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PubMed1996

Delayed toxic shock syndrome after functional endonasal sinus surgery.

Toxic shock syndrome (TSS) is an uncommon, severe, multisystem illness that may follow any surgical procedure. It usually occurs in the immediate postoperative period and is manifested by the sudden onset of a high fever and a variety of other signs and symptoms. The reported incidence of TSS after nasal surgery is 16 cases per 100,000 patients. We report five unusual cases of delayed TSS that occurred after functional endonasal sinus surgery in which no packing was used. Toxic shock syndrome developed in three children and two adults 5 days to 5 weeks postoperatively. All patients were treated successfully with no sequelae. The pathophysiologic features, clinical manifestations, and treatment of TSS are described in detail.

Adult↗

PubMedDate not supplied

Toxic shock syndrome: an opportunity for nursing intervention.

Toxic Shock Syndrome (TSS) is a potentially fatal illness caused by a particular strain of Staphylococcus aureus. The clinical presentation is similar to that of septic shock. The incidence of TSS peaked in the late 1970s and early 1980s, probably as a result of availability of super absorbent tampons. Although most commonly associated with menstruation, the overall incidence of menstrual and nonmenstrual TSS in men and women ranges from 1 to 3 per 100,000. There are almost equal numbers of menstrual and nonmenstrual cases of TSS identified annually. S aureus, the causative microorganism in cases of TSS, has been isolated from many body tissues. Toxic shock syndrome presents as a flu-like illness with high fever, vomiting, diarrhea, general malaise, and muscle weakness. Nursing and medical management focus on controlling or preventing potentially serious complications, such as adult respiratory distress syndrome, renal failure, electrolyte imbalances, disseminated intravascular coagulation, encephalopathy, and cardiomyopathy. Judicious use of tampons and barrier contraceptive devices may decrease the risk of developing TSS.

Adult↗

PubMedDate not supplied

Toxic shock syndrome occurring in children with abrasive injuries beneath casts.

Staphylococcal toxic shock syndrome has been reported in a number of nonmenstrual settings, including orthopedic patients with postoperative staphylococcal wound infections. We describe two cases of toxic shock syndrome in children with focal cutaneous staphylococcal infections occurring beneath casts placed for limb immobilization. These cases illustrate a new and potentially hidden site of staphylococcal infection leading to toxic shock syndrome.

Adolescent↗

PubMed1984

Toxicity of staphylococcal toxic shock syndrome toxin 1 in rabbits.

Strains of Staphylococcus aureus associated with toxic shock syndrome produce toxic shock syndrome toxin 1 (TSST 1), which is lethal to conventional rabbits and acts synergistically with gram-negative lipopolysaccharide. The lethal effect of TSST 1 was examined in specific-pathogen-free rabbits on the basis that these rabbits, being less colonized by gram-negative bacteria, would be less susceptible than conventional animals. Although there was no significant difference in mortality between specific-pathogen-free and conventional rabbits in response to 100 micrograms of TSST 1, there was a difference in response between Dutch belted rabbits and New Zealand white rabbits. Both specific-pathogen-free and conventional New Zealand white rabbits were more susceptible to TSST 1 than the Dutch belted strain. Pretreatment of conventional New Zealand white rabbits with polymyxin B neutralized the lethal effect of TSST 1.

Animals↗

PubMed1985

Effect of toxic shock syndrome toxin 1 on chicken embryos.

Staphylococcus aureus strains associated with toxic shock syndrome produce toxic shock syndrome toxin 1 (TSST1). This toxin has a variety of biological effects, including enhanced lethality in rabbits in the presence of sublethal amounts of lipopolysaccharide (LPS). Because chicken embryos are highly susceptible to LPS, the synergistic effect of TSST1 and LPS was examined in this system. Although TSST1 per se had no effect on chicken embryos, it potentiated the lethal effect of LPS. The 50% lethal dose of LPS was greatly reduced in the presence of up to 10 micrograms of TSST1 per ml. However, at high doses of TSST1 (greater than 100 micrograms/ml), no enhanced lethality was observed. The lowest dose of TSST1 tested which potentiated lethality was 10 ng/ml.

