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staphylococcal scalded skin syndrome

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The text is the summary of recent articles on staphylococcal scalded skin syndrome at 75 thresold from National Library of Medicine (NLM). This information is subject to NCBI's Disclaimer and Copyright notice.


Prompt empiric treatment with intravenous anti-staphylococcal antibiotic such as nafcillin, oxacillin, or flucloxacillin is essential until cultures are available to guide therapy [1]. If the patient is not improving, critically ill, or in communities where the prevalence of methicillin-resistant S [2]. Differential diagnosis includes toxic epidermal necrolysis, staphylococcal scalded skin syndrome, epidermolysis bullosa, and Stevens-Johnson syndrome [3]. This case report highlights staphylococcal scalded skin syndrome and its treatment, and future challenges [4]. The diagnosis of staphylococcal scalded skin syndrome was reached on clinical grounds and culture report [5].

Having a high clinical suspicion for staphylococcal scalded skin syndrome, early diagnosis/treatment, and following robust hygiene measures are imperative for the effective management of staphylococcal scalded skin syndrome [6]. Most of these infections are associated with milder Inflammation compared to normal [7]. We report a primary Immune Deficiency associated with a hyper-ige syndrome revealed by a staphylococcal scalded skin syndrome in a 5-year-old girl [8]. Genes encoding products producing high-level resistance (HLR) to mupirocin (mupA), fusidic acid resistance (fusB), resistance to macrolides and lincosamides (ermC and ermA), Panton-Valentine leukocidin (PVL) (lukS/lukF-PV), exfoliative toxins (eta and etb), and fibronectin binding protein A (fnbA) were investigated by PCRs in 102 selected preserved strains [9]. The Number of infections detected annually increased during the study years [10].

Immediate medication with parenteral anti-staphylococcal Antibiotics is mandatory [11]. Traditionally, frozen section has been used in dermatology to diagnose toxic Epidermal necrolysis, with some additional utility in staphylococcal scalded skin syndrome in the new born period [12]. We report a newborn Female with ruptured Bullae on the Face, Chest, back and Extremities with a clinical differential diagnosis that included staphylococcal scalded skin, bullous congenital ichthyosiform erythroderma/epidermolytic Hyperkeratosis and epidermolysis bullosa [13]. Aureus M060 isolated from a patient with staphylococcal scalded skin syndrome showed higher cytotoxic activity toward host Cells than that shown by MVs from three other clinical S [14]. Aureus MVs contained δ-hemolysin (Hld), γ-hemolysin, leukocidin D, and exfoliative Toxin C, but exfoliative Toxin A (ETA) was specifically identified in S [15].

The antibiotic therapy was changed to a combination of cefotaxime, flucloxacillin and clindamycin which rapidly stopped progression of the Exfoliation [16]. In the primary Lesion an ETA-producing Staphylococcus aureus strain was isolated [17]. Possible causes include lower Antibody levels against exfoliative toxins and Renal immaturity [18]. The subject of this report is unique in that he developed the largest Exfoliation described in literature [19]. Aureus often cause burn wound infections that can lead to complications caused by cross-infection [20].

Part I of this 2-part continuing Medical education article addresses common pitfalls involving site selection and Biopsy technique in the diagnosis of bullous diseases, Vasculitis, Panniculitis, connective tissue diseases, drug eruptions, graft-versus-host disease, staphylococcal scalded skin syndrome, Hair disorders, and neoplastic disorders [21]. From Neck of each mouse was isolated and identified endogenous exfoliative producing strain of S [22]. Detailed epidemiological and microbiological investigations were undertaken [23]. All eight isolates contained genes encoding exfoliative Toxin A (eta) and six of them contained genes encoding Toxin B (etb) [24]. Common among these are acute and Chronic graft-versus-host disease, erythema multiforme, Stevens-Johnson syndrome/toxic Epidermal necrolysis, Eruption of lymphocyte recovery, staphylococcal scalded skin syndrome, morbiliform drug eruptions, infections, and toxic erythema of Chemotherapy [25].

The diagnosis can be confirmed by a Skin Biopsy specimen, which can be expedited by frozen section processing, as staphylococcal scalded skin syndrome should be distinguished from life threatening toxic epidermal necrolysis [26]. The exfoliative toxins are spread haematogenously from a Localized source of infection, causing widespread Epidermal damage at distant sites [27]. Recent epidemiological studies have demonstrated that paediatric patients have an increased incidence of staphylococcal scalded skin syndrome during the summer and autumn [28].

References: 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 ,

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