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PubMed2002

Toxic shock syndrome following laparoscopic cholecystectomy.

Toxic shock syndrome has been described in three clinical situations: pediatric abscesses; menses, especially among women using highly absorbent tampons; and after surgery. The syndrome is marked by the sudden onset of fever, a sunburn-like rash, and hypotension, and is associated with recovery of toxin-producing Staphylococcus aureus, usually from small amounts of serous or seropurulent fluid. The syndrome usually begins 1 to 2 days after the procedure. To date, no cases have been reported after laparoscopic surgery. We describe a case of postoperative toxic shock syndrome in a 41-year-old woman who underwent laparoscopic cholecystectomy. She required a second operation, antimicrobial therapy, and blood pressure support and eventually recovered fully. Culture of the operative bed yielded S. aureus that produced enteroxin B. Surgeons should investigate vigorously any fever and hypotension developing in the first 24 to 48 hours after laparoscopy. Toxic shock syndrome should be considered in the differential diagnosis.

Adult↗

PubMed1981

Risk factors for staphylococcal toxic-shock syndrome.

Fifty-two cases of toxic-shock syndrome that occurred in January 1, 1976 through August 31, 1980, were reported to the Utah State Health Department between February 1 and August 31, 1980. The annual attack rate for Utah based on a six-month surveillance period was 14.4 per 100,000 women ages 12-49 years. All cases were in women who had onset of illness within two days of menses. Potential risk factors were investigated with a case-control study utilizing 29 women hospitalized with toxic-shock syndrome and 91 neighborhood female controls. Nine of the 29 (31%) women reported recurrences of similar illness. Use of tampons (p = 0.012) and use of a single brand of tampon-Rely-during the month of illness (p less than 0.005, RR =6.11) were associated with a significantly increased risk of acquiring toxic-shock syndrome. More controls were sexually active than women who had toxic-shock syndrome (p less than 0.05, RR - 0.277). This epidemiologic investigation of toxic-shock syndrome in menstrual-age women has identified tampons generally and a single brand specifically as significant risk factors in acquiring toxic-shock syndrome.

Adolescent↗

PubMed1986

The incidence of toxic shock syndrome in Northern California. 1972 through 1983.

In its 1982 report on toxic shock syndrome, the institute of Medicine, Washington, DC, identified population-based studies of the incidence of toxic shock syndrome over time based on hospital records as being a high priority for further research. We conducted such a study using records of hospitalizations in Northern California Kaiser-Permanente Medical Care Program facilities for the period from 1972 through 1983 among women and men aged 15 through 34 for illnesses considered possibly to be toxic shock syndrome. Of 6,688 hospitalizations reviewed, 54 were considered definite cases of toxic shock syndrome, and an additional nine were considered probable toxic shock syndrome. Four definite cases of toxic shock syndrome occurred in men, and 50 in women. The overall incidence of definite hospitalized toxic shock syndrome in men was 0.1 per 100,000 person-years, and in women 1.5 per 100,000 person-years. In women, an increase in the incidence of toxic shock syndrome was apparent by 1977; the rate peaked in 1980, decreased slightly in 1981 and 1982, and then almost doubled again in 1983. The temporal trend in the incidence of hospitalized toxic shock syndrome in women in the years 1977 through 1982 is consistent with the best available information on patterns of use of tampons containing higher-absorbency materials. The sharp increase in the incidence of hospitalized toxic shock syndrome in 1983 remains unexplained.

Adolescent↗

PubMed1982

Toxic shock syndrome: a perspective through the looking glass.

Toxic shock syndrome associated with Staphylococcus aureus was first described in 1978, although cases of patients with similar findings were reported as far back as 1927. Various strict clinical definitions for toxic shock syndrome have been proposed that still should include exclusionary data (titers, cultures) when possible. Epidemiologic studies of toxic shock syndrome confirm that it occurs in males and nonmenstruating females, but more commonly in menstruating females, especially those using tampons. Microbiologic studies have identified phenotypic characteristics of S. aureus strains associated with toxic shock syndrome but none have been shown to be causally related. The attentiveness of the lay press to toxic shock syndrome research should not divert investigators from an orderly scientific process and appropriate critical review.

