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PubMed1985

Induction of human interleukin-1 by toxic-shock-syndrome toxin-1.

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.

Bacterial Toxins↗

PubMed2005

Specific inhibitory action of anisodamine against a staphylococcal superantigenic toxin, toxic shock syndrome toxin 1 (TSST-1), leading to down-regulation of cytokine production and blocking of TSST-1 toxicity in mice.

Toxic shock syndrome toxin 1 (TSST-1), produced by Staphylococcus aureus (including methicillin-resistant S. aureus), is a superantigenic toxin responsible for toxic shock syndrome as well as neonatal TSS-like exanthematous disease. TSST-1 exhibits its deleterious effects by leading to the abnormal proliferation of, e.g., Vbeta2+ T cells and overproduction of proinflammatory cytokines. In the present study we examined the inhibitory effect of a Chinese herbal extract, anisodamine, on TSST-1 using human peripheral blood mononuclear cells (PBMCs). Anisodamine inhibited the production of proinflammatory cytokines better than interleukin-10 (an anti-inflammatory cytokine). The inhibitory effect of anisodamine was greater than that of any tropane alkaloid examined. Anisodamine acted directly on both monocytes and T cells in human PBMCs, and the effect was confirmed at the transcriptional level. Inhibition of NF-kappaB activation was also demonstrated. In contrast, no significant inhibition of Vbeta2+ T-cell proliferation was observed. In mice injected with TSST-1, anisodamine treatment significantly decreased serum proinflammatory cytokine levels and prevented TSST-1-induced death. These results suggest that anisodamine specifically acts against the production of cytokines (inflammatory cytokines in particular) and not against Vbeta2+ T-cell proliferation and that anisodamine may have a beneficial effect on TSST-1-associated disease.

Animals↗

PubMed1984

Phenotypic distinctiveness of Staphylococcus aureus strains associated with toxic shock syndrome.

Twenty Staphylococcus aureus strains from patients with toxic shock syndrome (TSS) and 20 from control patients (non-TSS) with infection but no clinical evidence of TSS were compared phenotypically in a collaborative, blinded, randomized study. TSS strains were significantly (P less than 0.05) more likely than non-TSS strains to produce various previously described but related toxic shock-associated proteins (pyrogenic exotoxin C, enterotoxin F, and TSS marker protein), as well as differing in other distinctive phenotypic characteristics, such as hemolysis, bacteriocin susceptibility, arsenate resistance, pigment production, and casein proteolysis. TSS strains were significantly less likely to carry plasmids than control strains. A combination of two variables--proteolysis and toxic shock-associated protein production--statistically accounted for all other phenotypic variations between TSS and non-TSS strains. Only proteolysis covaried with all other significant variables, suggesting a primary role in the phenotypic distinctiveness of TSS S. aureus strains and possibly in the pathogenesis of TSS.

Bacterial Proteins↗

PubMed1986

Toxic shock syndrome associated with TSST-1 producing coagulase-negative staphylococci.

Coagulase-positive staphylococci have been isolated from more than 95% of cases of toxic shock syndrome (TSS). Toxic shock syndrome toxin-1 (TSST-1) is produced in more than 90% of cases. A case is described of recurrent TSS in which a coagulase-negative staphylococcus was isolated from the vagina and produced TSST-1. No coagulase-positive staphylococci were isolated. Coagulase-negative staphylococci should be considered as causative agents in cases of TSS. Assay for TSST-1 should be performed on coagulase-negative staphylococci obtained from the appropriate clinical sites if no coagulase-positive staphylococci are isolated.

Adult↗

PubMed1999

Postoperative toxic shock syndrome caused by a highly virulent methicillin-resistant Staphylococcus aureus strain.

We report on a rare fatal case of postoperative toxic shock syndrome caused by infection with a highly virulent methicillin-resistant Staphylococcus aureus strain, designated Sak-1, which was found to be characteristic in its increased production of toxic shock syndrome toxin 1 in human whole blood (about 30-fold more than produced in Tod Hewitt broth). The strain also produced a high level of toxic shock syndrome toxin 1 in the circulating blood of mice experimentally infected with the strain.

