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Gram-negative endotoxins and staphylococcal toxic shock syndrome.

Strains of Staphylococcus aureus isolated from toxic shock syndrome (TSS) produce toxic shock syndrome toxin 1 (TSST1) which causes a shock-like illness in rabbits with many features similar to TSS in humans. TSST1 is lethal per se in rabbits and also acts synergistically with endotoxin to potentiate lethality. The mode of action of TSST1 is as yet unknown; it has been suggested that it may act by inhibiting the reticuloendothelial system thus allowing endotoxic shock to occur. Rabbits pretreated with polymyxin-B, which prevents the effect of endotoxin, were found to be protected from death by TSST1 indicating that endotoxin is indeed implicated in the pathogenesis of TSS. Specific pathogen-free rabbits which presumably have negligible levels of circulating LPS were susceptible to TSST1 suggesting that very small amounts of endotoxin are sufficient to potentiate lethality. The ways in which TSST1 may allow shock to occur is discussed.

Animals↗

Survey of tampon use and toxic shock syndrome, Tennessee, 1979 to 1981.

Thirty-eight cases of toxic shock syndrome were reported in Tennessee between January 1, 1979, and March 31, 1981. Thirty-one of these cases (82%) occurred in white women less than 30 years of age; none occurred in black women. We suspected that age and racial differences in tampon use could contribute to the relatively high risk of toxic shock syndrome in young white women. In March, 1981, we surveyed 1,136 Tennessee women regarding their past and current used of tampons. Age and race were related, not only to whether or not tampons were used but to the way tampons were used. "Continuous" tampon use during the most recent menstrual period was most common among young white women (61%), less common among older white women (42%), and least common among black women (23%). On the other hand, the brands, absorbency types, numbers, and usage patterns did not vary greatly with respect to age or race. Comparing each woman's tampon habits in March, 1981, with her usual habits in June, 1980, suggested a striking effect of publicity about the toxic shock syndrome. We estimate that 23% to 39% of the women surveyed changed their tampon habits in an attempt to reduce their risk of toxic shock syndrome.

Adolescent↗

Streptococcal toxic shock syndrome after breast reconstruction.

Streptococcal toxic shock syndrome (STSS) is an increasingly common disease entity but has rarely been described in the plastic surgery literature. We present the first known case of STSS associated with a reconstructive procedure. Two weeks postoperatively from a transverse rectus abdominis musculocutaneous flap for breast reconstruction, our patient presented with flulike symptoms and progressed rapidly to multiorgan failure. Though initially no nidus for infection was evident, the abdominal donor site was surgically debrided and found to contain group A Streptococcus. Following aggressive rehydration and antibiotic therapy, the patient gradually made a full recovery. In this case report, we review the presentation and epidemiology of STSS and compare it to the more common staphylococcal toxic shock syndrome. In addition, we discuss the management and outcomes of STSS, with an emphasis on raising clinical suspicion for this rare but dangerous entity.

Adult↗

Toxic shock syndrome in the burned patient.

Toxic shock syndrome (TSS) has gained notoriety because of its association with tampon use. However, there is an increasing awareness of the syndrome on many of the specialised burn units in hospitals through the United Kingdom. TSS primarily affects children with small-percentage burns, and it is this group of patients that normally would be expected to make an uneventful recovery. One unit, where 100-150 children are admitted per year, has seen four cases of confirmed TSS over a two-year period. There does not appear to be the same risk of TSS in adult burned patients, and this lower incidence may be the result of an increase in the production of antibodies to toxic shock toxins with increase in age.

Burns↗

The human immunodeficiency virus and nonmenstrual toxic shock syndrome: a female case presentation.

