PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “SCALDS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed2005

A clinical and microbiological comparison of Staphylococcus aureus toxic shock and scalded skin syndromes in children.

BACKGROUND: This study was designed to compare the clinical characteristics, toxin expression, virulence factors, and antimicrobial susceptibilities of staphylococci isolated from Taiwanese children with staphylococcal toxic shock syndrome (STSS) and staphylococcal scalded skin syndrome (SSSS). METHODS: Demographic characteristics, hospital course, and outcomes of the children were analyzed. Toxin-specific and virulence genes of the staphylococci were detected by polymerase chain reaction amplification. Antimicrobial susceptibilities were determined by disk diffusion and the Etest. RESULTS: Staphylococcus aureus was isolated from 16 children (6 in the STSS group and 10 in the SSSS group). Children with STSS tended to be older than those with SSSS, had a longer duration of hospitalization, and a much higher mortality rate. Community-associated methicillin-resistant S. aureus was isolated from 11 (68.8%) of 16 children. All of these isolates contained the ermB and mecA genes, but none had the mefA gene. All 16 isolates tested positive for the fnbA gene. The pvl and seb genes were more frequently found among S. aureus from the STSS group, compared with S. aureus from the SSSS group. We found that 67% (4 of 6) of the STSS isolates were genetically related. All of the S. aureus isolates were susceptible to vancomycin, gentamicin, doxycycline, and trimethoprim-sulfamethoxazole. Most isolates were resistant to clindamycin (63%), oxacillin (69%), and clarithromycin (81%). CONCLUSIONS: The most distinguishing feature of these isolates is the greater frequency of pvl and seb carriage among those from the STSS group. Most of the isolates were community-associated methicillin-resistant S. aureus that were highly resistant to macrolides but susceptible to trimethoprim-sulfamethoxazole. Vancomycin remains the initial drug of choice for treatment of STSS and SSSS. More studies are needed to determine the efficacy of trimethoprim-sulfamethoxazole in children with these syndromes.

Adolescent↗
PubMed1986

Staphylococcal scalded-skin syndrome.

Staphylococcal scalded-skin syndrome, an exfoliative dermopathy, affects neonatal and infant children. A classification of this disorder, as well as etiology and therapeutic modalities, is discussed. Topical medications such as used for treating partial-thickness burns cannot always be used in the newborn because of potential toxicity. Supportive therapy, specific antibiotics, and relatively inert dressings are recommended.

Diagnosis, Differential↗
PubMed1995

Staphylococcal scalded skin syndrome.

Staphylococcal scalded skin syndrome (SSSS) is a recognised clinical entity that affects primarily the very young and, in rare cases, the very old or the immunocompromised. Koch's postulates have been fulfilled in that: (i) Staphylococcus aureus is isolated from every case; (ii) S. aureus can reproduce the syndrome in an experimental animal model; (iii) a specific extracellular toxin can reproduce the syndrome; and (iv) antibody to the toxin can protect experimental animals. Although exfoliative toxin (ET) is responsible for the skin loosening seen in SSSS, it does not account for all the symptoms of the disease. Purified ET does not cause erythema in either neonatal mice or man, and the lesions are not painful unless the loosened epidermis is removed. This suggests that other factors, e.g., delta-haemolysin, are involved in the pathogenesis of this condition. Although much has been learned about the pathogenesis of the syndrome, we are still largely ignorant of the factors which govern host resistance to SSSS (i.e., intoxication by ET-producing strains of S. aureus). It is fortunate from the patient's point of view that the aetiological agent can be destroyed readily by the use of appropriate antibiotic therapy.

Animals↗
PubMed2005

Epidemiology of staphylococcal scalded skin syndrome in Germany.

Staphylococcal scalded skin syndrome (SSSS) is a blistering skin disorder caused by Staphylococcus aureus. The "Dokumentationszentrum schwerer Hautreaktionen", a unique population-based registry for severe skin reactions, included SSSS during a time period of 2 y in Germany. Statistical calculations indicated a low overall incidence between 0.09 and 0.13 cases per 1 million inhabitants per year with 95% confidence interval of [0-4]. The age distribution showed two clusters; one in young children and one in adults. The mortality rate was much lower in children than in adults. Young age was the main risk factor, whereas immunosuppression and consumptive infectious disease were the detected risk factors in adults.

Adolescent↗
PubMed2001

Staphylococcal scalded skin syndrome developing during burn treatment.