Female↗

PubMed1989

Toxic shock syndrome associated with poison oak dermatitis.

Toxic shock syndrome commonly occurs in menstruating women, but it is known to be associated with a variety of staphylococcal infections. We report a case of nonmenstrual toxic shock syndrome in an 11-year-old male who presented with altered consciousness and infected poison oak dermatitis of the feet. This is the first reported case of toxic shock syndrome associated with poison oak dermatitis. The signs and symptoms, laboratory findings, and treatment of toxic shock syndrome are reviewed.

Child↗

PubMed1992

A review of toxic shock syndrome: the need for education still exists.

Toxic shock syndrome is a multisystem disease that is believed to be caused by a toxin produced by Staphylococcus aureus. The syndrome can occur in persons of any gender, age or race and should be considered as a possible diagnosis in any patient displaying symptoms compatible with the illness. Most reported cases of toxic shock syndrome have occurred in young menstruating women and have been associated with the use of tampons. Toxic shock syndrome cases reported to the Centers for Disease Control have decreased substantially since May of 1980. The decreases in diagnosis and reporting may be attributed to diminished public and professional attention to the syndrome. In addition, it is likely that cases of the syndrome that do not meet the strict Centers for Disease Control case definition are not being diagnosed. Until more is understood about toxic shock syndrome, particularly its relationship to menstruation and tampon use, patient education remains a primary key to prevention. Women should be aware of the symptoms of toxic shock syndrome and, if symptoms occur, seek medical attention immediately.

Centers for Disease Control and Prevention, U.S.↗

PubMed1995

A mutation at histidine residue 135 of toxic shock syndrome toxin yields an immunogenic protein with minimal toxicity.

Structure-function studies have revealed that the region between amino acids 115 and 141 of toxic shock syndrome toxin 1 (TSST-1) constitutes a biologically active domain. A critical residue appears to be histidine 135, since a site-directed mutation that alters the histidine to alanine (H135A) results in a loss of mitogenic activity and an absence of toxicity as measured in a rabbit infection model of toxic shock syndrome. We have characterized the mutant toxin further and report here on its immunogenic activity in rabbits and on the protective ability of mutant-specific antibodies in two animal models of toxin-mediated shock. Antibodies raised in rabbits by immunization with the purified H135A are fully cross-reactive with staphylococcal TSST-1 and wild-type recombinant TSST-1 (rTSST-1) expressed in Escherichia coli. The H135A antibodies neutralized the mitogenic activity for murine splenic T cells equally well as did TSST-1-specific polyclonal and monoclonal antibodies. In addition, the H135A antibodies blocked the production of tumor necrosis factor by spleen cells stimulated with rTSST-1. The toxicities of rTSST-1 and H135A were compared in D-galactosamine (D-GalNH2)-sensitized MRL-lpr/lpr mice. The nontoxicity of H135A was confirmed in this murine model of superantigen-induced septic shock. No toxicity of H135A was demonstrable at doses of 60 micrograms, while doses of rTSST-1 as low as 2 micrograms caused significant mortality within 24 to 72 h after challenge. Furthermore, subsequent to challenge of mice with H135A, no elevation in the serum levels of interleukin-2 or tumor necrosis factor was measurable. Passive immunization with H135A antibodies also protected MRL-lpr/lpr mice against lethal challenge with rTSST-1. Finally, rabbits actively immunized with purified H135A did not succumb to infection with a transformed strain of Staphylococcus aureus expressing rTSST-1. Additional animal studies will be required to confirm the immunizing potential of H135A and the efficacy of H135A antibodies as a neutralizing antitoxin.

Animals↗

PubMed1986

Involvement of coagulase-negative staphylococci in toxic shock syndrome.

Coagulase-negative staphylococci that produce toxic shock syndrome toxin 1 (TSST-1) or a staphylococcal enterotoxin or both were isolated from various sources. Coagulase-negative strains that produce TSST-1 alone or with enterotoxin A were the only staphylococci isolated from seven patients with toxic shock syndrome. Two other toxic shock syndrome patients had coagulase-positive staphylococci also, but only the coagulase-negative strains produced TSST-1. Coagulase-positive and coagulase-negative strains that produced TSST-1 were isolated from two other toxic shock syndrome patients. In addition, coagulase-negative staphylococci that produced toxins were isolated from patients with other staphylococcal infections and from food implicated in a case of food poisoning.