Toxic shock syndrome (TSS) generally is associated with tampon use among menstruating women. Descriptions from the early 1980's detailed this sudden, multisystem, frequently fatal disease. The bacterial agent, Staphylococcus aureus produced exotoxins, which were quickly identified as the cause of TSS as well as a host of other systemic, bacterial infections. While S. aureus has become one of the more common bacterial pathogens in patients with Acquired Immune Deficiency Syndrome (AIDS), staphylococcal toxin-related disorders rarely have been reported in individuals infected with Human Immunodeficiency Virus (HIV) or individuals diagnosed with AIDS. To date all published cases of TSS attendant with HIV involved homosexual, hemophiliac, or drug injecting male patients. This report describes a woman infected with HIV and diagnosed with the classic array of symptoms found in toxic-shock syndrome, and provides information specific to women and their experience with HIV infection.

AIDS-Related Opportunistic Infections↗

Toxic shock syndrome after pilonidal cystectomy. Report of a case.

Toxic shock syndrome is an uncommon disease associated with staphylococcal infections. Although most frequently reported in menstruating women and associated with tampon use, toxic shock syndrome has been described following many types of surgical procedures. In this report we describe a case of toxic shock syndrome occurring in a previously healthy young man after elective surgery for a pilonidal cyst.

Adult↗

Treatment of toxic shock syndrome with endotoxin-neutralizing antibody.

The enhancement of host susceptibility to endotoxin (lipopolysaccharide, LPS) by toxic shock syndrome toxin-1 (TSST-1) is an important mechanism in the pathogenesis of toxic shock syndrome. In these studies, we sought to determine whether an endotoxin-neutralizing monoclonal antibody could be useful in the treatment of toxic shock syndrome. We isolated a murine monoclonal hybridoma (3-H3) which secreted monoclonal antibody (mAb) specific for Escherichia coli 0111:B4 LPS. Spleen cells cocultured with E. coli 0111:B4 LPS demonstrated up to a 60% decrease in mitogenic activity in the presence of 3-H3 mAb, but not control mAb, demonstrating that this antibody neutralized endotoxin in vitro. Rabbits pretreated with 3-H3 mAb or control mAb were injected intradermally with E. coli 0111:B4 LPS. One day later rabbits received E. coli 0111:B4 LPS intravenously to elicit the dermal Shwartzman reaction. Rabbits pretreated with 3-H3 mAb did not develop this reaction (0/6) compared to animals pretreated with control mAb (5/6), demonstrating that this antibody neutralized endotoxin in vivo (P less than 0.05). When this antibody was evaluated in a rabbit model of lethal toxic shock syndrome, rabbits pretreated with antibody demonstrated greater survival (8/14) than saline control animals (1/10) after challenge with TSST-1 and E. coli 0111:B4 LPS (P less than 0.05). Since the suspicion exists that low levels of endogenous LPS may potentiate TSST-1 activity during clinical toxic shock syndrome, we hypothesized that endotoxin-neutralizing antibodies could be useful in the treatment of this lethal disease process.

Animals↗

Toxic shock syndrome in scalded children.

Five patients showing clinical signs resembling the 'toxic shock syndrome' presented over a 4-month period at the Wessex Regional Burns Centre. Toxin-producing isolates of Staphylococcus aureus were made from wound swabs in four of the five patients. Four different phage types producing four different toxins were observed. Seven other patients yielded staphylococci from wound swabs but did not develop the toxic shock syndrome. In three of these latter patients the staphylococcus isolated was toxin producing. Since the syndrome carries a significant mortality risk it is desirable that it is recognized and treated without delay. To this end a simplified set of criteria for the identification of probable toxic shock syndrome cases is proposed. The observations suggest that toxic shock syndrome is more common than previously supposed. The syndrome may show a broad spectrum in its clinical presentation, and involve a wide range of staphylococcal phage types with possible involvement of several different enterotoxins.

Body Surface Area↗

Molecular topography of toxic shock syndrome toxin 1 as revealed by spectroscopic studies.

