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PubMed1986

Suppression of immunoglobulin-secreting cells from human peripheral blood by toxic-shock-syndrome toxin-1.

Toxic-shock syndrome toxin-1 (TSST-1), a nonspecific T lymphocyte mitogen, was shown to cause the suppression of immunoglobulin-secreting cells (ISCs) generated in pokeweed mitogen (PWM)-stimulated cultures of human peripheral blood mononuclear cells (PBMs). Greater than 90% suppression of the PWM-stimulated ISC response was achieved when 2 X 10(6) PBMs were cultured in the presence of 1 microgram of TSST-1. The nonspecific suppression induced by the toxin was dose related; amounts of TSST-1 as low as 1.0 ng/2 X 10(6) cultured cells caused significant suppression of the ISC response. TSST-1-induced suppression was due to the activation of a population of cells that secreted a soluble factor that mediated the resulting suppression. PBMs were activated by a 24-hr preincubation of 2 X 10(6) cells in the presence of 1 microgram of TSST-1 followed by repeated washing to remove residual toxin. These cells, when co-cultured with unstimulated PBMs and PWM, suppressed the normal ISC response. The supernatant factor, active at volumes of 10 microliters/2 X 10(6) PBMs, was generated by harvesting the supernatant fluid of TSST-1-activated cells. The results of these in vitro experiments confirm that TSST-1 is an immunosuppressing agent that affects human lymphocyte function and, in such a capacity, may play a role in the development of toxic shock syndrome in humans.

Adult↗

PubMed1994

Toxic shock syndrome in transsphenoidal neurosurgery.

An overlooked toxic shock syndrome (TSS) may lead to a fatal outcome. In neurosurgery a transsphenoidal approach with post-operative nasal tamponade may promote toxic shock syndrome without signs of local wound infection. By discussing the case history of a patient after hypophysectomy by the transsphenoidal route, we propose that after the appearance of the first signs of toxic shock syndrome, quick removal of the nasal tamponade is a life saving procedure.

Adenoma, Chromophobe↗

PubMed1989

Recurrent toxic shock syndrome.

While the classic manifestations of toxic shock syndrome in a high-risk patient are readily recognized, probable cases of the syndrome are often overlooked. This is especially true of nonmenstrual toxic shock syndrome, which may be associated with a variety of clinical conditions. There is a 30 percent risk of recurrence following the first episode of toxic shock. The roles of prophylactic antibiotics and oral contraceptives in reducing recurrences require further study.

Adult↗

PubMed1982

Postpartum patient with toxic shock syndrome.

A case is presented of postpartum toxic shock syndrome following a normal spontaneous vaginal delivery. Toxic shock syndrome to date has been reported in men, women, and children, the preponderance of cases (96%) being of women and usually at or near menses. Herein is reported a case of toxic shock syndrome occurring 14 hours post partum in a healthy young woman. This disease, which involves at least 3 major organ systems and also results in shock and a desquamating exanthem, must be borne in mind by all who care for the parturient. It is postulated that staphylococci plus blood and/or other unknown factors precipitate the disease.

Adult↗

PubMed1985

Toxic shock syndrome. I. Clinical exclusion of other syndromes by strict and screening definitions.

Several clinical definitions of toxic shock syndrome have been proposed and used in extensive epidemiologic and clinical studies. Most of these definitions suggest (but usually do not require) that there be sufficient laboratory studies to exclude other potentially similar syndromes. Simplified definitions which broaden the spectrum of toxic shock syndrome illness have also been proposed but not validated. In this study, clinical findings of consecutive hospitalized patients were compared: nine with toxic shock syndrome (confirmed by a modification of the collaborative strict case definition) and 120 with potentially similar diagnoses (bacteremia with shock, meningococcemia, Staphylococcus aureus bacteremia, scarlet fever, toxic epidermal necrolysis, acute rheumatic fever, leptospirosis, Rocky Mountain spotted fever, rubeola, Kawasaki syndrome, erythema multiforme, and Stevens-Johnson syndrome). None of the 120 controls satisfied the clinical criteria of the modified strict definition of toxic shock syndrome, demonstrating its exclusionary properties even in the absence of additional laboratory data. A "simplified" screening definition was constructed which might be applied early in illness (i.e., at admission) and this definition distinguished all the patients with toxic shock syndrome from all but three (2.5%) of the 117 analyzable patients with other mucocutaneous or potential infectious shock syndromes. Applied prospectively in the state of Colorado passive/active reporting system, the screening definition identified 24 potential toxic shock syndrome cases of which 19 (76%) eventually were confirmed as toxic shock syndrome. Before being adopted and widely used, clinical syndrome definitions should be documented to exclude other potentially overlapping syndromes or should require additional mandatory exclusionary laboratory data.

