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At least 19 recordsLinked to original sources
PubMed1989

Relative strength of the mitogenic and interleukin-2-production-inducing activities of staphylococcal exotoxins presumed to be causative exotoxins of toxic shock syndrome: toxic shock syndrome toxin-1 and enterotoxins A, B and C to murine and human T cells.

Several observations suggest that staphylococcal enterotoxins A, B and C (SEA, SEB and SEC, respectively), in addition to toxic shock syndrome toxin-1 (TSST-1), are causative exotoxins of toxic shock syndrome (TSS). Based on the view that polyclonal T cell activation with the causative exotoxins, resulting in over-production of lymphokines, is involved in the development of the pathological changes observed in TSS, we investigated the activities of these four exotoxins to induce proliferation and interleukin 2 production in murine and human lymphocytes by using in vitro culture systems. The results showed that all these exotoxins are strong polyclonal inducers of proliferation and interleukin 2 production in human T cells, whereas TSST-1 and SEA are strong and SEB and SEC are weak polyclonal inducers in murine T cells. These results suggest that SEA, SEB and SEC, in addition to TSST-1, are possibly involved as causative exotoxins in the development of the pathological changes observed in TSS.

Adult↗
PubMed1990

Therapy of toxic shock syndrome.

Toxic shock syndrome (TSS) is an acute febrile, exanthematous illness associated with multisystem failure including shock, renal failure, myocardial failure and adult respiratory distress syndrome (ARDS). It usually presents with fever, pharyngitis, diarrhoea, vomiting, myalgia, and a scarlet fever-like rash, and may progress rapidly (within hours) to signs of hypovolaemic hypotension such as orthostatic dizziness or fainting. The signs and symptoms of toxic shock syndrome should be recognised early to permit successful therapy. Patients are usually suffering from hypovolaemia due to leaky capillaries and fluid loss into the interstitial space, and consequently large volumes of fluid, both crystalloid (e.g. saline, electrolyte-solutions) and colloid (e.g. albumin, intravenous gamma-globulin), may be necessary to maintain adequate venous return and cardiac output. Patients with toxic shock syndrome usually have a focus of staphylococcal infection such as a surgical wound infection or soft tissue abscess, or they may have TSS associated with menstruation and use of a vaginal device such as tampons. The site of infection should be adequately drained and treated with antimicrobial therapy. Subacute complications including ARDS and myocardial failure require a thorough understanding of the underlying pathophysiology to ensure appropriate treatment. Recurrences of TSS can be avoided by appropriate antimicrobial treatment and avoidance of recurrent conditions which might favour staphylococcal toxin production (e.g. use of tampons during menstruation). More than 95% of patients survive toxic shock syndrome if appropriate therapy is instituted early.

Humans↗
PubMed1994

Advanced cervical carcinoma presenting with toxic shock syndrome.

Toxic shock syndrome is a multisystem disease which presents with a high fever, rash, gastrointestinal symptoms, and hypotension. A 58-year-old woman presented to the emergency room with these symptoms, hypotension and tachycardia. Because of vaginal spotting a pelvic examination was performed which demonstrated vulvo/vaginal erythema and a large vaginal mass consistent with an advanced cervical cancer with bilateral pelvic sidewall fixation. Cervical/vaginal biopsy demonstrated invasive squamous cell carcinoma and an initial chest X ray demonstrated multiple pulmonary metastases. After a total of 8 days of antibiotic therapy the patient received cis-platinum chemotherapy. The toxic shock syndrome was the presenting symptomatology in this patient with advanced cervical cancer. Toxic shock syndrome has been associated with the use of hyperabsorbent tampons as well as numerous other gynecologic procedures but has not been reported in patients with gynecologic cancer.

Anti-Bacterial Agents↗
PubMedDate not supplied

Hypercalcitoninemia, hypocalcemia, and toxic shock syndrome.