Adult↗

PubMed1999

Toxic-shock-like-syndrome due to Streptococcus pneumoniae sinusitis.

We describe a patient with Streptococcus pneumoniae sinusitis associated with a severe sepsis syndrome and desquamative rash whose clinical illness strongly resembled toxic-shock syndrome. Assay of convalescent serum for antibodies to toxic-shock syndrome toxin 1 was negative. This case suggests the possibility of an additional bacterial pathogen associated with toxic-shock syndrome.

Adult↗

PubMed2005

Fatal toxic shock syndrome associated with Clostridium sordellii after medical abortion.

Endometritis and toxic shock syndrome associated with Clostridium sordellii have previously been reported after childbirth and, in one case, after medical abortion. We describe four deaths due to endometritis and toxic shock syndrome associated with C. sordellii that occurred within one week after medically induced abortions. Clinical findings included tachycardia, hypotension, edema, hemoconcentration, profound leukocytosis, and absence of fever. These cases indicate the need for physician awareness of this syndrome and for further study of its association with medical abortion.

Abdominal Pain↗

PubMed2003

Molecular epidemiology of methicillin-resistant Staphylococcus aureus strains causing neonatal toxic shock syndrome-like exanthematous disease in neonatal and perinatal wards.

Neonatal toxic shock syndrome-like exanthematous disease (NTED) is a new neonatal disease caused by toxic shock syndrome toxin 1 (TSST-1). We conducted a prospective surveillance study and characterized the methicillin-resistant Staphylococcus aureus (MRSA) strains isolated from patients with NTED and compared them with the strains from patients with other MRSA infections and asymptomatic carriers. The study was performed in the neonatal intensive care unit and a general neonatal and maternal ward in the Tokyo Women's Medical University Hospital (TWMUH) from September to December 1998. Among 103 patients eligible for the study, MRSA was detected in 62 (60.2%) newborns; of these 62 newborns, 8 (12.9%) developed NTED, 1 (1.6%) had another MRSA infection, and 53 (85.5%) were asymptomatic MRSA carriers. Sixty-nine MRSA strains were obtained from the 62 newborns. DNA fingerprinting by pulsed-field gel electrophoresis showed two clusters: clone A with 8 subtypes and clone B. Sixty-seven of the 69 MRSA strains (97.1%) belonged to clone A, and type A1 was the most predominant (42 of 69 strains; 60.9%) in every neonatal and perinatal ward. All but one of the clone A strains had the TSST-1 and staphylococcal enterotoxin C genes. We also analyzed eight MRSA strains from eight NTED patients in five hospitals in Japan other than TWMUH. All the MRSA strains from NTED patients also belonged to clone A. These results suggest that a single clone that predominated in the neonatal wards of six hospitals might have caused NTED. However, the occurrence of NTED might not be dependent on the presence of an NTED-specific strain.

Anti-Bacterial Agents↗

PubMed1983

Toxic shock syndrome and lysogeny in Staphylococcus aureus.

Lysogeny, or the presence of temperate bacteriophage, was demonstrated, by means of two Staphylococcus aureus indicator strains, in 11 of 12 strains of S. aureus isolated from patients with toxic shock syndrome. Only 1 of 18 strains of S. aureus that were not associated with toxic shock syndrome showed the presence of bacteriophage. A laboratory strain of S. aureus was lysogenized by bacteriophage from two of the toxic shock-associated strains. These results add support to the theory that lysogeny by one or more bacteriophage in certain strains of S. aureus may be responsible for the pathogenesis of toxic shock syndrome.

Bacterial Toxins↗

PubMed1998

Novel therapies in streptococcal toxic shock syndrome: attenuation of virulence factor expression and modulation of the host response.

The systemic manifestations of severe invasive group A streptococcal infections, such as streptococcal toxic shock syndrome, are mediated by an overwhelming inflammatory response induced by streptococcal superantigens and other virulence factors. The high mortality rates associated with streptococcal toxic shock syndrome demonstrate a need for better therapy in these diseases. Novel strategies to attenuate or prevent streptococcal toxic shock syndrome at different stages of illness have been proposed. The most promising therapies include agents that by various mechanisms attenuate the inflammatory response or the action of streptococcal toxins/superantigens, or both.