Adolescent↗

PubMed2000

Inhibition of staphylococcal enterotoxin B-induced lymphocyte proliferation and tumor necrosis factor alpha secretion by MAb5, an anti-toxic shock syndrome toxin 1 monoclonal antibody.

Toxic shock syndrome (TSS) is primarily caused by toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin B (SEB). These toxins belong to a family of pyrogenic toxin superantigens (PTSAgs) produced by Staphylococcus aureus and exhibit several shared biological properties, including the induction of massive cytokine release and Vbeta-specific T-cell proliferation. The crystal structures of most PTSAgs are now published, and they demonstrate a striking similarity in conformational architecture even though their primary protein sequences are different. Despite these structural and immunobiological similarities, no cross-reactivity between TSST-1 and other PTSAgs has been demonstrated in serological or neutralization assays. Our laboratory has developed a neutralizing murine anti-TSST-1 monoclonal antibody (MAb5) which displayed cross-reactivity with SEB by enzyme-linked immunosorbent assay. The aim of the present study was to evaluate whether MAb5 can also cross-neutralize SEB-induced superantigenic activities in vitro. MAb5 was found to partially inhibit SEB-induced T-cell mitogenesis (63%) and tumor necrosis factor alpha (TNF-alpha) secretion (70%) in human peripheral blood mononuclear cells (PBMC) in a dose-dependent manner, while an isotypic anti-TSST-1 monoclonal antibody showed no effect. Epitope mapping revealed that MAb5 bound to TSST-1 residues 47 to 56 ((47)FPSPYYSPAF(56)) and to SEB residues 83 to 92 ((83)DVFGANYYYQ(92)), sequences that located in different regions of these toxins and are structurally dissimilar. SEB peptide (83)DVFGANYYYQ(92) was synthesized and found to also inhibit SEB-induced mitogenesis and TNF-alpha secretion in human PBMC. Our results demonstrate for the first time that MAb5 binds to different epitopes on TSST-1 and SEB that appear functionally important in inducing T-cell mitogenesis and TNF-alpha secretion in vitro.

Antibodies, Bacterial↗

PubMed1982

Epidemiologic comparisons of incidence of toxic shock syndrome.

Despite many imperfections in the nationwide reporting of toxic shock syndrome, the available data provide some useful information. The crude toxic shock morbidity rate has been estimated as approximately 0.50 per 100 000 United States population per year. This morbidity rate exceeds those for paralytic poliomyelitis, tetanus, tularemia, diphtheria, and typhoid fever, and is about one half of the rate for meningococcal infections and pertussis. The estimate of 8.9 cases of toxic shock syndrome per 100 000 menstruating women is similar to the crude rates for primary and secondary syphilis and mumps. From these comparisons, the incidence of toxic shock syndrome does not appear as low as some might suppose.

Epidemiologic Methods↗

PubMedDate not supplied

Toxic shock syndrome: case report of a postpartum female and a literature review.

Toxic shock syndrome is one of the best understood of the systemic inflammatory response syndromes. The mechanisms of disease have been extensively studied; however, no therapies have been developed that can effectively reverse the syndrome once the inflammatory response has begun. Although toxic shock syndrome classically has been associated with tampon use, multiple other etiologies exist including postpartum toxic shock, which usually affects patients in the immediate weeks following delivery. We present a case of toxic shock in a woman 10 weeks postpartum and review the literature regarding both menstrual-related and nonmenstrual-related toxic shock.

Adult↗

PubMed1982

Predictors of tampon use in adolescents after media coverage of toxic shock syndrome.

Adolescents who use tampons represent the population most susceptible to toxic shock syndrome. We surveyed 714 adolescents from two high schools and three hospital-based clinics to examine patterns of tampon use before and after media coverage on toxic shock syndrome. Predictors of behavior change in adolescent users of tampons were examined in the context of a theoretical model of preventive health behavior. Subjects were 168 adolescents, ages 13 to 19 (mean age, 15.19; mean gynecologic age, 3.4); 50% of the subjects were white; 19%, Asian; 16% black; 7%, Hispanic; and 6%, other. After extensive publicity on toxic shock syndrome, 33.9% of the subjects changed their habits of tampon use; 27.5% stopped using tampons and 6% decreased their use of tampons. Linear logistic regression analyses identified two factors that distinguished adolescents who decreased or stopped use of tampons after publicity on toxic shock syndrome from those who did not: greater likelihood of Rely tampon (Procter & Gamble) use before publicity (p = 0.014) and the belief that they were especially susceptible to toxic shock syndrome (p = 0.013).

Adolescent↗

PubMed1991

Toxic shock syndrome and tampons.

