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PubMed1992

Identification of HLA-DR alpha chain residues critical for binding of the toxic shock syndrome toxin superantigen.

Staphylococcal toxic shock syndrome toxin 1 (TSST-1) binds to major histocompatibility complex class II molecules, and the toxin-class II complexes induce proliferation of T cells expressing V beta 2 sequences. To define the residues involved in TSST-1 binding, a set of transfectants expressing 21 HLA-DR alpha chain mutants were analyzed for their abilities to bind and present TSST-1 and to present an antigenic peptide. Mutations at DR alpha positions 36 and 39 markedly decreased the ability of the DR7 molecule to bind and present TSST-1 but did not affect the ability to present an antigenic peptide. These data indicate that DR alpha residues 36 and 39, predicted to be located on an outer loop, are important in the formation of the TSST-1 binding site on DR molecules.

Amino Acid Sequence↗

PubMed1989

Ovine-associated Staphylococcus aureus protein with immunochemical similarity to toxic shock syndrome toxin 1.

A toxic shock syndrome toxin 1 (TSST-1) antibody-binding protein produced by an ovine-associated strain of Staphylococcus aureus was examined. The protein showed total identity to TSST-1 by immunodiffusion analysis. Western blots (immunoblots) of proteins separated by isoelectric focusing revealed that the TSST-1 antibody-binding protein had a pI of 8.6 rather than 7.0, the pI of standard TSST-1.

Animals↗

PubMed2004

[Probable toxic shock syndrome following pleural drainage].

Toxic shock syndrome (TSS) is rare complication after minor surgical procedure. A 22-year-old man was admitted our hospital with spontaneous pneumothorax on the right side. Few days after pleural drainage, he developed a high fever often over 40 degrees C and a rash, most demonstrating a truncal, "sunburn" pattern. Initially, he was diagnosed as right pylothorax, but the clinical course was not typical and antibiotic treatment was not effective. Two weeks later, desquamation of the hands and feet were noted, and methicillin-resistant Staphylococcus aureus (MRSA) isolated from the pleural effusion were identified as TSS toxin (TSST)-1 and enterotoxin-C producing. He was diagnosed as probable TSS, and recovered by steroid therapy. Early awareness and recognition of this disease is necessary for surgeons.

Adult↗

PubMed1991

Menstrually-related toxic shock syndrome.

Cases of suspect toxic shock syndrome reported to a state health department were studied. Retrospective examination of 53 definite and 29 probable cases of menstrually-related TSS revealed no significant differences in mean age, proportion with vaginal or cervical isolates of Staphylococcus aureus, proportion using tampons, proportion hospitalized and mortality.

Adult↗

PubMed1982

Toxic shock syndrome: relation to catamenial products, personal health and hygiene, and sexual practices.

In 1980, the discovery of an association between vaginal tampon use and toxic shock syndrome affected the lifestyles of menstruating women and the catamenial products industry. It made both the general public and the medical community more aware of all aspects of menstruation. The relation between developing toxic shock syndrome and tampon use is unclear; tampon fluid capacity (absorbency) remains the best predictive measure of that risk. No unique aspect of tampon use other than absorbency seems to increase the risk of developing toxic shock syndrome, and numerous hygiene and medical history factors do not seem to play a role in the pathogenesis of the disease. Studies in Minnesota, Wisconsin, and Iowa indicate that 70% to 75% of women between the ages of 15 and 24, the group with the highest risk of developing menstrual toxic shock syndrome, continued to use tampons after news media attention in 1980 on the association of the syndrome with tampon use. This rate of use is higher than the rate found for the general population by recent tampon market research.

Absorption↗

PubMed2002

Double mutant and formaldehyde inactivated TSST-1 as vaccine candidates for TSST-1-induced toxic shock syndrome.

Up to now there is no treatment for staphylococcal toxic shock syndrome, a disease mainly induced by toxic shock syndrome toxin-1(TSST-1). There is great demand in finding means to control the disease, one of them is the development of an effective and safe vaccine against TSST-1. In this study we constructed a series of vaccine candidates and investigated their biological activity, toxicity, and potential to invoke an immune response. TSST-1 was isolated from Stahylococcus aureus supernatants and recombinantly expressed as a N-terminal 6x histidine-tagged protein in Escherichia coli. In order to obtain molecules with minimal toxicity we constructed single mutants (G31R and H135A) and one double mutant (G31R/H135A) with both residues exchanged. We also detoxified native TSST-1 isolated from S. aureus, and recombinantly expressed TSST-1 by treatment with formaldehyde. Functional activity of native and recombinant TSST-1 and grade of inocuity of mutants and toxoids was determined by investigating mitogenity, T-cell activation, and cytokine release upon stimulation of human mononuclear cells with the vaccine candidates. All substances were tested in a rabbit immunization study. After primary immunization and three additional boosts all vaccinated animals developed antibody titers against TSST-1 and were protected against challenge with a lethal doses of superantigen potentiated with lipopolysaccharide.