Molecular characterization of toxic shock syndrome toxin 1 has been carried out and compared with a group of functionally related staphylococcal enterotoxins. The secondary structure analysis of the far-UV circular dichroic spectrum of toxic shock syndrome toxin 1 revealed 6.25% alpha-helix, 51.25% beta-pleated sheets, 9.0% beta-turns, and 33.5% random coils. The pattern, in general, was similar to the staphylococcal enterotoxins. Four antigenic sites have been predicted for toxic shock syndrome toxin 1 by using the secondary structure information in combination with the hydrophilicity calculation. The location of the antigenic sites, in general, agrees with the experimental results. Topographical analysis of the tyrosine residues as determined by second-derivative UV spectroscopy [Ragone, R., Colonna, G., Balestrieri, C., Servillo, L., & Irace, G. (1984) Biochemistry 23, 1871-1875] showed that six of nine tyrosine residues are exposed to aqueous solvent. Tryptophan fluorescence quenching studies with an anionic surface quencher, I-, and a neutral quencher, acrylamide, revealed that almost all of the tryptophan residues are buried in the protein matrix as their accessibility to the surface quencher is very low (17%). Since there are only three tryptophan residues in the amino acid sequence of the toxic shock syndrome toxin 1 and there is a tyrosine residue (Tyr-15, Tyr-115, and Tyr-153) next to each of the tryptophan residues (Trp-14, Trp-116, and Trp-154), it appears the tyrosine residues not exposed to the aqueous solvent are those next to the tryptophan residues. Functional implications of the topography of the tryptophan and tyrosine residues are assessed.

Bacterial Toxins↗

Nonmenstrual toxic shock syndrome: a review of 130 cases.

One hundred and thirty cases of toxic shock syndrome not associated with menstruation have been reported to the Centers for Disease Control, including 57 with onset in 1981 (12% of reported cases in 1981). These cases show that the syndrome occurs in a wide range of clinical settings and is associated with Staphylococcus aureus infections at a variety of sites: focal cutaneous and subcutaneous lesions, surgical-wound infections, postpartum infections, adenitis, bursitis, deep abscesses, and "primary" bacteremia. Although the clinical characteristics of nonmenstrual toxic shock syndrome are identical to those for menstrual toxic shock syndrome, the epidemiologic and demographic features are different. Of particular interest is the contrast in the racial distribution of the menstrual and nonmenstrual cases. Toxic shock syndrome can occur in persons of any age, race, or sex and must be considered in the differential diagnosis for any patient with a compatible illness.

Adolescent↗

Toxic shock syndrome in two CAPD patients with Staphylococcus aureus exit-site infection.

Toxic shock syndrome (TSS) is an illness defined by the occurrence of fever, rash, hypotension, multiple organ system dysfunction, and desquamation. Nonmenstrual TSS is often associated with surgical or nonsurgical cutaneous infections, which are rarely purulent or inflamed (Reingold AL, et al. Nonmenstrual toxic shock syndrome: a review of 130 cases. Ann Intern Med 1982; 96:871-4). Toxic shock syndrome associated with peritoneal exit-site infection but without peritonitis is extremely unusual (Sherbotie JR, et al. Toxic shock syndrome with Staphylococcus aureus exit-site infection in a patient on peritoneal dialysis. Am J Kidney Dis 1990; 15:80-3). We describe 2 patients that met the Centers for Disease Control case definition of TSS secondary to a peritoneal dialysis catheter exit-site infection with signs of mild inflammation and growth of Staphylococcus aureus, but with no evidence of peritonitis.

Adult↗

Toxic shock syndrome in Canada.

Fifty-three cases of toxic shock syndrome were reported in Canada from 1976 to 31 October 1981. Three of the 50 women with this syndrome died. Thirty-seven cases were associated with menstruation and all but one of these cases were in tampon users. Staphylococcus aureus has been isolated from eight patients, and enterotoxin was found in seven. The Canadian government has asked tampon manufacturers to print a warning statement on tampon boxes and to include a package insert informing users about toxic shock syndrome. Generally, the incidence of communicable disease in Canada is one tenth that of the United States, reflecting the population differential of 1:10 between the two countries. This ratio has not been found with respect to toxic shock syndrome.