Animals↗

PubMed1993

Toxic shock syndrome. Are you recognizing its changing presentations?

Nonmenstrual cases of toxic shock syndrome now occur at least as often as the classic menstrual cases. The syndrome has been reported in every conceivable clinical setting involving colonization or infection with Staphylococcus aureus and as a complication of surgical procedures, traumatic injuries, and local infections. Unusual clinical manifestations have been observed in patients with AIDS. Cases of toxic shock syndrome also have been linked to infection with toxin-producing strains of coagulase-negative staphylococci and group A streptococci. Knowledge of the expanding spectrum of toxic shock syndrome and early consideration of the disease in patients with fever, hypotension, rash, and/or multisystem disease are essential for timely diagnosis and optimum management.

Acquired Immunodeficiency Syndrome↗

PubMed1984

Toxic shock syndrome in children aged 10 years or less.

Eight children aged 10 years or less had toxic shock syndrome, and medical records were reviewed for seven of them. There were four boys and three girls, ranging in age from 5 5/12 to 10 8/12 years; all seven met the Centers for Disease Control case definition of toxic shock syndrome. One boy died. The illness was generally characterized by fever, followed by erythroderma, gastrointestinal complaints, and mucous membrane hyperemia. Based on the need for supplemental oxygen or mechanical ventilation, the girls tended to have milder courses than the boys. In four of four cultures performed prior to the institution of antibiotic therapy. Staphylococcus aureus grew from one or more sites. One boy also met the case definition of Kawasaki syndrome and has had multiple coronary artery aneurysms demonstrated in early and late follow-up. Toxic shock syndrome in these children was similar to published descriptions of toxic shock syndrome in series of adult patients, except that, as a group, the children had a greater incidence of respiratory embarrassment.

Age Factors↗

PubMed1982

Toxic shock syndrome associated with surgical wound infections.

In 13 cases of toxic shock syndrome (TSS) associated with postoperative wound infections, clinical findings were similar to those observed in cases of TSS in menstruating women. While local signs of a surgical wounds infection were minimal, Staphylococcus aureus was recovered from cultures of wounds in 12 of 12 patients; multiple blood cultures were negative for 11 of 11 patients. Toxic shock syndrome due to surgical wound infections accompanied a wide variety of surgical procedures in both men and women and was not necessarily associated with menstruation in women. The median interval between surgery and onset of TSS was two days. Toxic shock syndrome can develop in association with surgical wound infections caused by S aureus and should be considered in the differential diagnosis of postoperative fever and hypotension.

Adolescent↗

PubMed1984

Enhanced susceptibility of male rabbits to infection with a toxic shock strain of Staphylococcus aureus.

Artificial infection chambers in rabbits were infected with a toxic shock strain of Staphylococcus aureus in an attempt to determine the nature of the enhanced virulence of toxic shock strains relative to non-toxic shock strains of staphylococci. The results showed that rabbits immunized with either neutral or acidic proteins were protected from the lethal effects of these infections. Male rabbits were found to be significantly more susceptible to these infections than female rabbits. Castration rendered both sexes equally susceptible to lethal infections. Numerous tissues from all infected rabbits were examined histologically, and most of the pathological findings involved lymphoid tissue. Of special interest was the observation that unprotected male rabbits which died had evidence of lymphoid depletion and that surviving rabbits, both male and female, usually manifested lymphoid hyperplasia. No other pathological response was noted which would characterize these infections, but immunized rabbits had a diminished level of thymic cortex involution that was not different between the sexes.

Animals↗

PubMed1982

Toxic shock syndrome: management and long-term sequelae.