There has been a substantial reduction in the incidence of toxic shock syndrome in the 10 years since the association between tampons and toxic shock syndrome was first recognized. The decreased incidence is real, and not the result of decreased reporting to the passive surveillance system. The decreased incidence of menstrual toxic shock syndrome can primarily be explained by changes in the absorbency and composition of tampons available to the consumer. The reduction in the occurrence of menstrual toxic shock syndrome can be attributed to the withdrawal of Rely brand, which consisted of a unique composition, and subsequently to the lowering of absorbency of all brands of tampons. The conclusions of the early studies of toxic shock syndrome pointed the way to prompt public health interventions and resulted in the prevention of substantial morbidity.

Bacterial Toxins↗

PubMed1989

Postoperative toxic shock syndrome: a case report and review of the literature.

Toxic shock syndrome is a rare and potentially lethal postoperative complication. The recognition of this disorder can be delayed by the fact that the offending wounds in postoperative toxic shock syndrome are classically benign in appearance. The infrequency with which this syndrome is encountered can also prolong the interval between the onset of symptoms and institution of effective therapy. A case of toxic shock syndrome complicating an abdominoplasty performed at the Plastic Surgery Service of Walter Reed Army Medical Center is presented, and the literature available on toxic shock syndrome in the postoperative patient is discussed.

Abdomen↗

PubMed1986

Postoperative toxic shock syndrome after reconstructive surgery of the hand.

Toxic shock syndrome is a devastating and potentially lethal complication, which can occur in postoperative patients. Our experience with toxic shock syndrome after a reconstructive procedure on the hand is reported. An awareness of the clinical and laboratory manifestations of toxic shock syndrome was needed to facilitate its early recognition and treatment.

Adult↗

PubMed1986

Affinity purification of staphylococcal toxic shock syndrome toxin 1 and its pathologic effects in rabbits.

Toxic shock syndrome toxin 1 (TSST-1) was purified to apparent homogeneity by chromatofocusing and affinity chromatography. The amino acid composition of the toxin was very similar to that reported for TSST-1 by other investigators. The amino-terminal amino acid was serine. A partial specific volume of 0.73 ml/g was calculated for the toxin from the amino acid data, and a molecular weight of 19,200 +/- 1,300 was determined by hydrodynamic methods. New Zealand white rabbits of both sexes were equally susceptible to the lethal effects of the toxin; however, older rabbits (greater than 12 months) were far more susceptible than young adults or weanlings. The 50% lethal dose of TSST-1 in older rabbits was 50 to 60 micrograms/kg when injected subcutaneously and 20 to 30 micrograms/kg when injected intravenously. Enhancement of lethal endotoxin shock by TSST-1 could not be demonstrated when both toxins were injected subcutaneously; however, lethal shock did occur when endotoxin (10 micrograms/kg) was injected intravenously after TSST-1 had been injected by either the subcutaneous (50 to 60 micrograms/kg) or the intravenous (20 to 30 micrograms/kg) route. Endotoxin alone was not lethal at a dose of 500 micrograms/kg of body weight when injected subcutaneously. When injected intravenously, endotoxin at a dose of 500 micrograms/kg was not lethal in weanling males or in females in any age group; however, young (6 to 7 months) and adult (greater than 12 months) males were killed by endotoxin doses as low as 45 to 50 micrograms/kg. Histopathologic studies of rabbits by both sexes which died as a result of TSST-1 alone or in combination with endotoxin showed extensive damage to organs rich in lymphoid and mononuclear phagocytic cells such as the thymus, mesenteric lymph nodes, liver, and spleen. Severe congestion of these organs as well as erythrophagocytosis and lymphoid depletion in the spleen and mesenteric lymph nodes were noted. Congestion and hemorrhage were also found in the heart, lungs, trachea, and thymus. The systemic pathology produced by TSST-1 was strikingly similar to that seen in humans who had died of toxic shock syndrome and in rabbits with subcutaneous chamber inoculated with toxic shock case strains of Staphylococcus aureus. Rabbits that were not killed by the toxin suffered a very rapid and severe leukopenia followed by leukocytosis with a left shift. Lymphopenia was also noted as was a mild but persistent anemia. With the exception of the early leukopenia, very similar hematologic findings have been noted in humans with toxic shock syndrome.

Amino Acids↗

PubMed2002

Temporal sequence and functional implications of V beta-specific T cell receptor down-regulation and costimulatory molecule expression following in vitro stimulation with the staphylococcal superantigen Toxic shock syndrome toxin-1.

