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At least 1,117 records · Page 62Linked to original sources
PubMed1996

[Protective effect of ATP-MgCl2 on gut mucosa in burn rat].

In order to study the protective effect of ATP-MgCl2 on gut mucosal barrier function in trauma-induced stressed animal, full thickness burn of 30% total body surface area (TBSA) was produced in rats, and ATP-MgCl2 was injected intraperitoneally right after scald-injury. Malondialdehyde (MDA) contents of ileum mucosa were determined and morphological alteration in the ileum was observed under light microscope. The results showed that ileum mucosal MDA content increased significantly, accompanied by obvious morphological change, after the injury, whereas MDA content was maintained at the normal control level and pathological alteration in ileum tissue was abated after the use of ATP-MgCl2. It suggests that ATP-MgCl2 possesses a protective effect on gut mucosal barrier function of scald-injured rat, and the mechanism involved may be related to the inhibition of lipid peroxidation in gut mucosa.

Adenosine Triphosphate↗
PubMed1997

[Clinical and experiment study of cooling therapy on burned wound].

OBJECTIVE: To observe the subjective benefit of pain relief by cooling therapy when wound temperature drops to below 28 degrees C (threshold for pain). METHOD: 22 patients with partial-thickness burns who received cooling therapy showed 2 days early healing as compared with untreated burn wounds. As a first aid measure, prolonged cooling therapy (up to 30') was recommended. In experimental study, the protective effects with cooling therapy were observed in wistar rats with deep second degree burns. RESULTS: Lower epithelial cell activity and higher schiff alkaline values were seen in the wound skin tissue in the non cooling therapy than in early cooling therapy groups and healthy controls. The groups with early cooling therapy (at once, 10', 20' after scalded injuries) the epithelial cell activity maintained at 83%, 80%, 65%. CONCLUSION: The results suggest that cooling therapy can protect the epithelial cell activity to some extent after scalded injuries which may be associated with inhibition of lipid peroxide.

Adult↗
PubMed1996

[Gram-positive septic-toxic shock with bullae. Intraepidermal splitting as an indication of toxin effect].

A fourteen-year-old girl with acute otitis media died from gram positive sepsis and toxic shock despite intensive treatment. The definitive bacteriological results showed positive cultures for both S. aureus and S. pyogenes serotype A. In vitro the bacteria produced the bacterial superantigens TSST-1, enterotoxin A, enterotoxin C (S. aureus) and erythrogenic toxin C (S. pyogenes). The patient presented with large flaccid sterile bullae on her chest and arms as well as necrotizing fasciitis. Tzanck test showed keratinozytes without necrosis and no inflammatory cells. Frozen-section and conventional skin biopsy specimens revealed subcorneal intraepidermal cleavage. These cytological and histological findings are those of staphylococcal scalded skin syndrome (SSSS) and differ from bullous erysipelas or toxic epidermal necrolysis (TEN). Therefore bacterial exotoxins are most likely responsible for the intraepidermal blistering in our case just as in SSSS. Bullae are an unfavorable prognostic sign in gram positive toxic shock syndrome. Both Tzanck test and frozen-section biopsy are easy to perform and useful in the early and rapid recognition of gram positive bullous toxic shock syndrome.

Adolescent↗
PubMed2005

Lyell syndrome revisited: analysis of 18 cases of severe bullous skin disease in a burns unit.

Over the last few years, understanding of the pathophysiology of toxic epidermal necrolysis (TEN), or Lyell's disease, has substantially increased. However, differentiation of severe bullous skin disease remains a challenge for the clinician, and one that is often complicated by late patient referral. We performed a retrospective analysis of all patients with severe bullous skin disease, admitted between 1997 and 2002 to the Burn Centre, which is an integrated part of the Division for Plastic, Hand- and Reconstructive Surgery at the University Hospital of Zurich, Switzerland. We present an overview of our strategies and of the diagnostic and therapeutic difficulties encountered. The final diagnoses of the 18 patients referred to the unit were as follows: eight cases of TEN, one case of staphylococcal scalded-skin syndrome (SSSS), two cases of generalised drug eruption, one case of acute generalised exanthematic pustulosis and one case of febrile ulceronecrotic pityriasis lichenoides et varioliformis acuta (PLEVA). In two cases, the diagnosis remained unclear. In three cases, paraneoplastic origins were suspected but not demonstrated. The overall mortality rate was 33% (six of 18 patients). Remarkably, all patients with histologically confirmed TEN survived. Six of these patients were successfully treated with intravenous immunoglobulins (IVIG). The most common single causative drug inducing TEN (four cases out of eight) was Phenytoin. Establishing an accurate diagnosis-based on a skin biopsy, harvested at an early stage-is more important than ever, because more specific and effective therapeutic modalities are available. As these potentially life-threatening bullous skin disorders are rare, we recommend, that care be provided by an experienced interdisciplinary team, comprising a dermatologist, or dermatopathologist, an intensive care specialist and a plastic surgeon.

