SEARCH · PubMed Health

Results for “SHOCK, TOXIC”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

PubMedDate not supplied

Toxic shock syndrome in an adult male secondary to puncture wound.

The finding of toxic shock syndrome (TSS) is a rare, potentially fatal illness that physicians often associate with young, menstruating females. However, TSS is not exclusively a disease of females. We report the unusual case of an adult male patient who presented to the Emergency Department at Ruby Memorial Hospital in Morgantown with toxic shock syndrome secondary from a fish tooth suffered while trout fishing. The diagnostic features of TSS and treatment are also discussed in this article.

Adult↗

PubMedDate not supplied

[Toxic shock syndrome after reduction mammaplasty: a case report].

The clinical features of the toxic shock syndrome are well established. It is rapidly developing disease and may be lethal if not recognized and treated in time. Once the syndrome was associated with the use of tampon by menstruating women. Recently this syndrome has been reported as due to Staphylococcus aureus infection. A severe case of toxic shock syndrome in a 18-years-old patient after reduction mammoplasty is reported, and the importance of an early diagnosis is emphasized.

Acute Disease↗

PubMed1982

Toxic shock syndrome surveillance in the United States, 1980 to 1981.

Between 1 January 1980 and 18 October 1981, investigators from the Centers for Disease Control collected information on 1407 cases of toxic shock syndrome using a nationwide passive surveillance system. Ninety-two percent of the reported cases were associated with menstruation. Information available on the type of menstrual device used shows that 99% of the cases occurred in tampon users. Menstrual cases occurred predominantly in whites (98%) under the age of 25 (65%). The case/fatality ratio for menstrual toxic shock syndrome was 3.1% for cases with onset in 1981. The distribution of reported cases by date of onset showed a gradual increase in the number reported before the summer of 1980, a sharp increase during the summer and early fall of 1980, a marked decrease in the late fall of 1980, and a subsequent gradual decrease. Factors affecting the incidence and reporting of toxic shock syndrome during these periods include changes in the number of tampon users, changes in the availability and usage patterns of tampons, changes in the prevalence of toxin-producing strains of Staphylococcus aureus, improved recognition of the syndrome, and publicity.

Adolescent↗

PubMedDate not supplied

[Menstrual toxic shock syndrome].

A 15 year old girl presented twice with severe symptoms of multiorgan disease during a period of 4 weeks resulting in intensive care necessary to control illness. According to case definition criteria, a toxic shock syndrome was diagnosed on second admission. This could be confirmed by proof of TSST-1. Beside antibiotics, no specific treatment was used and complete clinical recovery occurred with symptomatic therapy. Discussing the menstrual toxic shock syndrome we point out different aspects of the pathogenesis of the disease including the possible role of tampon use. With regard to the results of several investigators, clinical symptoms of toxic shock syndrome could be the consequence of an uncontrolled immunologic reaction. Looking at this concept, more effective therapy may be available in the near future.

Adolescent↗

PubMed1995

Identification of class II major histocompatibility complex and T cell receptor binding sites in the superantigen toxic shock syndrome toxin 1.

Superantigens, in association with class II major histocompatibility complex (MHC) molecules, activate T cells bearing particular beta chain variable domains of the T cell receptor (TCR). Unlike conventional peptide antigens, superantigens bind as intact proteins to TCR and MHC molecules outside their peptide binding sites. To characterize these interactions at the molecular level, random point mutations were generated in the gene encoding toxic shock syndrome toxin 1, a bacterial superantigen associated with toxic shock syndrome. Functionally impaired mutants were identified based on their lack of murine and human T cell stimulatory activities, and experiments analyzing binding to human histocompatibility leukocyte antigen-DR molecules differentiated residues involved in MHC from TCR binding. The results showed that the great majority of mutations are clustered in two distinct regions of the toxic shock syndrome toxin 1 molecule. The class II MHC binding site is located in the hydrophobic region of the NH2-terminal domain, and the TCR binding site is primarily in the major central groove of the COOH-terminal domain. These studies provide insight into the interactions necessary for superantigen-mediated disease in humans.