The superantigen toxic shock syndrome toxin-1 (TSST-1) is implicated as the major cause of staphylococcal toxic shock syndrome. The temporal sequence of early signaling events in human peripheral blood mononuclear cells following TSST-1 stimulation was examined. TSST-1 induced rapid and complete down-regulation of V beta 2-specific T cell receptor (TCR), followed by transient CD154 expression on CD4(+) lymphocytes. This was sequentially followed by the up-regulation of CD86, CD80, CD40, and human leukocyte antigen-DR expression on CD14(+) monocytes. In contrast, S14N, a TSST-1 mutant toxin with a single amino acid substitution that is known to be impaired in interleukin (IL)--2, interferon (IFN)-gamma, and tumor necrosis factor (TNF)-alpha secretion, was deficient in both V beta 2-TCR down-regulation and CD154 and CD80/CD86 expression. Furthermore, pretreatment with monoclonal antibodies against V beta 2-TCR, CD80/CD86, and CD154 significantly inhibited TSST-1-induced IL-2, IFN-gamma, and TNF-alpha secretion. Taken together, these results indicate that early V beta-specific TCR activation, along with CD80/CD86 and CD154 costimulation, are key determinants of the TSST-1-induced proinflammatory cytokine response.

Antibodies, Monoclonal↗

PubMed1990

Tampon absorbency, composition and oxygen content and risk of toxic shock syndrome.

Tampon use has been identified as a major risk factor for toxic shock syndrome, although the etiologic role of tampons is not clearly understood. Two epidemiologic studies conducted to date have reported an association between tampon absorbency and risk of toxic shock syndrome. This finding is not corroborated by laboratory studies, however, which have suggested that absorbency may be a marker for other characteristics that create an environment conductive to the elaboration of toxic shock syndrome toxin 1. We used data from the previously reported Tri-state study to estimate simultaneously the effects of tampon oxygen content, absorbency and chemical composition. Although the data are sparse, oxygen content was more strongly associated with risk of toxic shock syndrome than either absorbency or chemical composition. The results suggest that it may be possible to develop a highly absorbent tampon that is not associated with a high risk of toxic shock syndrome.

Acrylates↗

PubMedDate not supplied

Clindamycin in the treatment of streptococcal and staphylococcal toxic shock syndromes.

OBJECTIVE: To evaluate the utility of clindamycin in the treatment of streptococcal and staphylococcal toxic shock syndromes. DATA SOURCES: Biomedical literature was accessed through MEDLINE (1966-December 1999). Key terms included clindamycin, streptococcal toxic shock, and staphylococcal toxic shock. DATA SYNTHESIS: Streptococcal and staphylococcal toxic shock syndromes are associated with a high mortality rate. beta-Lactams have been considered the drug of choice for the treatment of these serious infections, with the occasional use of adjunctive clindamycin, although no clinical evidence has been published to support this latter regimen. An evaluation of the information to propose the usefulness of clindamycin was conducted. CONCLUSIONS: Experimental laboratory evidence suggests utility of the adjunctive use of clindamycin in streptococcal and staphylococcal infections complicated by toxin production. Research using animal models comparing clindamycin plus beta-lactams with beta-lactams alone for the treatment of these infections would be useful.

Animals↗

PubMedDate not supplied

Identification of a new toxin from a strain of Staphylococcus aureus isolated from a patient with nonmenstrual toxic shock syndrome.

The extracellular products of a toxic shock syndrome toxin 1 (TSST-1)-negative isolate of Staphylococcus aureus (strain D4508) from a patient with nonmenstrual toxic shock syndrome were shown to possess toxic activity capable of producing shock and death when injected into rabbits. Fractionation of the extracellular products and the production of polyclonal antibodies to individual polypeptides identified the toxin as a single polypeptide of molecular weight 26,000. Immunoblot analyses showed the toxin to be antigenically related yet distinct from enterotoxins A, B, C, D, and E and unrelated to TSST-1.

Animals↗

PubMed1982

An enterotoxin-like protein in Staphylococcus aureus strains from patients with toxic shock syndrome.

An enterotoxin-like protein, tentatively labeled enterotoxin F, was isolated from Staphylococcus aureus strains taken from patients with toxic shock syndrome. Antibodies specific for enterotoxin F were prepared in rabbits. Use of these antibodies showed that 130 (91.5%) of 142 S. aureus strains from patients with toxic shock syndrome produced enterotoxin F. Strains from toxic shock patients in eight other countries were identified as enterotoxin F producers. Only a small number of S. aureus strains from sources other than patients with toxic shock syndrome were found to produce enterotoxin F. Twenty-one of 111 controls had low antibody titers (less than 1:100) to enterotoxin F whereas 86 of 92 toxic shock patients had low acute phase antibody titers (less than 1:100) to enterotoxin F. Eight of 52 patients had serum conversion as shown by an increase in antibody titer to enterotoxin F in sera taken 21 to 60 days after onset of the illness. It may be possible to identify persons susceptible to toxic shock syndrome by measuring their antibody titer to enterotoxin F.

Bacterial Toxins↗