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At least 37 records · Page 2Linked to original sources
PubMed1996

[Prolonged apnea after suxamethonium administration during staphylococcal toxic shock].

A toxic shock syndrome occurred after a femoral nail removal requiring revision surgery. After administration of suxamethonium (1 mg.kg-1), an apnoea prolonged over 45 minutes was observed. The trachea was extubated 105 minutes after suxamethonium administration. For the nail removal, two days before, the anaesthetic had been given by the same anaesthesiologist, with a similar protocol. Apnoea extended over 20 minutes. The day of the revision surgery, plasma cholinesterase activity was 410 UI.L-1 and reached 910 UI.L-1, 9 months later. Dibucaine number was 20 and fluorure number 17. The apnoea was in relation with a genetic plasma cholinesterase deficiency increased by the toxic shock syndrome. Shock and hepatic insufficiency were suspected to contribute to the decrease in plasma cholinesterase. Suxamethonium should be avoided in case of toxic shock syndrome.

Adult↗
PubMed2003

[Special features of intensive care of toxic shock syndrome. Review and case report of a TSST-1 associated toxic-shock syndrome with adult respiratory distress syndrome and multiple organ failure from a staphylococcal panaritium].

Toxic-shock-syndrome (TSS) is an acute febrile, exanthematous illness caused by toxins such as toxic-shock-syndrome-toxine-1 (TSST-1) and other endotoxines from staphylococcus aureus with an incidence of 0,5 per 100.000 inhabitants. Patients with menstrual toxic-shock-syndrome (menstrual-TSS) usually have TSS associated with menstruation and use of a vaginal device such as tampons. Other patients with non-menstrual toxic-shock-syndrome (non-menstrual-TSS) have a focus of staphylococcal infection such as a surgical wound infection or soft tissue abscess. TSS usually presents with fever, pharyngitis, diarrhoea, vomiting, myalgia and may progress rapidly (within hours) to signs of hypovolaemic hypotension and shock. In some cases TSS is associated with multisystem failure including shock, renal failure, myocardial failure and adult respiratory distress syndrome. In its acute phase the diagnosis of TSS is often uncertain because of its initial symptoms are non-specific and numerous conditions need to be considered in the differential diagnosis. But obviously less incidence, the signs and symptoms of toxic-shock-syndrome should be recognised early to permit successful therapy. The site of infection should be adequately drained and treated with antimicrobial therapy. Possible complications including ARDS and myocardial failure require a thorough understanding of its underlying pathophysiology to ensure appropriate intensive-care treatment. Only if appropriate therapy is instituted as early as possible, most of patients will be able to survive their toxic-shock-syndrome. In other cases TSS can be a rapidly progressive and perhaps lethal ending disease because of possible multiple organe failure such as ARDS.

Adolescent↗
PubMed1984

Toxic shock syndrome Staphylococcus aureus: effect of tampons on toxic shock syndrome toxin 1 production.

Tampons were tested for effect on growth and production of toxic shock syndrome toxin 1 by Staphylococcus aureus. Under good growth conditions, regular absorbency tampons had little effect on bacterial growth and inhibited toxin production two- to fourfold. In contrast, higher absorbency tampons had three different effects: 1) some tampons had no effect on bacterial growth but inhibited toxin production; 2) many tampons inhibited both growth and toxin production; 3) one tampon inhibited growth but increased exotoxin per cell. These effects were independent of degree of saturation of the tampons and were observed at incubation times of six, 12, and 18 hours. In no instance was the production of toxic shock syndrome toxin 1 per milliliter increased in the presence of tampons when compared with control.

Absorption↗
PubMed1987

A rabbit model of toxic shock syndrome that uses a constant, subcutaneous infusion of toxic shock syndrome toxin 1.