Animals↗

PubMed1988

Evaluation of single-dose cefazolin prophylaxis for toxic shock syndrome.

Otolaryngologists have increased their use of parenteral prophylactic antibiotics to prevent toxic shock syndrome following nasal surgery. This rare but potentially serious postoperative complication presumably requires nasal carriage of a toxigenic strain of Staphylococcus aureus by a susceptible patient. We investigated the effect of a single preoperative dose of intravenous cefazolin on nasal carriage of S aureus. Thirty patients were studied; 15 were S aureus carriers initially and 12 (80%) remained culture positive after prophylaxis and at the time surgery was completed. We conclude that this particular regimen is unlikely to have a major effect on the incidence of toxic shock syndrome following nasal surgery.

Cefazolin↗

PubMed1989

Risk involvement with Staphylococcus aureus exotoxins among pyogenic skin infections with special reference to toxic shock syndrome.

The sera of three patients involved in a non-menstrual toxic shock syndrome outbreak showed TSST-1 at a concentration above 40 ng/ml and no antibodies of IgG class against the toxin. A Staphylococcus aureus strain producing TSST-1 was isolated from one of the patients. S. aureus strains showing similar phage type and biotype patterns were isolated from 473 out of 876 close contacts with the patients involved in this outbreak. This carriage and spread was traced to pyogenic skin infections (mainly "folliculitis") among this population. Serological studies indicated that during the early phase of the outbreak anti TSST-1 titres were low then rose gradually. In a further related study the frequency of enterotoxin production was found 48.5% among staphylococci isolated from pyogenic skin infections. Our data indicated that pyogenic skin infections are potential source for toxic shock syndrome.

Antibodies, Bacterial↗

PubMed1991

Streptococcus pyogenes causing toxic-shock-like syndrome and other invasive diseases: clonal diversity and pyrogenic exotoxin expression.

Genetic diversity and relationships among 108 isolates of the bacterium Streptococcus pyogenes recently recovered from patients in the United States with toxic-shock-like syndrome or other invasive diseases were estimated by multilocus enzyme electrophoresis. Thirty-three electrophoretic types (ETs), representing distinctive multilocus clonal genotypes, were identified, but nearly half the disease episodes, including more than two-thirds of the cases of toxic-shock-like syndrome, were caused by strains of two related clones (ET 1 and ET 2). These two clones were also represented by recent pathogenic European isolates. A previous report of a relatively high frequency of expression of exotoxin A among isolates recovered from toxic-shock-like syndrome patients in the United States was confirmed; and the demonstration of this association both within clones and among distantly related clones supports the hypothesis that exotoxin A is a causal factor in pathogenesis of this disease. Near identity of the nucleotide sequences of the exotoxin A structural gene of six isolates of five ETs in diverse phylogenetic lineages was interpreted as evidence that the gene has been horizontally distributed among clones, presumably by bacteriophage-mediated transfer.

Bacterial Proteins↗

PubMed1995

Role of a carboxy-terminal site of toxic shock syndrome toxin 1 in eliciting immune responses of human peripheral blood mononuclear cells.