Journal Article↗

PubMed1987

Toxic shock syndrome and multiple-system organ failure after breast biopsy.

Toxic shock syndrome may result from postoperative staphylococcal wound infection. A case that occurred following a breast biopsy procedure for benign disease is reported. There was progressive multiple-system organ failure, and the patient was near death within 24 hours after a biopsy specimen of a benign fibroadenoma was obtained during an outpatient procedure. Early recognition and aggressive resuscitation are essential to prevent mortality after outpatient surgery complicated by toxic shock syndrome.

Adult↗

PubMed1980

Toxic shock syndrome, a newly recognized disease entity. Report of 11 cases.

The toxic shock syndrome has only recently been described. Eleven female patients aged 13 to 43 years (median 17) with toxic shock syndrome have been seen at the Mayo Clinic since August 1975. One patient died. Seven patients had one or more recurrences. As previously described, the syndrome was often life-threatening, afflicted mostly menstruating females, and was characterized by a very brief prodromal illness consisting of high fever, vomiting, diarrhea, conjunctivitis, headache, irritability, sore throat, myalgias, abdominal tenderness, and erythematous rash. The disorder can progress to hypotension or prolonged refractory shock, adult respiratory distress syndrome, diffuse intravascular coagulation with severe thrombocytopenia, and renal failure. Pancreatitis was observed in two cases. During convalescence, pronounced desquamation and peeling of the skin occurred. Numerous laboratory abnormalities are observed. In 5 of the 11 patients, Staphylococcus aureus was isolated from conjunctiva, oral cavity or nares, vagina, or stool. A recently described pyrogenic exotoxin was identified in the isolates of three patients; its etiologic role remains speculative. Therapy is mainly supportive. Antistaphylococcal therapy for the acute illness and for prevention of recurrences has not yet proved to be of any benefit. The role of vaginal tampons, if any, in the pathogenesis of this disorder remains unclear.

Adolescent↗

PubMed1996

Toxic shock syndrome: role of the environment, the host and the microorganism.

Toxic shock syndrome is a condition characterised by fever, rash and hypotension, and can be life-threatening. It was first described in 1978, since when many cases have been described and an association with tampon use during menstruation noted. In many cases there was concurrent infection with toxin-producing Staphylococcus aureus. It has since become clear, however, that the situation is more complex: the syndrome may occur in adults and children of both sexes, and may follow infection with bacteria other than S. aureus. Toxic shock syndrome requires a combination of susceptible host, toxin-producing bacterium and the right growth conditions within the host. The action of the toxin or toxins involved has proved difficult to elucidate. The most promising theory proposes that the toxins involved act as super-antigens, which cause massive T-lymphocyte proliferation, and production of the cytokines interleukin-1 and tumour necrosis factor.

Humans↗

PubMed1987

Nonproduction of toxic shock syndrome toxin 1 by coagulase-negative staphylococci.

We tested 187 strains of coagulase-negative staphylococci (CNS) for the production of toxic shock syndrome toxin 1 (TSST-1). A total of 111 CNS strains were isolated from the tampons of menstruating women and 74 were isolated from unused tampons. Two strains were isolated from the genital tract of a patient with toxic shock syndrome. Strains were cultivated by the membrane-over-agar method to enhance production of TSST-1, and culture supernatants were tested by two exquisitely sensitive enzyme-linked immunosorbent assays. None of the 187 CNS strains produced TSST-1. We conclude that CNS colonizing the genital tracts of menstruating women and unused tampons produce TSST-1 infrequently, if ever, and are unlikely to play a role in toxic shock syndrome.

Bacterial Toxins↗

PubMed1990

A single clone of Staphylococcus aureus causes the majority of cases of toxic shock syndrome.