We have developed a rabbit model of toxic shock syndrome that uses a subcutaneous infusion pump to administer toxic shock syndrome toxin 1 (TSST-1). A dose of 150 micrograms, infused at a constant rate over a period of 7 days, resulted in a characteristic illness highlighted by fever, conjunctival hyperemia, cachexia, and lethargy. The illness was uniformly fatal, with a mean interval until death of 3.2 +/- 0.4 days. Serial determinations of serum chemistries confirmed the multisystem nature of this illness. Rabbits developed profound hypocalcemia, with levels falling from 15.5 +/- 0.2 to 7.6 +/- 0.4 mg/dl under the influence of TSST-1. Blood urea nitrogen and creatinine rose dramatically, in the setting of oliguria or anuria. Serum glutamicpyruvic transaminase was the most reliable indicator of hepatic dysfunction, with the mean rising from 48 U/liter before administration of TSST-1 to 546 U/liter among rabbits surviving 2 days of the infusion. Creatine phosphokinase also rose dramatically in 10 of 16 rabbits. Rabbits demonstrated relative neutrophilia and lymphopenia as well as an increase in the partial thromboplastin time. Histopathologic examination demonstrated disease of multiple organs, particularly the liver, spleen, and lymph nodes, all of which demonstrated inflammation, thrombosis, hemorrhage, and erythrophagocytosis. The concurrent administration of prednisolone with TSST-1 prevented death in four of four rabbits and greatly lessened the morbidity. Rabbits were not protected from morbidity or mortality by the concurrent administration of polymyxin B. We believe that a constant, subcutaneous infusion of TSST-1 in rabbits provides a reproducible model for studying the pathogenesis of TSS.

Adrenal Cortex Hormones↗
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↗
PubMed1993

Toxicity of recombinant toxic shock syndrome toxin 1 and mutant toxins produced by Staphylococcus aureus in a rabbit infection model of toxic shock syndrome.

Menstrually associated toxic shock syndrome (TSS) is attributed primarily to the effects of staphylococcal exotoxin toxic shock syndrome toxin 1 (TSST-1). A region of the 194-amino-acid toxin spanning residues 115 through 144 constitutes a biologically active site. Several point mutations in the TSST-1 gene in that region result in gene products with reduced mitogenic activity for murine T cells. In this study we evaluated the toxicity of recombinant TSST-1 and several mutants of TSST-1 made by transformed Staphylococcus aureus during in vivo growth in a rabbit infection model of TSS. The toxicities of the transformed strains of S. aureus for rabbits correlated with the mitogenic activities of the recombinant toxins. An isolate originally obtained from a patient with a confirmed case of TSS (S. aureus 587) implanted in a subcutaneous chamber served as a positive control. TSST-1 produced in vivo led to lethal shock within 48 h, and a TSST-1-neutralizing antibody (monoclonal antibody 8-5-7) administered to rabbits challenged with S. aureus 587 prevented fatal illness. Rabbits infected with transformed S. aureus RN4220 expressing wild-type toxin (p17) or mutant toxins retaining mitogenic activity for T cells succumbed within a similar time frame. Blood chemistries of samples obtained from infected animals before death indicated abnormalities in renal and hepatic functions similar to those induced by parenteral injection of purified staphylococcal TSST-1. Mutant toxin 135 (histidine modified to alanine at residue 135) possessed only 5 to 10% of the mitogenic activity of wild-type toxin. Rabbits challenged with transformed S. aureus RN4220 expressing mutant toxin 135 exhibited only mild transient illness. Mutant toxin 135 retained reactivity with monoclonal antibody 8-5-7 and by several criteria was conformationally intact. Toxin from a double mutant, 141.144, with alanine substitutions at residues 141 (histidine) and 144 (tyrosine), also was devoid of mitogenic activity. In this case, antibody recognition was lost. Mutant toxins 115 and 141 were found to possess approximately half-maximal mitogenic activity. Rabbits challenged with S. aureus RN4220 expressing either 115 or 141 toxin succumbed to lethal shock. We conclude that the ability of TSST-1 to activate murine T cells in vitro and its expression of toxicity leading to lethal shock in rabbits are related phenomena.

Animals↗
PubMed1986

Imbalanced serum IgG subclass pattern in toxic shock syndrome patients: deficiency of specific IgG1 and IgG4 subclass antibodies to toxic shock syndrome toxin 1.

An imbalanced serum IgG subclass pattern was identified in 10 patients with toxic shock syndrome (TSS) showing remarkably low subclass levels of various combinations. IgG2 levels were significantly reduced as compared to normal controls. The IgG subclass-specificity of antibodies to toxic shock syndrome toxin (TSST-1) was investigated by a solid-phase radioimmunoassay. TSS-patients lacked pre-immunity to TSST-1 in all four IgG subclasses. Normally acquired immunity to the toxin as well as the serological response developing in two patients with TSS was generally restricted to IgG1 and IgG4. A strong booster response of all four IgG subclasses was seen in three patients with S. aureus septicaemia due to TSST-1 producing strains. The lack of specific IgG1 and IgG4 antibodies to TSST-1 and the low serum IgG subclass levels found in the TSS-patients could be of pathogenetic significance and help to explain the susceptibility to TSS in certain individuals.