Toxic shock syndrome is a multisystem illness frequently complicated by hypocalcemia. The etiology of the hypocalcemia, which may be severe, is not well understood. We report two cases of fatal toxic shock syndrome accompanied by severe hypocalcemia; each patient also had an inappropriately elevated serum calcitonin level, which in one case was as high as 179,000 pg/mL. Hypercalcitoninemia may be a cause of the low serum calcium levels as well as of certain clinical manifestations of toxic shock syndrome.

Adolescent↗
PubMed2004

Reductions in levels of bacterial superantigens/cannabinoids by plasma exchange in a patient with severe toxic shock syndrome.

Toxic shock syndrome is a rare but potentially fatal toxin-mediated febrile illness. We report a case of toxic shock syndrome complicated by life-threatening organ dysfunction with high toxin-1 and staphylococcus enterotoxin type A levels that were successfully reduced by early introduction of plasma exchanges. The report shows the time course of the concentrations of anandamide and 2-arachidonyl glyceride and confirms that early introduction of plasma exchange can result in a rapid reduction of circulating toxins and mediators in the treatment of life-threatening multiple organ dysfunction.

Adolescent↗
PubMed1985

Animal studies of toxic shock syndrome.

Toxic shock syndrome (TSS) was first described in 1978 and since that year over 2990 cases have been reported to the Communicable Disease Center. The estimated case-fatality rate is 5.6%. The disease is characterized by fever, hypotension, rash, desquamation, and involvement of at least three other organ systems. Approximately 85% of the cases are menstrually related and tampon use has been identified as a risk factor. The remaining 15% of the cases occur in both sexes and are not specifically related to age or geographic location. In all cases where sought there is evidence for infection by Staphylococcus aureus. Nearly all S. aureus isolates are phage type 52/29 and elaborate a unique exotoxin (toxic shock toxin). This review explores both the successful and unsuccessful attempts to induce toxic shock or a TSS-like syndrome in animals other than man. The review identifies the baboon as an animal model of TSS and discusses the clinical and pathologic sequellae, in this species, after exposure to purified toxic shock toxin.

Animals↗
PubMed2000

Toxic shock syndrome.

Toxic shock syndrome (TSS) is an acute febrile illness accompanied by watery diarrhea, sunburn rash, vomiting, hypotension, and multiple organ involvement. When it was initially recognized 20 years ago, TSS was primarily associated with menstruation. Since then, the frequency of menstrual TSS has decreased dramatically. Staphylococcus aureus is the cause of menstrual TSS and is also responsible for about half of all cases of nonmenstrual TSS. Since the late 1980s, Streptococcus pyogenes has been shown to cause a nonmenstrual TSS-like illness, with a higher mortality rate. The mechanism of TSS is attributable to bacterial endotoxins that impede the body's immune system and cause the release of cytokines, which are responsible for the clinical manifestations of the disease. Early recognition and treatment of TSS are important factors in improving patient survival. Patients should be treated with parenteral antibiotics that are highly effective against staphylococci and streptococci. They should also receive fluid resuscitation and vasopressors. Some patients require intubation, dialysis, or immunoglobulin therapy.

Journal Article↗
PubMed1983

Toxic shock syndrome.

Toxic shock syndrome (TSS) is an exotoxin-mediated illness that occurs primarily in young menstruating women who use tampons. The syndrome ranges from a potentially fatal disease characterized by hypotension and failure in multiple organ systems to a less severe condition commonly misdiagnosed as a nonspecific viral illness or gastroenteritis. Physicians should recognize that an exanthematous, febrile illness that recurs during menstruation or that occurs primarily in the postoperative or postpartum period and in association with staphylococcal infections may be TSS even in the absence of requisite diagnostic criteria. Unless TSS can be excluded with reasonable certainty, appropriate cultures should be obtained, with treatment initiated presumptively. In all menstrual cases, women should be advised to avoid tampon use indefinitely.

Adolescent↗
PubMed1988

Post-traumatic toxic shock syndrome.

Toxic shock syndrome (TSS) associated with Staphylococcus occurs most commonly in menstruating women, although cases in both sexes have been reported. This report describes a severe case of TSS after a relatively minor stab wound. The male patient exhibited all of the major characteristics of this multisystem disease including anuric renal failure. TSS, which can be fatal, may result from surgical and traumatic wound infections and demands prompt recognition and treatment.