Animals↗

PubMed1984

Purification and characterization of Staphylococcus aureus FRI 1169 and 587 toxic shock syndrome exotoxins.

An exotoxin was purified from a toxic shock toxin (TST)-producing Staphylococcus aureus strain, FRI 1169, and another exotoxin was purified from a pyrogenic exotoxin C (PEC)-producing S. aureus strain, 587. Both strains had been isolated from toxic-shock syndrome patients. The two exotoxins were purified by the same method of ion-exchange chromatography, chromatofocusing, and gel filtration. After purification, those exotoxins gave a line of identity against an anti-TST serum and also were immunologically similar to TST in a double-diffusion test. In sodium dodecyl sulfate-polyacrylamide gel electrophoresis, each exotoxin gave a single band with a relative mobility identical to that of the other. Their molecular weights (24,000), isoelectric points (7.0), amino acid compositions, and NH2-terminal amino acid sequences (the first four residues) were identical. Both produced fever and enhanced host susceptibility to lethal endotoxin shock in rabbits, comparable with PEC. These findings show that the two exotoxins are the same protein, which is assumed to be TST. When injected into rabbits, the culture supernatant of strain 587 showed biological activity like that described above, whereas the culture supernatant neutralized with anti-TST immunoglobulin did not. This showed that PEC-producing strain 587 does not produce any toxin with these biological activities in rabbits except TST.

Amino Acid Sequence↗

PubMed1982

Pathologic findings in twelve fatal cases of toxic shock syndrome.

Pathologic changes in 12 fatal cases of toxic shock syndrome occurred in the vagina, cervix, lung, liver, and kidney. Desquamation and ulceration of the cervical and vaginal mucosa were seen in all six cases where adequate specimens were submitted. Hyaline membrane formation characteristic of "shock lung" was found in all lung tissues. Periportal inflammation was found in all liver specimens and acute tubular necrosis was seen in eight of the 12 kidney specimens. Although not specific for toxic shock syndrome, the findings are consistent with the hypothesis that the illness is caused by a staphylococcal toxin.

Adolescent↗

PubMed1991

[Toxic shock syndrome in a 6-year-old male].

Toxic shock syndrome, caused by an exotoxin of staphylococcus aureus is very rare in children. On admission, beside the shock, abdominal problems as vomiting, diarrhoea and a developing adynamic ileus were outstanding in our patient. Not before additional symptoms as staphylococcal pneumonia with bacteriemia occurred and later desquamation of palms and feet, diagnosis of toxic shock syndrome could be confirmed.

Child↗

PubMed1988

Toxic shock syndrome associated with use of a nasal tampon.

Toxic shock syndrome has been noted to occur with nasal surgery, both with and without packing. A new synthetic sponge, described as a nasal tampon, has become available for use as packing after surgery. Herein is reported the first case of toxic shock syndrome associated with the use of this nasal tampon.

Adult↗

PubMed1998

Exanthematous disease induced by toxic shock syndrome toxin 1 in the early neonatal period.

BACKGROUND: We have seen a number of patients who developed systemic exanthema and thrombocytopenia in the first week of life. Although nearly 100% of the patients were carriers of meticillin-resistant Staphylococcus aureus (MRSA), no clear link between MRSA and this exanthematous disease has yet been made. METHODS: 20 neonates with exanthema and thrombocytopenia were selected for study. To see whether superantigenic exotoxins from MRSA are involved in the pathogensis of the exanthematous disease, we studied the production of these exotoxins by MRSA isolates from the neonates. We studied the expression of T-cell-receptor Vbeta and CD45RO in T cells taken from four of the neonates. We also analysed the DNA sequences of 16 cloned Vbeta2-positive T-cell-receptor-chain genes taken from two of the neonates. FINDINGS: Although most of the patients recovered within 5 days of onset of the exanthematous disease without any active treatment, two preterm infants died in the recovery phase. All patients showed colonisation by MRSA. The MRSA produced toxic shock syndrome toxin-1 (TSST-1). The number of T cells positive for T-cell-receptor Vbeta2, reactive to TSST-1, was increased in the four patients studied (p<0.0001), and these T cells expressed CD45RO (p=0.0185). None of the Vbeta2 clones had the same junctional sequences. INTERPRETATION: The polyclonal expansion of Vbeta2-positive T cells in patients colonised by TSST-1-producing MRSA suggests that the pathogenic micro-organism of this neonatal exanthematous disease is S aureus, mainly MRSA, and that in its pathogenesis it activates T cells by TSST-1. Although the pathogenesis of both this exanthematous disease and toxic shock syndrome are fundamentally the same, a diagnosis of toxic shock syndrome cannot be made in this case, based on the clinical criteria for toxic shock syndrome. We propose neonatal toxic-shock-syndrome-like exanthematous disease (NTED) as the name for this disease.