Acute Disease↗
PubMed1989

Toxic shock syndrome caused by a strain of Staphylococcus aureus that produces enterotoxin C but not toxic shock syndrome toxin-1.

An 8-month-old infant presented with pneumonia and pleural effusion associated with clinical manifestation of toxic shock syndrome. A Staphylococcus aureus strain isolated from the pleural fluid produced enterotoxin C, but not toxic shock syndrome toxin-1 or other enterotoxins. Acute and convalescent sera showed an antibody rise to enterotoxin C but not to toxic shock syndrome toxin-1. These findings support the possibility that enterotoxin C was the primary toxin associated with this infant's illness.

Bacterial Toxins↗
PubMed1999

Staphylococcus aureus isogenic mutant, deficient in toxic shock syndrome toxin-1 but not staphylococcal enterotoxin A production, exhibits attenuated virulence in a tampon-associated vaginal infection model of toxic shock syndrome.

Since menstrual toxic shock syndrome (MTSS) is associated with a predominant clone of Staphylococcus aureus which produces both toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin A (SEA), we sought to clarify the role of TSST-1 in a tampon-associated vaginal infection model in New Zealand White (NZW) rabbits, using isogenic tst+/sea+ S. aureus mutants in which tst was inactivated by allelic replacement. Rabbits infected with the tst-/sea+ strain became ill within 3 days, with fever, weight loss, conjunctival hyperemia, and lethargy. Mortality was significantly higher with the tst+/sea+ strain compared to its tst-/sea+ isogenic derivative (4/13 vs. 0/14; p < 0.05, Fisher's exact test, 2-tailed). Mean fever index was higher (p < 0.005; t test, 2-tailed) and weight loss more sustained among survivors in the tst+/sea+ group. Furthermore, culture filtrates from the tst+/sea+ strain induced a significantly greater response in mitogenesis and TNF alpha secretion from rabbit splenocytes in vitro compared to the tst-/sea+ isogenic derivative. Thus, regardless of the role of SEA, TSST-1 significantly contributed to both morbidity and mortality in this tampon-associated vaginal infection model in NZW rabbits. This is the first demonstration of the potential role of TSST-1 and SEA in the pathogenesis of MTSS with a MTSS-associated clinical S. aureus strain in a relevant animal model.

Animals↗
PubMed1986

Non-menstrual toxic shock syndrome. A case report and a review of non-menstrual toxic shock syndrome in Western Europe.

Having been confronted with a post-operative toxic shock syndrome, we made a study of European literature and were struck by the more favorable course the disease promptly took when penicillinase-resistant antibiotics were used. We suggest that a new case, based on bacteriological analysis and phagotyping of the offending organism and wound appearance, was prevented by us when immediate antibiotic treatment was given.

Adult↗
PubMedDate not supplied

Passive protection of rabbits infected with toxic shock syndrome-associated strains of Staphylococcus aureus by monoclonal antibody to toxic shock syndrome toxin 1.

The effectiveness of passive immunization was assessed in an infection model of toxic shock syndrome (TSS) in which monoclonal antibody to TSS toxin 1 (TSST-1) was administered intravenously to rabbits. Previously implanted infection chambers were inoculated with Staphylococcus aureus strains RN4710 and D4508. The former strain carries the TSST-1 gene on plasmid pRN6201; the latter is a TSST-1-negative clinical isolate obtained from a patient with nonmenstrual TSS. Purified monoclonal antibody, MAb 8-5-7 (IgG), was administered in two doses of approximately 1.25 mg each 24 hours before and 24 hours after infection. MAb 8-5-7 provided complete protection against both the TSS-like syndrome and the mortality that occurred in unprotected rabbits infected with strain RN4710 but did not provide complete protection in rabbits infected with strain D4508; three of the five rabbits either displayed signs of illness or died despite treatment. Western-blot analyses of the extracellular proteins produced by strains RN4710 and D4508 that used MAb 8-5-7 as a probe revealed that only TSST-1 produced by RN4710 reacted with the antibody. Thus, if MAb 8-5-7 partially protected animals against infections with strain D4508, the protection appears to have been nonspecific.

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↗