Bacterial Toxins↗

PubMedDate not supplied

Endotoxin is not an essential mediator in toxic shock syndrome.

The hypothesis that toxic shock syndrome toxin 1 (TSST-1) exerts its deleterious effects in toxic shock syndrome (TSS) primarily by enhancing the lethality of small amounts of endogenous endotoxin derived from mucosal colonization with gram-negative bacteria was assessed by evaluating two means of inactivating endotoxin in rabbit models of TSS. In both of these models, toxins and TSST-1 are allowed to diffuse constantly from a subcutaneous depot. Immunologic inactivation of endotoxin with antiserum to the core lipopolysaccharide did not change the clinical course or mortality among animals infected with live TSS-associated staphylococci or among animals with a subcutaneous depot of TSST-1. Anti-TSST-1 was successful in preventing disease and death in these models. Pharmacologic inactivation of endotoxin by pretreatment or continuous treatment with polymyxin B did not prevent illness or mortality in the toxin depot model. Endotoxin thus appears not to be an essential mediator in TSS, since TSS-like illness develops and progresses despite inactivation of endotoxin in animal model systems that are faithful both physiologically and clinically to TSS in humans.

Animals↗

PubMed1985

Studies on staphylococci from toxic shock syndrome in France, 1981-1983.

Staphylococci from 22 cases of toxic shock syndrome with onsets between 1981 and March 1983 have been studied. Another four cases were detected by abstract surveillance. Three of these patients died. The case histories show that the syndrome occurs in women during menstruation as well as in males and in children, and is associated with Staphylococcus aureus infections. The production of enterotoxins (A, B, C) and toxic shock toxin by S. aureus isolates from toxic shock syndrome was investigated. Twenty-two of the 23 isolates were found to be toxigenic: 7 produced enterotoxin A, 8 produced enterotoxin B, 3 produced enterotoxin C and 13 produced toxic shock toxin. The latter was found with enterotoxin A in five cases, and with enterotoxins A and B in only one case. Sixty-three percent of 46 S. aureus strains isolated from the vagina of patients with diseases other than toxic shock syndrome produced toxin; eight of these strains produced toxic shock toxin.

Adolescent↗

PubMed2001

Inhibition of staphylococcal enterotoxin A-induced superantigenic and lethal activities by a monoclonal antibody to toxic shock syndrome toxin-1.

Staphylococcal toxic shock syndrome is caused by a family of related superantigens that includes toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxins (SEs) A, B, and C. The cross-inhibitory activity against SEA by a novel anti-TSST-1 monoclonal antibody (MAb), MAb5, which also cross-inhibits SEB-induced superantigenic activities, was investigated. MAb5 blocked SEA binding to human monocytes, cross-neutralized SEA-induced T cell mitogenesis and TNF-alpha secretion in human peripheral blood mononuclear cells, and prevented lethality in mice. Epitope mapping revealed that MAb5 binds to residues SEA(154-161) within the central alpha helix that is structurally highly conserved among TSST-1, SEA, and SEB. The cross-inhibitory activity of MAb5 is likely due to steric hindrance of this conserved motif, although the precise function of this motif shared among related staphylococcal superantigens remains to be further elucidated.

Amino Acid Sequence↗

PubMed1991

Toxic shock syndrome: an update.

Since late 1979 to early 1980, when toxic shock syndrome achieved notoriety, a substantial body of data has demonstrated that vaginal Staphylococcus aureus infections, particularly those occurring during menstruation, account for most cases of toxic shock syndrome in women of reproductive age. Among those patients with onset during menstruation, tampon use has been identified as the most important risk factor. Although menstrually associated cases have been observed among users of all brands and styles of tampons, the use of selected "super absorbent" brands and styles has been associated with an increased risk of toxic shock syndrome. Although the tampon characteristics responsible for the associated risk of toxic shock syndrome remain poorly understood, both absorbency and chemical composition appear to be important variables in this relationship. In response to studies demonstrating this relationship and legal pressures, tampon manufacturers have removed chemical constituents previously used to enhance absorbency, such as polyester foam, carboxymethylcellulose, and polyacrylate rayon, and have markedly reduced tampon absorbency. Coinciding with these changes, the reported number of menstrually related cases of toxic shock syndrome has dropped substantially, although they continue to account for 50% to 70% of all cases of toxic shock syndrome in women of reproductive age.