Acute Kidney Injury↗
PubMed1986

Immunological protection of rabbits infected with Staphylococcus aureus isolates from patients with toxic shock syndrome.

Toxic shock syndrome toxin-1 (TSST-1) isolated from the growth medium of Staphylococcus aureus 1169 and 555 was used to immunize male rabbits before infection with either a TSST-1+ or a TSST-1- strain of S. aureus isolated from cases of TSS. None of the immunized rabbits died as a result of the infections, whereas 50% of the nonimmunized rabbits infected with the TSST-1- strain, D4508, and 75% of those infected with the TSST-1+ strain, 555, died. Western blots of crude extracellular protein preparations probed with sera from immunized rabbits indicated that the TSST-1- strain produces a 30,000-molecular-weight protein that cross-reacts with antiserum to TSST-1. Because both organisms caused similar diseases in rabbits, we propose to designate the cross-reacting protein as TSST-2.

Adolescent↗
PubMed1989

Mastitis and toxic shock syndrome.

Toxic shock syndrome (TSS) secondary to mastitis or breast abscess is only seldom described. We report a case of definite TSS due to postpartum staphylococcal mastitis which evolved over a period of 3 weeks to a breast abscess, recurring after 2 months. Only the episode of acute mastitis was complicated with TSS, while Staph. aureus could be isolated during the period of mastitis from milk and during drainage of the second breast abscess.

Abscess↗
PubMed1990

Toxic shock syndrome.

Toxic shock syndrome (TSS) is a severe multi-system disorder resulting from a Staphylococcus aureus exotoxin. Primary presenting features consist of fever, hypotension, vomiting and diarrhea, and a diffuse macular erythroderma with later desquamation. Treatment is supportive accompanied by drainage and debridement of infection and antibiotics. TSS may occur following any infection with Staphylococcus aureus and is a well-documented complication of nasal surgery. Otolaryngologists should be aware of the manifestations of this disorder and its treatment. A case is presented, along with a review of the literature and management of TSS.

Bandages↗
PubMed1981

The clinical spectrum of toxic shock syndrome.

Toxic shock syndrome (TSS) is a recently recognized acute multisystem illness that may recur. Epidemiologic links with menstruation and use of tampons have been identified. We report the cases of seven patients (six women and one man), 12 to 31 years old, seen over nine months, who met the criteria for TSS. Four were menstruating at onset. All had hypotension, fever, erythematous rash and distal desquamation. A prodrome of myalgias and diarrhea occurred in all patients. Clinical features of the acute illness included pharyngitis, conjunctivitis, leukocytosis and renal dysfunction (7), hepatobiliary abnormalities (6), mental confusion (6) and coagulopathy (4). In three patients, examination of cerebrospinal fluid showed abnormalities. The illness progressed in three patients to adult respiratory distress syndrome and significant cardiac dysfunction. Staphylococcus aureus was isolated from mucosal sites in six. The disease recurred in two. There were no deaths. Possible transmissibility was illustrated by two patients, a married couple, with simultaneous illnesses. Pathophysiologic features of TSS suggest a toxicogenic cause. Management consists of early recognition, vigorous fluid resuscitation, inotropic support as needed, discontinuation of tampon use and treatment with antistaphylococcal antimicrobic drugs.

Adolescent↗
PubMed1997

[Toxic shock syndrome].

Toxic shock syndrome (TSS) is a rare, life-threatening, acute multisystem illness usually characterized by sudden onset of high fever, diffuse sunburn-like erythroderma and a variety of other signs and symptoms. It may progress rapidly to hypotension and shock with multiple organ failure. Its exact cause is unknown, but in almost all cases there has been an infection with exotoxin-producing strains of phage group I Staphylococcus aureus. Although initially described in association with the use of superabsorbent tampons in menstruation, TSS has complicated a variety of surgical procedures. Recently in head and neck surgery attention has focused on absorbent packing materials, such as those used in postoperative nasal care. TSS developed in a 12-year-old 28 hours after tonsillectomy, nasal septoplasty and inferior turbinectomy in which absorbent packing material was used. It is important to maintain a high index of suspicion for TSS in all postoperative patients with fever, hypotension and erythroderma.

