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      Unusual staphylococcal toxic shock syndrome presenting as a scarlet-like fever

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          Abstract

          Diagnosis of nonmenstrual staphylococcal toxic shock syndrome (TSS) is often challenging. A female medical colleague had a rare entity, a staphylococcal pharyngitis complicated by TSS. The diagnosis was confirmed by isolation of tst-positive Staphylococcus aureus in throat culture and by identification of a specific Vβ2 expansion pattern of her T lymphocytes. Recent improvements in microbiology can be of great help for the diagnosis of nonmenstrual TSS.

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          Most cited references14

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          Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngitis: 2012 update by the Infectious Diseases Society of America.

          The guideline is intended for use by healthcare providers who care for adult and pediatric patients with group A streptococcal pharyngitis. The guideline updates the 2002 Infectious Diseases Society of America guideline and discusses diagnosis and management, and recommendations are provided regarding antibiotic choices and dosing. Penicillin or amoxicillin remain the treatments of choice, and recommendations are made for the penicillin-allergic patient, which now include clindamycin.
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            Gram-positive toxic shock syndromes.

            Toxic shock syndrome (TSS) is an acute, multi-system, toxin-mediated illness, often resulting in multi-organ failure. It represents the most fulminant expression of a spectrum of diseases caused by toxin-producing strains of Staphylococcus aureus and Streptococcus pyogenes (group A streptococcus). The importance of Gram-positive organisms as pathogens is increasing, and TSS is likely to be underdiagnosed in patients with staphylococcal or group A streptococcal infection who present with shock. TSS results from the ability of bacterial toxins to act as superantigens, stimulating immune-cell expansion and rampant cytokine expression in a manner that bypasses normal MHC-restricted antigen processing. A repetitive cycle of cell stimulation and cytokine release results in a cytokine avalanche that causes tissue damage, disseminated intravascular coagulation, and organ dysfunction. Specific therapy focuses on early identification of the illness, source control, and administration on antimicrobial agents including drugs capable of suppressing toxin production (eg, clindamycin, linezolid). Intravenous immunoglobulin has the potential to neutralise superantigen and to mitigate subsequent tissue damage.
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              Toxic-shock syndrome associated with phage-group-I Staphylococci.

              Seven children (aged 8--17 years) presented with a high fever, headache, confusion, conjunctival hyperaemia, a scarlatiniform rash, subcutaneous oedema, vomiting, watery diarrhoea, oliguria, and a propensity to acute renal failure, hepatic abnormalities, disseminated intravascular coagulation, and severe prolonged shock. One patient died, one had gangrene of the toes, and all have had fine desquamation of affected skin and peeling of palms and soles during convalescence. Five patients were studied prospectively. Staphylococcus aureus related to phage-group I was isolated from mucosal (nasopharyngeal, vaginal, tracheal), or sequestered (empyema, abscess) sites, but not from blood. This organism produces an exotoxin which causes a positive Nikolsky sign in the newborn mouse and which is biochemically, pathologically, and immunologically distinct from phage-group-II stapphylococcal exfoliatin.
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                Author and article information

                Contributors
                Journal
                New Microbes New Infect
                New Microbes New Infect
                New Microbes and New Infections
                Elsevier
                2052-2975
                18 August 2015
                November 2015
                18 August 2015
                : 8
                : 10-13
                Affiliations
                [1) ]Service of Infectious Diseases, Department of Medical Specialties, Switzerland
                [2) ]Intensive Care Unit, Department of Anaesthesiology, Pharmacology and Intensive Care, Switzerland
                [3) ]Bacteriology Laboratory, Department of Laboratories and Genetic Medicine, University Hospitals of Geneva, Geneva, Switzerland
                [4) ]Hospices Civils de Lyon, CIRI, Université Lyon 1, Inserm U1111, CNRS UMR5308, Ecole Normale Supérieure de Lyon, Centre National de Référence des Staphylocoques, Lyon, France
                [5) ]St Helens Clinical Commissioning Group, United Kingdom
                Author notes
                [] Corresponding author: D.O. Andrey, Service of Infectious Diseases, University Hospitals Geneva, 4, Rue Gabrielle-Perret-Gentil, CH-1211 Geneva 14, Switzerland diego.andrey@ 123456hcuge.ch
                Article
                S2052-2975(15)00064-5
                10.1016/j.nmni.2015.08.002
                4590715
                57a27708-1dfb-488b-b1ff-5aae5c7801af
                © 2015 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 7 March 2015
                : 15 July 2015
                : 7 August 2015
                Categories
                Original Article

                non menstrual tss,scarlet fever,staphylococcus aureus,strepa rapid antigenic test,vbeta t lymphocytes expansion

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