Staphylococcus aureus toxic shock syndrome toxin 1 (TSST-1) is involved in the pathogenesis of toxic shock syndrome and perhaps other staphylococcal diseases. Recently, the C-terminal part of the TSST-1 toxin has been shown to be responsible for mitogenic activity in animal models. We studied the role of the C-terminal structural unit of TSST-1 with regard to proliferation, cytokine release (tumor necrosis factor alpha [TNF-alpha], interleukin-6 [IL-6], and IL-8), mRNA expression for IL-6, IL-8, IL-10, TNF-alpha, and CD40 ligand (CD40L), synthesis of immunoglobulin E (IgE), IgA, IgG, and IgM, CD23 expression, and soluble CD23 (sCD23) release from human peripheral blood mononuclear cells (PBMC). For this purpose, we used the recombinant wild-type TSST-1 (p17) mutant toxin Y115A (tyrosine residue modified to alanine) and toxin H135A (histidine residue modified to alanine). Unmodified toxin p17 and mutant toxin Y115A, at a concentration below 5 ng, to a lesser degree, induced a strong proliferation. Toxin p17 followed by toxin Y115A was the most pronounced inducer for mRNA expression for IL-10 and CD40L and cytokine generation (mRNA and protein) for TNF-alpha, IL-6, and IL-8. Mutant protein H135A failed to activate human PBMC. Both toxins p17 and, to a lesser degree, Y115A significantly suppressed IL-4- and anti-CD40-induced synthesis of all four Igs as well as IL-4-induced CD23 expression and sCD23 release. Mutant toxin H135A failed to do so. Thus, our data show that a region in the C terminus of TSST-1 is responsible not only for mitogenic activity but also for additional immunomodulating biological activities of TSST-1. More specifically, histidine residue H135A of the 194-amino-acid toxin appears to be critical for the expression of biological activities in a human in vitro model.

Antigens, CD↗

PubMed1996

The toxic shock syndromes.

Because of the frequency with which Staphylococcus aureus and Streptococcus pyogenes infections occur, physicians are quite familiar with the diversity of their clinical presentations. In the 1970s, however, shock associated with multiorgan failure was described in menstruating female patients as well as in male patients following a variety of surgical procedures, such as rhinoplasty. This previously undescribed presentation of S. aureus infection, termed staphylococcal toxic shock syndrome, was associated with unique strains of S. aureus. In the mid-1980s, the emergence of streptococcal toxic shock syndrome was heralded by several case reports describing patients with group A streptococcal infections associated with shock and organ failure. This article compares the differences in the epidemiologic, clinical, and pathophysiologic features of the toxic shock syndromes.

Anti-Bacterial Agents↗

PubMed1996

Fatal group A streptococcal infection with toxic shock syndrome: complicating minor orthopedic trauma.

Since 1987, reports have appeared of a streptococcal toxic shock syndrome in various clinical settings. None have appeared in the orthopaedic literature. Between 1989 and 1991 at our institution three patients with relatively minor orthopaedic injuries or procedures died of group A streptococcal infections complicated by toxic shock syndrome. The manifestations of this syndrome included rapid progression of systemic sepsis, necrotizing soft-tissue infections, acute renal failure, adult respiratory distress syndrome, and coagulopathy. All three patients died despite aggressive resuscitative measures and surgical debridement. Optimal treatment of this life-threatening process requires early recognition, aggressive surgical debridement, appropriate antibiotic management, and intensive care unit support.

Adult↗

PubMed1990

[A patient with toxic shock syndrome following correction of the nasal septum].

A male aged 30 suffered from toxic shock syndrome after septorhinoplasty with positioning of a tampon. Initial treatment consisted of removing the tampon and supportive care, as a result of which the patient recovered. The patient was a carrier of Staphylococcus aureus which produced toxic shock syndrome toxin-I (TSST-I). Anti-TSST-I antibodies were already found in the serum in the initial phase of the disease.

Adult↗

PubMed1998

Streptococcal toxic shock syndrome presenting as suspected child abuse.

Natural disease processes can predispose individuals to develop external body lesions that mimic traumatic injury. This can be particularly problematic in pediatric cases in which clinicians are alerted to the problems of child abuse. Streptococcal toxic shock syndrome is a systemic infectious illness that can manifest itself with erythematous and necrotizing skin lesions. We report a fatal case of streptococcal toxic shock syndrome in a 4-year-old girl who presented with skin lesions that were initially thought to be traumatic in origin. A report of possible child abuse was filed with the state. Based on the morphologic findings and bacteriologic culture results at autopsy, these lesions and the cause of death in this case were instead determined to result from streptococcal toxic shock syndrome.

Cause of Death↗

PubMed2002

Mucosal tolerance to a bacterial superantigen indicates a novel pathway to prevent toxic shock.