Bandages↗
PubMed1983

Staphylococcal scalded skin syndrome, toxic shock syndrome, and Kawasaki disease.

Three dramatic clinical syndromes have been compared and contrasted. Of these, staphylococcal scalded syndrome is most readily recognized and least likely to have a morbid or fatal outcome. It is easy to confuse toxic shock syndrome and Kawasaki disease. Since the case fatality rate is significant in both of these diseases, and the management so different, proper recognition of the disease by its external features is critical.

Adolescent↗
PubMedDate not supplied

Ecology of toxic shock syndrome: amplification of toxic shock syndrome toxin 1 by materials of medical interest.

Historically, the literature suggests that staphylococcal exoproteins, including enterotoxins, are stimulated by various physicochemical ecologic factors, many of which have been shown to stimulate production of toxic shock syndrome toxin 1 (TSST-1). The propensity of different fibers and other substances to amplify TSST-1 production in toxic shock syndrome-associated strains of Staphylococcus aureus, as well as a comparative analysis of the underlying mechanisms of TSST-1 production, are reported. Two hundred twenty intravaginal devices or other products and materials and 60 experimental controls were examined for their propensity to induce TSST-1 production. Certain materials are superior to unaltered cotton in providing a more absorbent fiber--nutrients are efficiently drawn in, concentrating protein between fibers, and thereby creating an ideal physicochemical environment for the amplification of TSST-1 and other toxins. The greatest stimulation of TSST-1 was observed with (in decreasing order): polyester and carboxymethyl cellulose, polyacrylates, viscose rayon, gelatin foam, polyurethane, and cotton. No toxin was found with nasal tampons (polymer of polyvinyl acetal) or with vaginal cups (an elastomeric polymer). Results are discussed in terms of specific ecologic parameters from historical as well as recent perspectives.

Bacterial Toxins↗
PubMedDate not supplied

Risk of developing toxic shock syndrome associated with toxic shock syndrome toxin 1 following nongenital staphylococcal infection.

Few risk factors for nonmenstrual toxic shock syndrome (TSS) have been identified. This study sought to determine at what rate and under what circumstances nongenital toxigenic Staphylococcus aureus infections led to TSS. Clinical isolates of S. aureus were examined for the production of TSS toxin 1 (TSST-1), and available sera from infected patients were tested for antibody to this toxin. Twenty-six percent of 810 isolates produced TSST-1. Isolates from children were more likely to be positive for TSST-1 than were those from adults. None of 57 patients with TSST-1-positive staphylococcal infection and a TSST-1 antibody titer of greater than or equal to 1:100 developed TSS. Eight of 65 tested patients with TSST-1-positive isolates had antibody below the presumably protective level of 1:100. Two of these patients had definite TSS, three had probable or possible TSS, and three probably did not have TSS. In patients lacking protective antibody to TSST-1, the interval between acquisition and infection with staphylococci, the type and amount of toxins produced, the site of infection, and still-unclarified aspects of host susceptibility may all affect the rate and severity of TSS.

Adult↗
PubMed2003

Effects of total body irradiation and cyclosporin a on the lethality of toxic shock syndrome toxin-1 in a rabbit model of toxic shock syndrome.

Toxic shock syndrome (TSS) may be mediated by superantigen-activated T cells, a theory we tested in rabbits, which are more susceptible to the lethal effects of superantigens, such as TSS toxin-1 (TSST-1), than are mice. Rabbits exposed to 10 cGy of total body irradiation exhibited T cell deficiency, with profound depletion of splenic lymphocytes and circulating CD4(+) lymphocytes, as well as an inability to manifest delayed-type hypersensitivity. Nevertheless, these rabbits remained completely susceptible to TSST-1, indicating that TSS can occur in the setting of marked immunosuppression.

Animals↗