Streptococcal toxic shock-like syndrome

Wolf, J. E.

doi:10.1001/archderm.131.1.73

Cited by 10 publications

(3 citation statements)

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“…The biological basis for the severity of GAS NF may relate to their capacity to produce one or more pyrogenic exotoxins (type A, B or C) that vary in their capacity to induce erythema, pyrogenicity, systemic toxicity, multiorgan system failure, vascular permeability changes, and shock. 6,11 One of the striking characteristics of this series is that both for GAS and non-GAS NF, the initial diagnosis was frequently incorrect, which may have resulted in delayed therapy and likely contributes to the high fatality rate of this series. In most cases, the diagnosis of erysipelas or cellulitis was the first to be made, underscoring the absence of specificity of the clinical signs in the early stages of the infectious process, irrespective of the causative germ.…”

Section: Discussionmentioning

confidence: 99%

The importance of serum creatine phosphokinase level in the early diagnosis and microbiological evaluation of necrotizing fasciitis

Simonart

Nakafusa

Narisawa

2004

Acad Dermatol Venereol

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Section: Discussionmentioning

confidence: 99%

The importance of serum creatine phosphokinase level in the early diagnosis and microbiological evaluation of necrotizing fasciitis

Simonart

Nakafusa

Narisawa

2004

Acad Dermatol Venereol

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“…The latter two agents can be released from streptococci either by beta-lac-tam antibiotics [35^37] or by cationic proteins from neutrophils (reviewed in [35]). Streptococcal cell wall components are also known to be involved in the generation by macrophages of TNF-K and additional cytokines, nitric oxide and in the induction of toxic shock syndrome [26,27,38,39]. Phospholipids and azo-dyes might neutralize both the cell-bound and cell-free SLS and the attack complex of complement.…”

Section: Discussionmentioning

confidence: 99%

Gamma globulin, Evan's blue, aprotinin A PLA2 inhibitor, tetracycline and antioxidants protect epithelial cells against damage induced by synergism among streptococcal hemolysins, oxidants and proteinases: relation to the prevention of post-streptococcal sequelae and septic shock

Ginsburg¹

1998

FEMS Immunology and Medical Microbiology

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An in vitro model was employed to study the potential role of streptococcal extra-cellular products, rich in streptolysin O, in cellular injury as related to streptococcal infections and post-streptococcal sequelae. Extra-cellular products (EXPA) rich in streptolysin O were isolated from type 4, group A hemolytic streptococci grown in a chemostat, in a synthetic medium. EXPA induced moderate cytopathogenic changes in monkey kidney epithelial cells and in rat heart cells pre-labeled with 3H-arachidonate. However very strong toxic effects were induced when EXP was combined with oxidants (glucose oxides generated H2O2, AAPH-induced peroxyl radical (ROO.), NO generated by sodium nitroprusside) and proteinases (plasmin, trypsin). Cell killing was distinctly synergistic in nature. Cell damage induced by the multi-component cocktails was strongly inhibited either by micromolar amounts of gamma globulin, and Evan's blue which neutralized SLO activity, by tetracycline, trasylol (aprotinin), epsilon amino caproic acid and by soybean trypsin inhibitor, all proteinase inhibitors as well as by a non-penetrating PLA2 inhibitor A. The results suggest that fasciitis, myositis and sepsis resulting from infections with hemolytic streptococci might be caused by a coordinated 'cross-talk' among microbial, leukocyte and additional host-derived pro-inflammatory agents. Since attempts to prolong lives of septic patients by the exclusive administration of single antagonists invariably failed, it is proposed that the administration of 'cocktails' of putative inhibitors against major pro-inflammatory agonizes generated in inflammation and infection might protect against the deleterious effects caused by the biochemical and pharmacological cascades which are known to be activated in sepsis.

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“…The biological basis for the severity of GAS NF may relate to their capacity to produce one or more pyrogenic exotoxins (type A, B or C) that vary in their capacity to induce erythema, pyrogenicity, systemic toxicity, multi-organ system failure, vascular permeability changes and shock [3, 4, 5]. NF other than that due to GAS involves the participation of one or more anaerobes and/or of non-group-A streptococci, Staphylococcus aureus and enteric organisms, and may be associated with a less fulminant evolution and a better outcome.…”

Section: Introductionmentioning

confidence: 99%

Group A Beta-Haemolytic Streptococcal Necrotising Fasciitis: Early Diagnosis and Clinical Features

Simonart

2004

Dermatology

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Necrotising fasciitis (NF) due to group A β-haemolytic streptococci (GAS) is a rare but still life-threatening soft-tissue infection characterised by rapidly spreading inflammation and subsequent necrosis of the muscle fascia and of the surrounding tissues. Previous studies have emphasised that the outcome of patients with NF depends essentially on early diagnosis and treatment, consisting of extensive surgical debridement, along with appropriate antibiotic therapy. However, one of the striking features of the published series of GAS NF is that there was a delay in diagnosis in several cases, which underscores the difficulty of the early diagnosis of the condition. The goal of this article was to review the clinical features and diagnostic tools that could facilitate the early recognition of GAS NF.

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Streptococcal toxic shock-like syndrome

Cited by 10 publications

References 0 publications

The importance of serum creatine phosphokinase level in the early diagnosis and microbiological evaluation of necrotizing fasciitis

The importance of serum creatine phosphokinase level in the early diagnosis and microbiological evaluation of necrotizing fasciitis

Gamma globulin, Evan's blue, aprotinin A PLA2 inhibitor, tetracycline and antioxidants protect epithelial cells against damage induced by synergism among streptococcal hemolysins, oxidants and proteinases: relation to the prevention of post-streptococcal sequelae and septic shock

Group A Beta-Haemolytic Streptococcal Necrotising Fasciitis: Early Diagnosis and Clinical Features

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