Enterotoxins with superantigenic properties secreted during systemic Staphylococcus aureus infection are responsible for toxic shock. We show that intranasal administration of staphylococcal enterotoxin A (SEA), but not a recombinant SEA lacking superantigenic activity, protected mice against lethal systemic SEA challenge. Protection was superantigen specific since intranasal exposure to SEA would not protect against death caused by subsequent toxic shock syndrome toxin 1 systemic challenge. Protection was neither due to selective depletion of SEA-specific T-cell receptor Vbeta families nor due to production of neutralizing anti-SEA antibodies. Importantly, the production of interleukin 10 (IL-10) induced by "tolerization" (that is, by the induction of immunological tolerance) contributed to the observed protection against lethal superantigen-triggered disease. In support of this notion we found that (i) significantly increased levels of IL-10 in sera of "tolerized" animals (that is, animals rendered tolerant) and (ii) IL-10(-/-) mice could not be tolerized by mucosal SEA administration. Altogether, this is the first study to show that mucosal tolerance to a superantigen is readily triggered by means of immunodeviation.

Animals↗

PubMed1988

Effect of dilution rate and Mg2+ limitation on toxic shock syndrome toxin-1 production by Staphylococcus aureus grown in defined continuous culture.

A toxic shock syndrome isolate of Staphylococcus aureus was grown in a chemostat, in a defined synthetic medium of six amino acids, glucose, two vitamins and salts. Steady states were achieved under limiting and replete Mg2+ conditions and at a range of relative specific growth rates. The biomass and toxic shock syndrome toxin-1 (TSST-1) were estimated at each condition. Under Mg2+ limitation the biomass and TSST-1 production rates were reduced compared to Mg2+ replete conditions. Optimal TSST-1 production occurred at 0.81 relative specific growth rate.

Bacterial Toxins↗

PubMed1988

Scarlet fever can mimic toxic shock syndrome.

We describe a patient who presented with a widespread erythematous rash, diarrhoea, confusion, pre-renal uraemia and hyponatraemia. The diagnosis of staphylococcal toxic shock syndrome seemed likely as she was menstruating and there was no evidence of pharyngitis. A rising ASO titre confirmed a streptococcal aetiology and thus 'toxic' scarlet fever. Toxic shock syndrome and toxic scarlet fever are compared.

Adult↗

PubMed1982

Statistical methods in the study of toxic shock syndrome.

Analysis of statistical methods used in matched case-control studies of toxic shock syndrome shows that matching has implications for validity and precision of the studies and for the choice of analysis techniques. The studies considered accounted for the matching in the analysis, either by the Mantel-Haenszel or Miettinen-Pike-Morrow approach to 1-to-M matched designs, or by the use of conditional maximum likelihood fitting of logistic regression models. Methods of dealing with confounding and effect modification in the (matched) logistic regression model are presented in the context of studies of toxic shock syndrome. The varied statistical techniques used in these studies were generally appropriate to the matched design except that nonmatching variables were not thoroughly considered as effect modifiers or confounders.

Carboxymethylcellulose Sodium↗

PubMed1994

Toxic shock syndrome after functional endonasal sinus surgery: an all or none phenomenon?

Reported cases of toxic shock syndrome (TSS) following nasal surgery or functional endonasal sinus surgery (FESS) are uncommon. Classic TSS is a serious multisystem disorder resulting from Staphylococcus aureus phage I toxic shock syndrome toxin 1 (TSST-1), and it is characterized by fever, rash, hypotension, mucosal hyperemia, vomiting, diarrhea, and laboratory evidence of multisystem organ dysfunction. TSS cases following nasal surgery have been associated with nasal packing, mucosal barrier violation, prior S aureus phage I colonization, as well as low antitoxin antibody levels. Of the 1700 FESS procedures performed at our institution, 3 cases were complicated by classic TSS, with 2 additional patients having a postsurgical course compromised by a milder degree of TSS. Diagnostic criteria, clinical presentation, management, and etiology are discussed, and the possibility of a continuum from mild-to-classic TSS is addressed.

Adolescent↗