Acute Disease↗
PubMed1985

Screening of clinical S. aureus-isolates for the production of exfoliative toxin. A methodological study.

Screening S. aureus-isolates for the production of exfoliative toxin (ET) and discrimination between its two known variants (ETA, ETB) by immunodiffusion (ID), isoelectric focusing (IEF) and animal experiment were assessed methodologically using isolates from a patient with bullous impetigo and a patient with Ritter von Rittershain's disease. Only by animal assay one of the isolates could be identified as ET-producer. ID was used for the discrimination between ETA and ETB. It is concluded that the in-vivo assay for ET-production using live staphylococci can not yet be replaced by ID and IFE and that in patients with staphylococcal scalded skin syndrome swabs should be taken from multiple lesions und all S. aureus isolates obtained should be screened for ET-production to prevent false-negative results. Lysotyping alone gives no proof of ET-production since types II 55/71 and II 3A/3C do not produce ET in all cases and toxinogenic S. aureus strains of phage groups I and III have been described.

Adolescent↗
PubMed1997

The structure of Staphylococcus aureus epidermolytic toxin A, an atypic serine protease, at 1.7 A resolution.

BACKGROUND: Staphylococcal epidermolytic toxins A and B (ETA and ETB) are responsible for the staphylococcal scalded skin syndrome of newborn and young infants; this condition can appear just a few hours after birth. These toxins cause the disorganization and disruption of the region between the stratum spinosum and the stratum granulosum--two of the three cellular layers constituting the epidermis. The physiological substrate of ETA is not known and, consequently, its mode of action in vivo remains an unanswered question. Determination of the structure of ETA and its comparison with other serine proteases may reveal insights into ETA's catalytic mechanism. RESULTS: The crystal structure of staphylococcal ETA has been determined by multiple isomorphous replacement and refined at 1.7 A resolution with a crystallographic R factor of 0.184. The structure of ETA reveals it to be a new and unique member of the trypsin-like serine protease family. In contrast to other serine protease folds, ETA can be characterized by ETA-specific surface loops, a lack of cysteine bridges, an oxyanion hole which is not preformed, an S1 specific pocket designed for a negatively charged amino acid and an ETA-specific specific N-terminal helix which is shown to be crucial for substrate hydrolysis. CONCLUSIONS: Despite very low sequence homology between ETA and other trypsin-like serine proteases, the ETA crystal structure, together with biochemical data and site-directed mutagenesis studies, strongly confirms the classification of ETA in the Glu-endopeptidase family. Direct links can be made between the protease architecture of ETA and its biological activity.

Amino Acid Sequence↗
PubMed1998

The clinician's choice of antibiotics in the treatment of bacterial skin infection.

The development of modern antibiotics has vastly improved the therapy of cutaneous bacterial infections, particularly those caused by Staphylococcus aureus. This organism and beta-haemolytic streptococci are the most common cutaneous pathogens. A growing body of evidence suggests that proteins from S. aureus and some strains of streptococci can act as superantigens and cause polyclonal T-cell activation by binding directly to antigen-presenting cells. This process is a likely explanation of Kawasaki's syndrome as well as staphylococcal and streptococcal toxic shock syndrome. Sudden aggravation of atopic dermatitis, contact dermatitis and some cases of psoriasis can be similarly explained. Bacterial toxins can precipitate the staphylococcal scalded skin syndrome. Specific and effective eradication of bacteria and programmes to prevent recurrences are important, particularly in immune suppressed persons. Topical antibiotics used primarily for superficial infections of limited extent and for the prevention of recurrences in carriers of S. aureus should be combined with the use of topical disinfectants. The treatment of selected bacterial skin infections based on clinical examples will be discussed. These include secondarily infected dermatoses, cellulitis and streptococcal carriage in the ano-genital region and staphylococcal folliculitis and nasal carriage.

Administration, Topical↗
PubMed2003

Targetting of desmoglein 1 in inherited and acquired skin diseases.