Bacterial Toxins↗

PubMed2005

Toxic shock syndrome in children: epidemiology, pathogenesis, and management.

Toxic shock syndrome (TSS) is an acute, toxin-mediated illness, like endotoxic shock, and is characterized by fever, rash, hypotension, multiorgan involvement, and desquamation. TSS reflects the most severe form of the disease caused by Staphylococcus aureus and Streptococcus pyogenes. A case definition for staphylococcal TSS was well established in the early 1980s and helped in defining the epidemiology. Since the late 1980s, a resurgence of highly invasive streptococcal infections, including a toxic shock-like syndrome, was noted worldwide and a consensus case definition for streptococcal TSS was subsequently proposed in 1993. Both TSS and the toxic shock-like syndrome occur at a lower incidence in children than in adults. Changes in the manufacturing and use of tampons led to a decline in staphylococcal TSS over the past decade, while the incidence of nonmenstrual staphylococcal TSS increased. Nonmenstrual TSS and menstrual TSS are now reported with almost equal frequency. The incidence of streptococcal TSS remains constant after its resurgence, but varies with geographic location. Streptococcal TSS occurs most commonly following varicella or during the use of NSAIDs. Sites of infection in streptococcal TSS are much deeper than in staphylococcal TSS, such as infection caused by blunt trauma, and necrotizing fasciitis. Bacteremia is more common in streptococcal TSS than in staphylococcal TSS. Mortality associated with streptococcal TSS is 5-10% in children, much lower than in adults (30-80%), and is 3-5% for staphylococcal TSS in children.TSS is thought to be a superantigen-mediated disease. Toxins produced by staphylococci and streptococci act as superantigens that can activate the immune system by bypassing the usual antigen-mediated immune-response sequence. The host-pathogen interaction, virulence factors, and the absence or presence of host immunity determines the epidemiology, clinical syndrome, and outcome. Early recognition of this disease is important, because the clinical course is fulminant and the outcome depends on the prompt institution of therapy. Management of a child with TSS includes hemodynamic stabilization and appropriate antimicrobial therapy to eradicate the bacteria. Supportive therapy, aggressive fluid resuscitation, and vasopressors remain the main elements. An adjuvant therapeutic strategy may include agents that can block superantigens, such as intravenous immunoglobulin that contains superantigen neutralizing antibodies.

Adolescent↗

PubMed1982

Toxic shock syndrome. A fatal case with autopsy findings.

Although the clinical and laboratory features of the toxic shock syndrome have recently been further defined, the pathologic lesions attending this disorder are as yet primarily unstudied. We present the autopsy findings in a fatal case of toxic shock syndrome, which occurred in a 17-year-old girl. These observations are used as a focus for the discussion of possible pathophysiologic mechanisms operative in this disease and are contrasted with autopsy findings in several other pathologic entities that are often confused with toxic shock syndrome.

Adolescent↗

PubMed1984

Induction of human interleukin-1 by a product of Staphylococcus aureus associated with toxic shock syndrome.

Certain strains of Staphylococcus aureus associated with toxic shock syndrome elaborate material that induces human blood monocytes to secrete interleukin-1 (IL-1). IL-1 was detected both by its ability to cause fever in rabbits using the leukocytic pyrogen (LP) assay and by its mitogenic activity towards thymocytes in the so-called lymphocyte-activating factor (LAF) assay. Anti-human IL-1 prevents the manifestation of both activities. Filtrates of control strains of S. aureus manifest neither activity. Thus, culture filtrates derived from toxic shock syndrome (TSS)-associated strains cause biphasic fever in rabbits when injected intravenously. The fever lasts several hours. Plasma taken at the peak of the fever and injected into a second set of rabbits produces a brief monophasic fever typical of LP. Further, human monocytes release LP when incubated with TSS filtrates in vitro. The monocyte products also stimulate the proliferation of mouse thymocytes in the presence of phytohemagglutinin in a manner characteristic of LAF. A bacterial filtrate is much less effective without an intermediate incubation with monocytes. The stimulation of monocyte IL-1 production is easily quantified, provides a simple method of assaying the TSS toxin, and since it involves human cells, is directly relevant to the human disease. The assay was used to monitor the purification of TSS toxin. Only 0.1 ng/ml of the purified material is required to induce monocyte IL-1 production. It is thus more potent than endotoxin. In contrast to endotoxin, its effect is not blocked by polymyxin B. We conclude that in TSS the sudden fever and probably other components of the acute phase response may be attributed to a massive release of IL-1.