Little information is available on the optimal management of toxic shock syndrome and on its sequelae. The most appropriate antibiotic treatment, the efficacy of colloid infusions, and the potential role of gamma globulin preparations have not yet been completely ascertained. Coagulase-positive staphylococci associated with toxic shock syndrome had minimal inhibitory concentrations of 0.06 microgram/mL or less to rifampin, 0.25 microgram/mL or less to gentamicin, and 0.50 microgram/mL or less to both nafcillin and clindamycin. In the 36 patients studied abnormal chest roentgenograms were commoner in those who had received albumin than in those who had not. Radioimmunoassay showed antibody titers to staphylococcal enterotoxin F, a marker protein in toxic shock syndrome, of 1:4000 or more for intravenous gamma globulin (12/15 lots) and 1:40 000 or more for intramuscular gamma globulin. Major sequelae of toxic shock syndrome include late-onset rash, compromised renal function, cyanotic extremities, and prolonged neuromuscular abnormalities.

Adolescent↗

PubMed1999

Involvement of enterotoxins G and I in staphylococcal toxic shock syndrome and staphylococcal scarlet fever.

We investigated the involvement of the recently described staphylococcal enterotoxins G and I in toxic shock syndrome. We reexamined Staphylococcus aureus strains isolated from patients with menstrual and nonmenstrual toxic shock syndrome (nine cases) or staphylococcal scarlet fever (three cases). These strains were selected because they produced none of the toxins known to be involved in these syndromes (toxic shock syndrome toxin 1 and enterotoxins A, B, C, and D), enterotoxin E or H, or exfoliative toxin A or B, despite the fact that superantigenic toxins were detected in a CD69-specific flow cytometry assay measuring T-cell activation. Sets of primers specific to the enterotoxin G and I genes (seg and sei, respectively) were designed and used for PCR amplification. All of the strains were positive for seg and sei. Sequence analysis confirmed that the PCR products, corresponded to the target genes. We suggest that staphylococcal enterotoxins G and I may be capable of causing human staphylococcal toxic shock syndrome and staphylococcal scarlet fever.

Enterotoxins↗

PubMed1988

Postpartum toxic shock syndrome: a report of a case.

We describe a case of a 29-year-old Japanese woman with toxic shock syndrome which occurred 6 days after a normal vaginal delivery. This is the second case of postpartum toxic shock syndrome in Japan, so far as we know. Staphylococcus aureus was isolated from the uterine cavity. The isolate was coagulase type II and it produced both enterotoxin C and toxic shock syndrome toxin-1. The clinical course and laboratory data for this patient were in conformance with previously reported typical postpartum toxic shock syndrome, except for the onset time after delivery, because the previously reported postpartum TSS cases were clearly divided into two groups, early onset within 3 days of delivery and late onset 2 or more weeks after delivery.

Adult↗

PubMed1992

[Toxic shock syndrome after Cesarean section].

A case of toxic shock syndrome (TSS) after caesarean section is reported. Strains Staphylococcus aureus (phage type 80/42E/81/83A--mixed type) producing toxic shock syndrome toxin-1 in very great grantities amounts were isolated from the surgical wound. The diagnosis is often difficult in non-menstrual cases in which TSS is not expected.

Adult↗

PubMed1986

A hospital discharge code review of toxic shock syndrome in Wisconsin.

The Wisconsin Division of Health conducted a review of discharge coding for 142 (97%) of the state's general care hospitals for the period 1980-1983 to evaluate the use of International Classification of Diseases codes for toxic shock syndrome and to estimate completeness of reporting of recognized hospitalized cases of the syndrome to the Division of Health. Hospital use of code 040.89 (other bacterial diseases-other) recommended for toxic shock syndrome by the National Center for Health Statistics in January 1981 increased from 23% of Wisconsin hospitals in 1980 to 92% in 1983. The sensitivity of this code for toxic shock syndrome increased from 54% to 85% from 1981 to 1983; study population specificity was stable at approximately 95%, and the predictive value was 65% in 1981 and 70% in 1983. The use of codes 785.50 (shock, unspecified) and 785.59 (nontraumatic shock-other) frequently assigned to toxic shock syndrome was also assessed; all measures of their utility decreased in proportion to the increasing use of 040.89. The coding review identified 20 previously unreported cases of toxic shock syndrome; the 10 confirmed and 10 probable cases represent 4% and 21% of the state's 223 confirmed and 47 probable cases with onsets in 1980-1983. Results indicate that a National Center for Health Statistics coding recommendation for a disease of emerging significance can result in relatively uniform coding of the illness, which can provide a tool for case finding and surveillance evaluation for hospitalized cases.