Desmoglein 1 is a member of the desmosomal cadherin family that comprise the desmogleins and desmocollins. The desmoglein 1 gene (DSG1) is centromeric to the desmoglein gene cluster and spans approximately 45 kb of 18q12, comprising 15 exons. The transcript encodes a precursor protein of 1049 amino acids that is cleaved to yield a mature protein of 1000 residues. This mature protein is expressed in certain specialized epithelia, and in the epidermis is expressed within the superficial layers. Within the desmosome the extracellular domain of the protein is essential for calcium dependent heterophilic binding to the desmocollins, whereas the intracellular domain is essential for binding to the desmosomal plaque protein, plakoglobin. Desmoglein 1 has been implicated in several human diseases. Mutations within the extracellular domain lead to autosomal dominant striate palmoplantar keratoderma, whereas autoantibodies and strains of Staphylococcus aureus target the extracellular domain in the acquired bullous disorders pemphigus foliaceus and staphylococcal scalded skin syndrome, respectively. Therefore, intact and functionally active desmoglein 1 is essential to epidermal integrity. Here, we review the expression, protein structure, genetics, and molecular interactions of desmoglein 1 and outline the role it plays within the desmosome and how it becomes defective in human disease.

Cytoskeletal Proteins↗
PubMed2003

Desmoglein as a target in autoimmunity and infection.

Clinical phenotypes of most diseases are complex. However, once the mechanism behind the scene is clarified, the nature shows amazing beauty. There is a simple logic behind a complex disease. The exact molecular mechanism of the blister formation in staphylococcal scalded skin syndrome (SSSS) remained to be elucidated for 3 decades since exfoliative toxin was discovered by Melish and Glasgow in 1970. A knowledge accumulated to understand the pathogenesis of pemphigus and cell-cell adhesion of keratinocytes led us to solve this question. Desmoglein 1, which is a cadherin type cell-cell adhesion molecule in desmosomes, is targeted in two different skin diseases, pemphigus foliaceus, and SSSS. In pemphigus foliaceus IgG autoantibodies are developed against desmoglein 1 and inhibit its adhesive function with resultant blister formation in the superficial epidermis. In SSSS, exfoliative toxin produced by Staphylococcus aureus specifically binds and cleaves desmoglein 1 with resultant blister formation at the identical site.

Animals↗
PubMed1987

Influence of focal growth conditions on the pathogenesis of toxic shock syndrome.

Patients with toxic shock syndrome (TSS) had sequestered focal sites colonized or infected with Staphylococcus aureus significantly more frequently than did patients with scalded skin syndrome. Growth conditions within the infected foci of four patients with TSS included nearly physiological levels of pH, pO2, pCO2, protein, calcium, and magnesium. Two strains of S. aureus had typical TSS phenotypes (production of TSS toxin-1 [TSST-1] and protease), which were optimally expressed in vitro under conditions similar to those documented in vivo (6% CO2, pH 7.0, aerobic, high levels of protein). Altering any one of these growth factors significantly decreased production of TSST-1. In protein-containing media, depletion of divalent cations had a less-profound effect on organism growth and TSST-1 production. The unique in vivo environment in patients with non-menstrual TSS is similar to conditions associated with tampon use during menstruation. Growth conditions may play an important role in the expression of S. aureus phenotype and the pathogenesis of TSS.

Bacterial Toxins↗
PubMed2004

Mechanisms of blister formation by staphylococcal toxins.

Many children suffer from the bacterial skin diseases bullous impetigo and staphylococcal scalded skin syndrome (SSSS). Staphylococcus aureus, which produces exfoliative toxins (ETs), causes these diseases. Recently, it was proven that ETs cleave the cell adhesion molecule desmoglein (Dsg) 1, which plays an important role in maintaining the proper structure and barrier function of the epidermis. Surprisingly, Dsg1 is also the antibody target in the autoimmune disease pemphigus foliaceus. Skin biopsies from pemphigus foliaceus patients show the same pathology as those from bullous impetigo and SSSS patients. The crystal structure of ET suggests that it is a serine protease with an inactive catalytic site, which may become activated when ET binds a specific receptor. This receptor binding is thought to cause a change in conformation that exposes the catalytic site. It has recently been shown that Dsg1 specifically binds and activates ET, which in turn cleaves the bound Dsg1 at only one peptide bond. This process is absolutely dependent on the calcium-dependent conformation of Dsg1. These data suggest that ETs have a very high specificity for human Dsg1, and that S. aureus uses ETs to disrupt the barrier of the human epidermis in order to survive and proliferate on the human body.

Blister↗
PubMedDate not supplied

The burn unit as a resource for the management of acute nonburn conditions in children.

Burn units bring together resources to manage large complex wounds, organ failures, and the hypermetabolic response to injury. These resources can also facilitate management of other problems such as purpura fulminans, toxic epidermal necrolysis, staphylococcal scalded skin syndrome, and major mechanical soft-tissue injuries. During a recent 10-year interval 2.4% of all acute admissions to a regional pediatric burn facility were in this category and form the basis for this review.

Acute Disease↗
PubMed2000

Neonatal skin disorders: a review of selected dermatologic abnormalities.