Genetic relationships among 315 isolates of the bacterium Staphylococcus aureus expressing toxic shock syndrome toxin-1 (TSST-1) recovered primarily from humans with toxic shock syndrome (TSS) in five countries on two continents were determined by analyzing electrophoretically demonstrable allelic variation at 20 chromosomal enzyme loci. Forty-nine distinctive electrophoretic types (ETs), representing multilocus enzyme genotypes, were identified. Cluster analysis of the ETs revealed two major phylogenetic divisions separated at a genetic distance of 0.35 and seven branches diverging from one another at distances greater than or equal to 0.20. A single clone (ET 41) accounted for 88% of cases of TSS with a female urogenital focus and 53% of TSS cases involving nonurogenital (predominantly wound) infections. With few exceptions, strains representing different phylogenetic lines had characteristic TSST-1 gene (tst) restriction fragment length polymorphism patterns obtained by digestion of genomic DNA with Cla I. Strains recovered from ovine and bovine hosts with mastitis were genotypically distinct from the major human TSS clone. The expression of TSST-1 in cell lineages representing the total breadth of multilocus genotypic diversity in the species S. aureus as a whole is interpreted as evidence that the TSST-1 gene is evolutionarily old. The recovery of a single clone from the majority of individuals afflicted with TSS having a urogenital focus and from the genital tract of a large proportion of asymptomatic female carriers strongly suggests that this clone is especially well adapted for colonization of these anatomic sites.

Animals↗

PubMed1999

Intravenous immunoglobulin as adjunctive treatment for streptococcal toxic shock syndrome associated with necrotizing fasciitis: case report and review.

Streptococcal toxic shock syndrome (STSS) is caused by infection with a toxicogenic strain of Streptococcus pyogenes. Clinical manifestations may be those of a mild illness, characterized by malaise, fever, and muscle pain, to severe sepsis and multisystem organ failure. The syndrome may be associated with several invasive infections including necrotizing fasciitis. Treatment is primarily surgical debridement of infected tissue with supportive care, antibiotics, and hemodynamic monitoring. Intravenous immunoglobulin (IVIG) is reported to have beneficial effects in the management of STSS associated with necrotizing fasciitis. The agent was successful in conjunction with surgical excision and antibiotics in a patient with necrotizing fasciitis, toxic shock, and multisystem organ failure. On the basis of this experience and a thorough literature review, we concur that IVIG may be a useful adjunct in the treatment of STSS associated with necrotizing fasciitis.

Adolescent↗

PubMed1982

Staphylococci associated with toxic shock syndrome in the United Kingdom.

Only 15 cases of menstrual toxic shock syndrome were reported in the United Kingdom by 31 October 1981. The women affected used tampons of various brands. Staphylococcus aureus was isolated from the vaginas of 12 women. Two distinct strains were isolated from three women. Most strains were phage group I or nontypable strains related to them and were resistant only to penicillin, cadmium, and arsenate. Enterotoxin F was produced by strains from 10 of 12 patients and by 20% to 30% of strains from other sources--including healthy people. Its production was particularly common among control phage group I vaginal isolates. The reason for the rarity of toxic shock syndrome in the United Kingdom as compared to the United States is still unknown. There does not seem to be a low prevalence of toxigenic strains, but factors such as immunity to toxin and a difference in tampon use may be important and need further study.

Adolescent↗

PubMedDate not supplied

Streptococcal toxic shock syndrome with initial manifestation of abdominal pain and cholecystitis.

Streptococcal toxic shock syndrome with the initial manifestation of abdominal pain and cholecystitis is rare. We report the case of a 10-year-old boy who presented with abdominal pain, cholecystitis and shock initially. Acute respiratory distress syndrome, renal and hepatic insufficiency and disseminated intravascular coagulation developed soon after admission. Skin rash and desquamation were found subsequently during the recovery phase. The blood and sputum cultures were sterile. Acute and convalescent plasma from the patient showed increased anti-streptolysin O titer (ASLO titer). Measurement of the ASLO titer on Day 11 after the onset of disease had an ASLO titer of 242 IU/ml (N Latex ASL, Dade Behring Marburg GmbH, USA), and the ASLO titer on Day 21 after the onset of disease showed an increase to 875 IU/ml. These clinical findings and the plasma analysis were consistent with streptococcal toxic shock syndrome.

Abdominal Pain↗