Toxic Shock Syndrome: Management and Long-Term Sequelae

Chesney, P. Joan; Crass, Barbara A.; Polyak, Marcia B.; Wand, Philip J.; Warner, Thomas F.; Vergeront, James M.; Davis, Jeffrey P.; Tofte, Robert W.; Chesney, Russell W.; Bergdoll, Merlin S.

doi:10.1016/s0022-5347(17)53522-3

Cited by 5 publications

(10 citation statements)

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“…Only two records, but it was mentioned in at least five of the 17 cases of staphylococcal scarlet fever (data not shown). strains of the 43 isolates associated with these syndromes produced additional toxins other than exfoliatins; one strain Classically, the erythroderma associated with TSS most often involves flushing of the skin and not the fine papular scarlatiniwas shown to concomitantly produce ETA and enterotoxin SEA, while another was shown to produce both TSST-1 and form rash associated with streptococcal or staphylococcal scarlet fever [17,20,36]. However, we were unable to make any ETA.…”

Section: Methodsmentioning

confidence: 91%

Toxin Involvement in Staphylococcal Scalded Skin Syndrome

et al. 1997

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Staphylococcus aureus strains isolated from children with scalded skin syndrome (15 with generalized exfoliative syndrome, 28 with bullous impetigo, and 17 with staphylococcal scarlet fever). All strains isolated from patients with generalized exfoliative syndrome or bullous impetigo produced ETA and/or ETB and caused a Nikolsky's sign when injected subcutaneously into newborn mice. In contrast, exfoliative toxin was detected in an S. aureus strain from only one of 17 cases of staphylococcal scarlet fever; the 16 other S. aureus strains produced TSST-1 and/or an enterotoxin. In conclusion, enterotoxins or TSST-1 are more frequently associated with staphylococcal scarlet fever than are exfoliative toxins. Hence staphylococcal scarlet fever may well represent an abortive form of toxic shock syndrome rather than a milder form of staphylococcal scalded skin syndrome.

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Section: Methodsmentioning

confidence: 91%

Toxin Involvement in Staphylococcal Scalded Skin Syndrome

et al. 1997

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“…61 In the case of TSST-1mediated TSS, the protective role of anti-TSST-1 antibody is supported by evidence showing that: (i) in virtually all cases of TSS caused by TSST-1, anti-TSST-1 antibodies are either undetectable or present in low amounts during the acute phase of TSS; (ii) TSS caused by TSST-1 is extremely rare in individuals with significant levels of anti-TSST-1 antibody; and (iii) recurrence of TSS is associated with the absence of anti-TSST-1 antibody in convalescent serum. 48,54,62,63 Less than half of all individuals with MTSS develop protective levels of anti-TSST-1 antibody in convalescent sera specimens, and those that do not are at significant risk of recurrence. 54,63 Antibodies to TSST-1 of the IgG class cross the placenta and may provide protection against TSS and Kawasaki syndrome in infants younger than 6 months.…”

Section: Pathogenesis Of S Aureus Toxin-mediated Diseasementioning

confidence: 99%

“…2,83,85 A fine erythematous maculopapular rash occurs later in the acute course in a significant proportion of survivors. 62,87 A characteristic manifestation of TSS is desquamation of skin of the hands and feet (including palms, soles, fingers and toes) which occurs 10-21 days after disease onset, and this is also described in other superantigenmediated disease states such as streptococcal toxic shock syndrome and Kawasaki's disease. 2,7,86 Telogen effluvium (which occurs as a result of disturbed metabolism and keratinization of the hair and nails resulting in hair loss and disordered nail growth) can occur after 4-16 weeks, with restoration of normal growth occurring 5-6 months following recovery.…”

Section: Clinical Features Of S Aureus Toxin-mediated Disease Toxic mentioning

confidence: 99%

“…However, it is generally agreed that an antimicrobial agent with activity against S. aureus (preferably a β-lactam agent) (see Table 5) should be given to all patients with suspected TSS with the aim of reducing or eliminating the organism burden. 2,4,62,82,86 There is evidence from in vitro studies that non-βlactam agents that inhibit bacterial protein synthesis such as gentamicin or clindamycin can reduce TSST-1 production from enterotoxin-producing S. aureus strains. [95][96][97] As this reduction in TSST-1 expression has also been demonstrated in the in vivo setting for clindamycin, 96 it is often suggested that clindamycin be added to the primary antistaphylococcal agent in the treatment of suspected TSS.…”

Section: Antimicrobial Therapymentioning

confidence: 99%

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Recognition and management of Staphylococcus aureus toxin‐mediated disease

Rj¹

2005

Internal Medicine Journal

128

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The ubiquitous human pathogen Staphylococcus aureus is capable of producing a formidable range of extracellular toxins that can have significant deleterious effects on the host. Toxic shock syndrome (TSS) results from infection or colonization with a strain of S. aureus that produces staphylococcal enterotoxin(s). The key features of TSS are widespread erythroderma occurring in association with profound hypotension and multiple organ dysfunction. As morbidity and mortality from TSS are appreciable, early recognition of TSS combined with intensive supportive management is critical. Staphylococcal foodborne disease (SFD) is caused by contamination of food during preparation or serving by preformed S. aureus enterotoxin(s). Symptom-onset is abrupt and the disease may be severe enough to warrant hospitalization, but it is usually self-limiting and does not require specific antistaphylococcal therapy. Staphylococcal scalded skin syndrome (SSSS) results from colonization or infection with a strain of S. aureus that produces epidermolytic toxin(s). SSSS ranges in severity from trivial focal skin blistering to extensive, life-threatening exfoliation. This review discusses the epidemiology, pathogenesis, diagnosis, and management of TSS, SFD and SSSS.

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“…It failed to produce these toxins but did elaborate enterotoxin F, which is characteristic of strains associated with the toxic shock syndrome.2 3 Tolerance to both nafcillin and vancomycin has been documented in staphylococci associated with the toxic shock syndrome but is rare. 4 The clinical importance of in vitro tolerance remains controversial, but this phenomenon is more important when the syndrome is associated with endocarditis than it is in most cases, in which a bactericidal antimicrobial regimen is not mandatory.…”

Section: Commentmentioning

confidence: 99%