Female↗

PubMed1987

Toxic shock syndrome (TSS) in children.

Toxic shock syndrome is uncommon in the prepubertal age group. Two children presented with pyrexia, macular erythroderma, vomiting, hypotension and rapid deterioration of consciousness. One child had severe neurological involvement. The diagnosis of toxic shock syndrome was established in both cases by the exclusion of other causes and by culturing staphylococcus aureus. We postulate that the neurological manifestations were caused by a direct neurotoxic action of the staphylococcal-produced toxin. Both children made a complete recovery.

Child↗

PubMedDate not supplied

Magnesium and the pathogenesis of toxic shock syndrome.

Excess production of toxic shock syndrome toxin 1 by appropriate strains of Staphylococcus aureus occurs when the organisms are grown in an environment deficient in Mg++. Since many of the fibers previously used in tampons combine with Mg++, an explanation for the pathogenesis of menstrually related toxic shock syndrome presents itself. Pitfalls in the reproduction of these experiments have been investigated and include attention to inoculum size, to the effect of washing the inoculum to rid it of magnesium from the parent culture, and related variables. The growth of staphylococci in magnesium-deficient medium is slower than in the usual culture media, making it necessary that the effect of magnesium deficiency be examined after sufficient incubation to permit maximal toxin production to occur. When these variables are taken into account, a coherent theory to explain the pathogenesis of menstrual TSS emerges. Absorbency of tampons, which correlates with the capacity to absorb Mg++, becomes, as has been suggested, a surrogate for the magnesium effect. The observations raise the possibility of a safer tampon, one in which the magnesium content is regulated to cause the staphylococci not to be in a magnesium-deficient environment.

Bacterial Toxins↗

PubMed1994

Case report: toxic shock syndrome arising from cellulitis.

Toxic shock syndrome is a febrile, multiorgan illness related to toxins elaborated by staphylococcal or streptococcal infections. In the 1980s, most cases were associated with menstruation. More recently, many cases now are unrelated to menses. In this article, the authors describe a case of a nonmenstruating woman with toxic shock syndrome, associated with cellulitis of her arm. Cultures of the arm grew Staphylococcal aureus, which produced enterotoxin B.

Adult↗

PubMed1981

Toxic shock syndrome.

Eight cases of toxic shock syndrome, confirmed by Center for Disease Control criteria, involved women who were menstruating and were tampon users. Each patient had severe febrile illness with rash, associated hypotension, renal and liver function abnormalities, pharyngitis and vaginitis. An examination of the literature indicates that cases that were reported as adult Kawasaki disease may actually have been toxic shock syndrome.

Adolescent↗

PubMed1988

[Severe hypophosphoremia in a toxic shock syndrome].

A case of toxic shock syndrome occurring during a menstrual period, and associated with severe hypophosphataemia, is reported. The patient was a 21-year old woman using tampons. On the fourth day, she developed encephalopathy with decreased consciousness and hyperventilation. Severe hypophosphataemia was noted. A phage-group-1 Staphylococcus aureus, producing TSST-1 and enterotoxin A, was isolated from vaginal, pharyngeal and skin sites. Pathogenesis and role of hypophosphataemia in toxic shock syndrome are emphasized.

Adult↗

PubMed1986

Toxic shock syndrome after augmentation mammaplasty.

Toxic shock syndrome was first described in children in 1978. Two years later the strong connection between this disease and the colonization of vaginal tampons with certain strains of Staphylococcus aureus was noted. Even from the earliest descriptions, however, it has been clear that the same clinical picture may be caused by staphylococcal infections elsewhere, and that the presence of foreign materials in the body is not mandatory. We describe a patient with toxic shock syndrome after augmentation mammaplasty.

Adult↗