We report a case of staphylococcal scalded skin syndrome (SSSS) in a 5-year-old girl who had been hospitalized for burn treatment. When she developed an upper respiratory tract infection, she manifested extensive erythema and exfoliation. There was a purulent discharge from the ulcer caused by the burn, and exfoliation was observed in the surrounding area. Based on clinical symptoms and laboratory data, SSSS was diagnosed and treated with antibiotics, resulting in subsidence. Staphylococcus aureus was isolated from the posterior nasopharynx and the skin erosion and was proved to produce exfoliative toxin A (ETA). Infection from an asymptomatic carrier of an ET-producing strain was suspected, but we failed to identify the origin, in spite of a thorough inspection of the mother, nurses, and physician. SSSS is occasionally reported as a hospital-acquired infection. We should study the frequency of asymptomatic carriers of ET-producing strains so that we can formulate strategies to prevent such infections.

Arm↗
PubMed2001

Staphylococcal scalded skin syndrome in a healthy adult.

We report a case of staphylococcal scalded skin syndrome (SSSS) in a 65-year-old healthy woman. Fever, purulent conjunctivitis, and exfoliation of the skin in the gluteal region were noted. A scarlatiniform rash was observed on the body, and this erythema was followed by generalized desquamation. Staphylococcus aureus was isolated from her eye discharge, posterior nasopharynx, and the erosive surface of the skin. All the investigated strains produced exfoliative toxin B, but none produced toxic shock toxin-1 (TSST-1) or enterotoxin. The patient was treated with antibiotics and fluid supplementation, resulting in subsidence. This case is thought to have been caused by an abortive form of SSSS or a scarlatiniform variant, which is very rare in healthy adults.

Aged↗
PubMed2005

Netherton syndrome: report of two Taiwanese siblings with staphylococcal scalded skin syndrome and mutation of SPINK5.

Netherton syndrome (NS) is a severe autosomal recessive ichthyosis. It is characterized by congenital ichthyosiform erythroderma, trichorrhexis invaginata, ichthyosis linearis circumflexa, atopic diathesis and frequent bacterial infections. Pathogenic mutations in SPINK5 have recently been identified in NS. SPINK5 encodes lymphoepithelial Kazal-type-related inhibitor (LEKTI), a new type of serine protease inhibitor involved in the regulation of skin barrier formation and immunity. We report two Taiwanese brothers with NS. The patients had typical manifestations of NS with an atopic diathesis and recurrent staphylococcal infections, including staphylococcal scalded skin syndrome (SSSS) since birth. Horny layers were obtained by skin surface biopsy for electron microscopy from lesional skin of both patients and from normal controls. All 33 exons and flanking intron boundaries of SPINK5 were amplified for direct sequencing. The ultrastructure of the stratum corneum (SC) was characterized by premature degradation of corneodesmosomes (CDs) with separation of corneocytes. A homozygous 2260A --> T (K754X) mutation of SPINK5 was found in both patients. Staphylococcal exfoliative toxin A (ETA) is a serine protease capable of cleaving desmoglein 1, an important adhesive molecule of CDs, and can cause separation of the SC, resulting in SSSS. The premature degradation of CDs found in our patients may be attributable to insufficient LEKTI, and possibly also to colonization/infection of ETA-producing Staphylococcus aureus. Mechanisms involved in the pathogenesis of the skin barrier defect in NS are proposed. Further study is needed to prove this hypothesis.

Base Sequence↗
PubMed1991

Diffuse cutaneous mastocytosis mimicking staphylococcal scalded-skin syndrome: report of three cases.

Three cases of diffuse cutaneous mastocytosis (DCM) were at first incorrectly diagnosed as staphylococcal scalded-skin syndrome. In the first patient, at age 1 day the disease was recognized promptly by simple techniques such as Darier's sign and Tzanck smear. Much delay in making the diagnosis occurred in the other two patients, however: almost 1 year and 15 years, respectively. Bullous manifestations in mastocytosis occur only in the first two or three years. In the first months the disease can be dangerous and life threatening. To distinguish mastocytosis from vesicular and bullous neonatal disorders, one should perform Darier's sign and a Tzanck smear. The diagnosis is confirmed by histopathologic studies. Treatment of the bullous manifestations is symptomatic, with zinc oxide paste and oral antihistamines, which may provide some relief. In addition, cimetidine and sodium cromoglycate may be beneficial. At a later age psoralen plus ultraviolet A therapy may also relieve the symptoms. Particular foods and medicines can liberate histamine and should be restricted as much as possible in extremely affected patients. Special care should be taken when these patients are to undergo anesthesia. The risk of complications during and after anesthesia is also present in other forms of mastocytosis.

Adolescent↗
PubMed1993

Pyomyositis and staphylococcal scalded skin syndrome.

Pyomyositis is a rare musculoskeletal infection in non-tropical countries. We report a child who had pyomyositis complicated by staphylococcal scalded skin syndrome. This complication has not previously been described in patients with pyomyositis. Early diagnosis of pyomyositis was made by ultrasound examination, and percutaneous needle drainage under ultrasound guidance was performed. Pus aspirated and blood cultures grew Staphylococcus aureus. No open surgical drainage was required and resolution of the abscess was documented by serial ultrasound examinations.