Adolescent↗

PubMed1987

Toxic shock syndrome after chemical face peel.

Two cases of toxic shock syndrome following chemical face peel are reported. Toxic shock syndrome is a severe toxin-mediated multisystem disease. The major signs are fever, rash, desquamation, and hypotension. It can occur in males as well as females and is not necessarily related to menstruation. The surgical wound does not usually appear infected. Early recognition is the hallmark of successful treatment. Therapy is symptomatic, with aggressive administration of fluids. Antistaphylococcal agents are used. Prophylactic antibiotics are not necessarily recommended.

Chemexfoliation↗

PubMed1996

T-cell activation and proliferation in a case of recurrent menstrual toxic shock syndrome.

A case of menses-related toxic shock syndrome with a relapse within 9 days is presented. Cervical smear of the patient yielded growth of a Staphylococcus aureus strain which produced toxic shock syndrome toxin-1 (TSST-1). Serum antibody against TSST-1 were absent in the first sample which was obtained in the acute phase and did not increase significantly within 5 weeks. We studied the proliferative response of the patient's T cells during and after the acute phase of disease to evaluate whether they have been rendered unresponsive to TSST-1. We could not detect any reduction in the T cell proliferation at any time. Peripheral T cells of the patient were analysed flow-cytometrically at two different times to determine the expression of the T cell activity markers CD25 and HLA-DR. The expression of HLA-DR was increased during the acute phase and had declined significantly at the time of the second analysis; the CD25 expression remained constant.

Adolescent↗

PubMed1987

[IgG antibodies to toxic shock syndrome toxin-1 (TSST-1) in human sera].

IgG antibodies against toxic shock syndrome toxin-1 (TSST-1) in 2002 human sera were determined using an enzyme-linked immunosorbent assay. The results indicate a very early common exposure to TSST-1 in German males and females. The antibody titers are increasing up to the age of 20. They continue to increase further from the mid-thirties, reaching a peak level in the mid-fifties. Toxic shock syndrome is rarely described in Germany. It is possible, therefore, that most of the infections with TSST-1 producing S. aureus are of a subclinical nature. An atypical, less dramatic course than the commonly known toxic shock syndrome is also discussed.

Adolescent↗

PubMed1996

Crystal structure of a biologically inactive mutant of toxic shock syndrome toxin-1 at 2.5 A resolution.

Toxic shock syndrome toxin-1 (TSST-1) is one of a family of staphylococcal exotoxins recognized as microbial superantigens. The toxin plays a dominant role in the genesis of toxic shock in humans through a massive activation of the immune system. This potentially lethal illness occurs as a result of the interaction of TSST-1 with a significant proportion of the T-cell repertoire. TSST-1, like other superantigens, can bind directly to class II major histocompatibility (MHC class II) molecules prior to its interaction with entire families of V beta chains of the T-cell receptor (TCR). The three-dimensional structure of a mutant (His-135-Ala) TSST-1 was compared with the structure of the native (wild-type) TSST-1 at 2.5 A resolution. The replacement of His 135 of TSST-1 with an Ala residue results in the loss of T-cell mitogenicity and toxicity in experimental animals. This residue, postulated to be directly involved in the toxin-TCR interactions, is located on the major helix alpha 2, which forms the backbone of the molecule and is exposed to the solvent. In the molecular structure of the mutant toxin, the helix alpha 2 remains unaltered, but the His to Ala modification causes perturbations on the neighboring helix alpha 1 by disrupting helix-helix interactions. Thus, the effects on TCR binding of the His 135 residue could actually be mediated, wholly or in part, by the alpha 1 helix.

Bacterial Toxins↗