) from surgical specimens of human tonsil and of thymocytes (19) obtained from surgical specimens removed during open heart surgery were as described.Normal human fibroblasts were grown from skin biopsies, propagated, and harvested as described (20). Interferon y (IFN-y) treatment of fibroblasts was performed as described (20) L-Cell Transfectants. The L-cell transfectants expressing HLA class II molecules used in this study were gifts of R. Karr (University of Iowa, IA) and were prepared by transfection of the respective full-length cDNA clones (DRa, DR4f3I, DPw4a, DPw4p, DQ7a, and DQw3,8) in the expression vector pcD together with the pSV2-neo plasmid into DAP.3 murine L-cell fibroblasts (21). Cells were grown in tissue culture plates in complete RPMI 1640 medium containing G418 (250 jug/ml; GIBCO, Grand Island, NY) and were harvested by incubation for 15-20 min in isotonic phosphate-buffered saline (pH 7.4; PBS) containing 0.53 mM EDTA.Toxins. TSST-1 was prepared as described (22) and iodinated using chloramine-T. The mean specific activity of the labeled toxin was 950 Ci/mmol (range, 230-1700 Ci/m...
Strains of Staphylococcus aureus isolated from patients with toxic shock syndrome (TSS) make a characteristic protein known as toxic-shock-syndrome toxin-1 (TSST-1), but the role of this protein in the pathogenesis of TSS is not certain. We have purified TSST-1 by using a combination of alcohol precipitation, isoelectric focusing, and gel chromatography. TSST-1 has an isoelectric point of 7.2 and a molecular weight of 23,100, in accordance with previously published determinations for this protein, and is serologically identical to pyrogenic exotoxin C and staphylococcal enterotoxin F. In highly purified form, TSST-1 is a potent inducer of interleukin-1 production by human monocytes, as quantitated in a thymocyte-proliferation assay. This capability is not attributable to contamination by other staphylococcal products or gram-negative endotoxin and can be blocked by hydrocortisone. Many features of TSS suggest that induction of interleukin-1 by TSST-1 in vivo may play a central role in the elaboration of this disease.
We studied the effect of toxic-shock-syndrome toxin-1 (TSST-1) on production of tumor necrosis factor (TNF) by human monocytes. Adherent mononuclear cells were stimulated with TSST-1 and their supernatants assayed for TNF by using L929 cells in a cytotoxicity assay. TSST-1 stimulated production of TNF over a wide range of concentrations. The cytotoxicity of monocyte supernatants was neutralized by antibody to TNF but not by antibody to interleukin-1 or by normal rabbit serum. TSST-1 and lipopolysaccharide (LPS) had a synergistic effect on monokine production. Monocytes "primed" with TSST-1 produced more interleukin-1 and TNF in response to LPS than did unprimed cells. Treating monocytes with LPS before TSST-1 and co-incubating the two agents with cells for 24 h also enhanced monokine production under some circumstances. These studies suggest a role for TNF in the pathogenesis of toxic shock syndrome, as a consequence of induction by TSST-1 alone or the synergistic effects of several bacterial products.
The goal of this study was to develop and validate clinical prediction rules for bacteremia and subtypes of bacteremia in patients with sepsis syndrome. Thus, a prospective cohort study, including a stratified random sample of 1342 episodes of sepsis syndrome, was done in eight academic tertiary care hospitals. The derivation set included 881 episodes, and the validation set included 461. Main outcome measures were bacteremia caused by any organism, gram-negative rods, gram-positive cocci, and fungal bloodstream infection. The spread in probability between low- and high-risk groups in the derivation sets was from 14.5% to 60.6% for bacteremia of any type, from 9.8% to 32.8% for gram-positive bacteremia, from 5.3% to 41.9% for gram-negative bacteremia, and from 0.6% to 26.1% for fungemia. Because the model for gram-positive bacteremia performed poorly, a model predicting Staphylococcus aureus bacteremia was developed; it performed better, with a low- to high-risk spread of from 2.6% to 21.0%. The prediction models allow stratification of patients according to risk of bloodstream infections; their clinical utility remains to be demonstrated.
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