Child↗
PubMed1996

[A case of staphylococcal scalded skin syndrome caused by exfoliative toxin-B producing MRSA].

We experienced a 6 month-old infant who suffered from staphylococcal scalded skin syndrome (SSSS), whose mother used steroid ointment for the infant's erythematous skin rash for 2 days. On the 3rd day, the infant was admitted to our hospital with fever, erythema on the trunk and extremities, and flaccid blisters and erosions at periorificial areas and the neck. Nikolsky's sign was positive. S. aureus was cultured from the throat, conjunctival inflammatory lesion and exudates. The biological characteristics of the isolates were coagulase type I, enterotoxin-nonproducing, TSST-1-nonproducing, protease pattern: D type, and plasmid profile: 563 kbp. The investigation of exfoliative toxin (ET) revealed negative for ET-A but positive for ET-B, proved by polymerase chain reaction (PCR). The isolated strain of S. aureus was demonstrated to be methicillin-resistant (MRSA), which was further defined to be positive for mec A gene by PCR method. It will be possible for such toxigenic ET-B producing MRSA to gain the dominant status in NICU or closed areas.

Base Sequence↗
PubMed2001

Toxin levels in serum correlate with the development of staphylococcal scalded skin syndrome in a murine model.

Staphylococcal scalded skin syndrome (SSSS) is an exfoliative dermatitis that results from infection with exfoliative toxin-producing Staphylococcus aureus. SSSS is seen primarily in infants and children. Here we ask if there is a specific maturation process that protects healthy adults from this syndrome. For these studies, an active recombinant exfoliative toxin A (rETA) was used in a neonatal mouse model. A time course generated on the susceptibility to the toxin as a function of mouse age indicated that BALB/c mice developed the characteristic symptoms of SSSS until day 7 of life. Between day 7 and day 8 of life there was a dramatic decrease in susceptibility, such that mice at day 9 of life were resistant to the effects of the toxin. This time course corresponds approximately to the time needed for maturation of the adaptive immune response, and SSSS in adults is often identified with immunocompromised states. Therefore, mice deficient in this response were examined. Adult mice thymectomized at birth and adult SCID mice did not develop the symptoms of SSSS after injection with the toxin, indicating that the adaptive immune response is not responsible for the lack of susceptibility observed in the older mice. SSSS in adults is also associated with renal disorders, suggesting that levels of toxin in serum are important in the development of the disease. rETA was not cleared as efficiently from the serum of 1-day-old mice compared to clearance from 10-day-old mice. Ten-day-old mice were given repeated injections of toxin so that the maximal level of toxin was maintained for a sustained period of time, and exfoliation occurred in these mice. Thus, whereas the adaptive immune response is not needed for protection of adult mice from SSSS, efficient clearance of the toxin from the bloodstream is a critical factor.

Aging↗
PubMed2006

Antimicrobial agent of susceptibilities and antiseptic resistance gene distribution among methicillin-resistant Staphylococcus aureus isolates from patients with impetigo and staphylococcal scalded skin syndrome.

The susceptibilities to antimicrobial agents of and distributions of antiseptic resistance genes in methicillin-resistant Staphylococcus aureus (MRSA) strains isolated between 1999 and 2004 in Japan were examined. The data of MRSA strains that are causative agents of impetigo and staphylococcal scalded skin syndrome (SSSS) were compared with those of MRSA strains isolated from patients with other diseases. The susceptibilities to antiseptic agents in MRSA isolates from patients with impetigo and SSSS were higher than those in MRSA isolates from patients with other diseases. The distribution of the qacA/B genes in MRSA strains isolated from patients with impetigo and SSSS (1.3%, 1/76) was remarkably lower than that in MRSA strains isolated from patients with other diseases (45.9%, 95/207). Epidemiologic typings of staphylococcal cassette chromosome mec (SCCmec) and pulsed-field gel electrophoresis (PFGE) showed that MRSA strains isolated from patients with impetigo and SSSS had type IV SCCmec (75/76), except for one strain, and 64.5% (49/76) of the strains had different PFGE types. In addition, the patterns of restriction digestion of all tested qacA/B plasmid in MRSA isolates having different PFGE types were identical. The results showed that a specific MRSA clone carrying qacA/B was not prevalent, but qacA/B was spread among health care-associated MRSA strains. Therefore, it was concluded that the lower distribution rate of qacA/B resulted in higher susceptibilities to cationic antiseptic agents in MRSA isolated from patients with impetigo and SSSS.

Anti-Bacterial Agents↗
PubMed1988

Staphylococcal scalded skin syndrome in two immunocompetent adults caused by exfoliatin B-producing Staphylococcus aureus.