The skin serves many purposes, acting as a barrier to infection, protecting internal organs, contributing to temperature regulation, storing insulating fats, excreting electrolytes and water, and providing tactile sensory input. This article focuses on a review of normal skin structure and function and selected neonatal skin disorders. The disorders reviewed are Staphylococcal scalded skin syndrome, epidermolysis bullosa, and the ichthyoses. The basis for each skin disorder is presented. Nursing management and skin care are incorporated into the review of each selected disorder.

Epidermolysis Bullosa↗
PubMed1988

Microbiologic characteristics of exfoliative toxin-producing Staphylococcus aureus.

Exfoliative toxin (ET) production, phage types and antibiotic susceptibilities of 74 strains of Staphylococcus aureus isolated from patients with generalized staphylococcal scalded skin syndrome or bullous impetigo were studied. Of 74 staphylococcal isolates, 61 strains were found to produce ET by the newborn mouse assay method and the latex agglutination method. Fifteen strains were positive for ET-A, 32 for ET-B and 14 for both ET-A and ET-B. Among 61 ET-producing strains 27 (44%) were classified as Phage Group II, 16 (26%) as Group III, and 14 (23%) as Groups I and III. Of 27 Phage Group II strains 14 produced ET-A and 13 produced both ET-A and ET-B, but no strain was positive solely for ET-B. On the other hand 15 of 16 Phage Group III strains and all 14 Phage Group I and III strains produced only ET-B. It was demonstrated that the phage types of staphylococci were closely related to ET types. Characteristically the minimal inhibitory concentrations of penicillin G against ET-producing strains were less than 2 micrograms/ml, in contrast to other pathogenic staphylococci, 60 to 70% of which are highly penicillin G-resistant.

Adolescent↗
PubMed1990

Action of staphylococcal exfoliative toxins on epidermal cell cultures and organotypic skin.

In the staphylococcal scalded skin syndrome, spontaneous intraepithelial cleavages are due to the exfoliative toxins A or B (ETA or ETB). Until now, these toxins have been studied either on epidermis or on organotypic skin cultures. In the present study, we compare the effects of these toxins on human keratinocyte cell cultures to those on human and mouse organotypic skin cultures. With concentrations of ETA or ETB of 1 mg/ml for 3 hours, spontaneous intraepithelial cleavages were noted in both cell and organotypic cultures. Keratinocyte cell cultures were as sensitive as organotypic skin cultures to these toxins. Since keratohyaline granules may represent a possible binding site for ETA or ETB, we tried to correlate the expression of keratohyaline granules with the appearance of intraepithelial clefts due to the toxins. However, when cultured in liquid medium, epithelia were not differentiated enough to allow the detection of the binding site of ETA-ETB.

Animals↗
PubMed1995

Rapid identification by polymerase chain reaction of staphylococcal exfoliative toxin serotype A and B genes.

A new system was designed to detect staphylococcal exfoliative toxin A (ETA) and B (ETB) genes by the polymerase chain reaction (PCR). The primer pairs for the ETA gene (eta) were 20 and 20-mer, and its PCR product was a 741-bp eta fragment, while the primer pairs for the ETB gene (etb) were also 20 and 20-mer, and its PCR product was a 629-bp etb fragment. When these primers were simultaneously used in the PCR, the two types of ET were clearly detected as two bands in an ETA and ETB double-producer using only one colony within 3 hr. We examined 66 strains of Staphylococcus aureus isolated from patients with staphylococcal scalded skin syndrome (SSSS) and compared the results obtained by ELISA and PCR. The same results were obtained for 56 of the strains, i.e., 30 strains were ETA producers, 20 strains were ETB producers, and 6 strains were double-producers. However, positive results were obtained for 5 of the 10 non-ET-producing strains. Two of these strains were judged by PCR as ETA producers and three as ETB producers. Thus, PCR is very sensitive and rapid in detecting ETA and ETB gene fragments in colonies isolated from patients with SSSS.

Base Sequence↗
PubMed2000

An exfoliative toxin A-converting phage isolated from Staphylococcus aureus strain ZM.

Exfoliative toxin A (ETA) causes staphylococcal scalded-skin syndrome in children. The gene for ETA was believed to be coded by the chromosomal DNA. We isolated temperate phages from an ETA-producing strain, ZM, using a restriction minus strain, 1039, as an indicator. One of the prophages, designated phi-ZM-1 mediated lysogenic conversion of ETA. The polymerase chain reaction assay of the eta gene revealed that phage phi-ZM-1 carries the structural gene for ETA.

Exfoliatins↗
PubMed2005

Recognition and management of Staphylococcus aureus toxin-mediated disease.

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.

Anti-Bacterial Agents↗