Animals↗

PubMed1984

Toxic shock syndrome in Oregon. Risk of recurrence.

To define the risk of having a recurrence of toxic shock syndrome, we collected information on 53 cases (42 definite and 11 probable cases) that occurred in Oregon between Jan 1, 1980, and May 30, 1982. For the 777 person-months for which follow-up information was available, only one probable recurrent case of toxic shock syndrome occurred. The low frequency of recurrences may be associated with the high frequency (91%) with which beta-lactamase-resistant antibiotics were used in initial episodes of toxic shock syndrome and with the relatively low proportion (44%) of menstruating women who resumed the use of tampons after their first episode.

Adolescent↗

PubMed1981

Toxic shock syndrome: clinical and laboratory features in 15 patients.

Toxic shock syndrome is a recently recognized illness with serious morbidity and mortality that occurs primarily in healthy menstruating women who use tampons. Thirteen women and two men were evaluated; two of the women died in spite of seemingly appropriate therapy. All patients had a temperature of 38.9 degrees C or greater, hypotension of syncope, a skin rash with subsequent desquamation, mucous membrane inflammation, and laboratory evidence of multiple organ dysfunction. Staphylococcus aureus was isolated from the cervix or vagina in eight women and from soft-tissue infections in both men. Two patients were bacteremic. The significant heterogeneity in the clinical manifestations, laboratory abnormalities, and therapeutic requirements among patients may result in diagnostic confusion and inappropriate therapy. Although toxic shock syndrome appears to be associated with tampon usage and S. aureus, the pathogenesis remains unknown.

Adolescent↗

PubMed1988

Serologic responses to toxic shock syndrome (TSS) toxin-1 in menstrual and nonmenstrual TSS.

Toxic shock syndrome toxin-1 (TSST-1) is implicated as the major exotoxin associated with menstrual toxic shock syndrome. The role of TSST-1 in nonmenstrual TSS is less certain. We examined serum IgG responses to TSST-1 in 16 nonmenstrual (9 female, 7 male) and 14 menstrual TSS patients, and in 87 women and 66 men as age-matched healthy controls, using an enzyme-linked immunosorbent assay (ELISA). Relative ELISA titers were expressed as percent activity of a mid level serum standard tested concurrently. Based on 95% confidence estimates for predicting a negative titer (20.6 +/- 8.2%) using sera in which TSST-1 specific IgG was demonstrated to be absent by western blot, 24% of control women and 9% of control men lacked TSST-1 specific IgG in the random survey (p less than 0.05, Fisher's exact test). Relative titers in acute sera of menstrual TSS women (26.2 +/- 5.2%, mean +/- S.E.), but not nonmenstrual TSS women (71.8 +/- 18.6%), were significantly lower than those of control women (78.9 +/- 7.3%, p less than 0.01, Mann-Whitney test). Acute titers from male TSS patients (37.0 +/- 15.6%) were also significantly lower than those in control men (114.6 +/- 11.0% (p less than 0.05). Antibody titers from menstrual TSS women and TSS men remained low during convalescence. Nevertheless, seroconversion to TSST-1 was demonstrated by western blot in 7 of 10 patients in whom TSST-1 positive S. aureus was isolated, but in neither of two patients without toxigenic S. aureus.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Streptococcal toxic shock syndrome in a postpartum woman. Case report and review of the literature.

A case of streptococcal toxic shock syndrome in a 29-year-old postpartum woman is described. The patient presented with hypotension, coagulation defects, adult respiratory distress syndrome and scarlet exanthema as a complication of hemolytic group A streptococcal endometritis. One hundred and twenty-two other cases of streptococcal toxic shock syndrome in the literature are reviewed and the criteria of the syndrome discussed. Streptococcal toxic shock syndrome seems to be increasing along with more frequent invasive streptococcal infections in several countries. It is therefore important to recognize and treat the infection as early as possible to minimize the risk of mortality.

Adult↗