An exfoliatin B-producing strain of Staphylococcus aureus was isolated from two adults with typical staphylococcal scalded skin syndrome (SSSS). One patient developed desquamation after a local staphylococcal infection of the hand, and the other developed exfoliation after nosocomially acquired staphylococcal endocarditis. Neither patient was immunocompromised, had evidence of renal insufficiency, or manifested other potential risk factors for SSSS. Purified toxin, isolated from the causative organisms, produced a Nikolsky sign in neonatal mice. The toxins were shown to be exfoliatin B by biochemical and immunologic methods and heretofore had been described only in children with SSSS. Analysis of plasmid DNAs from both strains revealed a 23-megadalton plasmid with identical restriction endonuclease digestion fragments. One isolate belonged to phage group II (3B/3C/6/7/47/54/55), whereas the other isolate belonged to phage groups I and III (7/29/52/52A/53/54/80). The observation that a non-phage group II exfoliatin-producing strain of S. aureus may produce SSSS in adults indicates the need to better define the diagnostic criteria for SSSS. Immunocompetent adults may remain susceptible to some strains of exfoliatin B-producing S. aureus.

Bacterial Toxins↗
PubMed1998

Staphylococcal scalded-skin syndrome complicating wound infection in a preterm infant with postoperative chylothorax.

The course of infection in a 3-week-old premature newborn suffering from extensive dermatitis with flaccid blisters is described. Staphylococcus aureus was recovered from a local wound infection around a chest tube inserted to drain a postoperative chylothorax. The strain isolated tested positive for the eta gene for exfoliative toxin A, the causative agent of staphylococcal scalded-skin syndrome (SSSS). In this case, prematurity and loss of chylus with consecutive lymphopenia may have contributed to development of SSSS.

Chylothorax↗
PubMed2005

Clinical manifestations of staphylococcal scalded-skin syndrome depend on serotypes of exfoliative toxins.

We sought a possible correlation between the clinical manifestations of staphylococcal scalded-skin syndrome (SSSS) and the serotype of exfoliative toxins (ET) by PCR screening of the eta and etb genes in Staphylococcus aureus strains isolated from 103 patients with generalized SSSS and 95 patients with bullous impetigo. The eta gene and the etb gene were detected in, respectively, 31 (30%) and 20 (19%) episodes of generalized SSSS and 57 (60%) and 5 (5%) episodes of bullous impetigo. Both genes were detected in 52 (50%) episodes of generalized SSS and 33 (35%) episodes of bullous impetigo. To explain this link between etb and generalized SSSS, we examined the distribution of ETA- and ETB-specific antibodies in the healthy population (n = 175) and found that the anti-ETB antibody titer was lower than the anti-ETA titer. Thus, ETA is associated with bullous impetigo and ETB is associated with generalized SSSS, possibly owing to a lower titer of anti-ETB neutralizing antibodies in the general population.

Adolescent↗
PubMed1997

Staphylococcal scalded skin syndrome in an adult. Identification of exfoliative toxin A and B genes by polymerase chain reaction.

A 68-year-old man developed areas of erythema with flaccid bullae and wrinkling on his face, upper extremities, chest, right buttock, and shins. Histological examination revealed an intraepidermal cleavage with a sparse cellular infiltration in the dermis, consistent with a diagnosis of staphylococcal scalded skin syndrome. Cultures from an abscess of his right knee joint and his blood were both positive for Staphylococcus aureus. Both S. aureus isolates were confirmed to be double-producers of ETA and ETB using the polymerase chain reaction. The use of nonsteroidal anti-inflammatory drug seemed to be one of the predisposing factors in this patient.

Aged↗
PubMed2002

Molecular mechanisms of blister formation in bullous impetigo and staphylococcal scalded skin syndrome.

Bullous impetigo due to Staphylococcus aureus is one of the most common bacterial infections of man, and its generalized form, staphylococcal scalded skin syndrome (SSSS), is a frequent manifestation of staphylococcal epidemics in neonatal nurseries. Both diseases are mediated by exfoliative toxins (ETs), which show exquisite pathologic specificity in blistering only the superficial epidermis. We show that these toxins act as serine proteases with extremely focused molecular specificity to cleave mouse and human desmoglein 1 (Dsg1) once after glutamic acid residue 381 between extracellular domains 3 and 4. Mutation of the predicted catalytically active serine to alanine completely inhibits cleavage. The mutated ETs bind specifically to Dsg1 by immunofluorescence colocalization and by coimmunoprecipitation. Thus, ETs, through specific recognition and proteolytic cleavage of one structurally critical peptide bond in an adhesion molecule, cause its dysfunction and allow S. aureus to spread under the stratum corneum, the main barrier of the skin, explaining how, although they circulate through the entire body in SSSS, they cause pathology only in the superficial epidermis.

Amino Acid Sequence↗