Adolescent↗

Selective expansion of T cells expressing V beta 2 in toxic shock syndrome.

Infection with Staphylococcus aureus and the production of toxic shock syndrome toxin-1 (TSST-1) have been implicated in the pathogenesis of toxic shock syndrome. Previous in vitro studies have demonstrated that TSST-1 is a powerful but selective stimulator of human T cells, and that the majority of activated cells express the TCR V beta 2 gene segment. We therefore studied patients with toxic shock syndrome using a modification of the PCR to determine if expansion of V beta 2+ T cells is a marker of the in vivo disease process. Five of eight patients studied demonstrated markedly elevated levels of circulating V beta 2+ T cells, whereas none showed significantly elevated levels of T cells expressing other V beta gene segments. The results suggest that toxin-mediated T cell activation, which involves a large fraction of the human T cell repertoire, may be critical in the pathogenesis of this disease.

Antigens, CD↗

Knowledge of toxic shock syndrome among adolescent females: a need for education.

Toxic shock syndrome (TSS) has been identified as a potentially fatal but preventable illness that causes disease, disability, and premature death, especially among adolescent females using high absorbency tampons. In 1983 the authors surveyed 129 high school girls in three midwestern senior high schools to determine the relationship between choice of a menstrual product and knowledge about toxic shock syndrome. The study found that the knowledge level of adolescent females about TSS was fragmented and inaccurate. No significant relationship was found between choice of a menstrual product and knowledge about TSS; very little variation existed between the scores for napkin users, regular tampon users, and high absorbency tampon users. Results of the study are discussed in terms of the implications for the health of adolescent females. Recommendations are offered for utilizing health professionals, parents, and the news media in the development of toxic shock education programs.

Adolescent↗

Toxic shock syndrome, contraceptive methods, and vaginitis.

To elucidate further the etiology of toxic shock syndrome, we assessed the effects of certain contraceptive methods and recent history of vaginal infection on the incidence of toxic shock syndrome, with confounding effects of other risk factors controlled. We found a strong but imprecise positive association between toxic shock syndrome and tubal ligation (rate ratio = 7.9, 90% confidence interval 1.4 to 42.7). We also observed a negative association with oral contraceptives (rate ratio = 0.49, 90% confidence interval 0.22 to 1.1) and a positive association with a recent history of vaginitis (rate ratio = 2.1, 90% confidence interval 1.2 to 3.9).

Contraceptive Devices, Female↗

[Correlation in Staphylococcus aureus infections between toxic shock syndrome toxin-1 production and clinical feature].

Toxic shock syndrome (TSS) is caussed by toxic shock syndrome toxin-1 (TSST-1) of Staphylococcus aureus. We studied the incidence of TSST-1 production by the clinical isolates of S. aureus, in order to clarify the possibility of TSS caused by S. aureus. One hundred and seventeen clinical isolates of S. aureus were tested. Of 117 strains, 74 were methicillin-cephem resistant S. aureus (MRSA), and 43 were methicillin-cephem sensitive S. aureus (MSSA). TSST-1 production and penicillinase (PCase) activity were measured by means of reversed passive Latex aggulutination method and acidmetric assay, respectively. The incidences of TSST-1 production by PCase positive MRSA, PCase negative MRSA, PCase positive MSSA and PCase negative MSSA were 92% (55/60), 78% (11/14), 21% (7/33) and 0% (0/10), respectively. TSS occurred in a patient with chronic complicated pyelonephritis after endopyelotomy for hydronephrosis. In this patient, PCase positive MRSA which produced TSST-1 was isolated from urinary tract, and he was cured after administration of arbekacin. These results indicsate that methicillin-cephem resistance and PCase production are the risk factors for TSST-1 production in S. aureus.

Bacterial Toxins↗