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Staphylococcal scalded skin syndrome is a rarely reported superficial desquamating eruption found in patients who have otherwise toxic conditions. Its early recognition and treatment can be lifesaving. A case of staphylococcal scalded skin syndrome is reported in a patient with chronic liver failure.
Staphylococcal Scalded Skin Syndrome (SSSS) is a disease primarily of young children, characterized by exfoliative dermatitis caused by exfoliative toxin producing Staphylococcus aureus. We had three cases of SSSS with varied dermatological manifestations-diffuse/scarlitiniform erythema, generalized exfoliation, sand paper skin texture, flaccid bullae, erosions, seborrheic dermatitis like scaling and cracking in skin creases which can be confused with other skin conditions. Hence, a high index of suspicion, early diagnosis and prompt treatment is imperative.
Staphylococcal scalded skin syndrome (SSSS) may cause significant morbidity in children. It is common practice for adhesive occlusive dressings to be used to apply topical local anaesthetic prior to venepuncture. We report two cases in which removal of these dressings from children with SSSS caused injury and discomfort in areas previously free from blistering. We recommend that an alternative method of topical anaesthetic application is used to minimize skin trauma in these patients.
Staphylococcal scalded skin syndrome (SSSS), not previously recorded as a chronic disease, persisted for 2 years in a 50-year-old woman with epilepsy and cerebellar ataxia. Lesions initially suggestive of erythema multiforme and toxic epidermal necrolysis evolved over 2 years into those typical for SSSS, with extensive erosions and subcorneal blisters, showing an epidermal split at the granular cell layer. Exfoliatin A-producing phage I-III Staphylococcus aureus, previously linked only to acute mild adult cases of SSSS, was cultured from purulent discharge in the patient's eyes, ears and open skin lesions. The roles of epilepsy and antiepileptic medications are discussed as possible predisposing factors.
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.
Staphylococcal scalded skin syndrome describes a spectrum of superficial blistering skin disorders caused by the exfoliative toxins of Staphylococcus aureus. In its severe form, the exfoliation can spread to cover the entire body surface area. Two S. aureus exfoliative toxin serotypes affecting humans have been identified, but their purpose and mechanism of action have remained elusive. Based on their interaction with human and mouse epidermis, their three-dimensional structure and site-directed mutagenesis studies, it is speculated that they act as atypical serine proteases, and desmoglein-1 has now been identified as the specific epidermal substrate. Recent studies also suggest that the toxins may have a unique superantigenic activity. Clinically, new rapid diagnostic tests have been developed, including one that is able to detect the toxins directly from serum. With early diagnosis and appropriate management, mortality in children remains low and long-term complications are rare because the lesions are superficial and heal rapidly without scarring. In adults, however, the condition carries a mortality of almost 60% despite aggressive treatment, usually because of serious underlying illness. The recent developments in our understanding of the exfoliative toxins should lead to new and improved diagnostic and therapeutic strategies, including the use of specific antixoxins to prevent exfoliation.
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Staphylococcal exfoliative toxin (ET) is an extracellular product of Staphylococcus aureus isolated from patients with staphylococcal scalded skin syndrome (SSSS) which includes Ritter's disease, bullous impetigo and staphylococcal scarlet fever, and has been regarded as the causative agent of SSSS. The ET has not only a splitting effect at the granular layer of skin in human and mice but also an immunogenicity to human and mice. Using experimental animals and clinical specimens of patients with or without SSSS, the immunological investigation were performed and following results were obtained. 1) When some inbred and congenic resistant strains of mice were immunized with serotype A ET (ETA), they were divided into the high anti-ETA antibody producers (high responders) and the low responders. The gene controlling antibody response to ETA in mice is located in the I-A subregion in the major histocompatible complex (H-2 complex), and its function seems to be at least related to antigen recognition at the T-lymphocyte level. 2) Neonatal mice are generally susceptible to ETA regardless of their H-2 haplo-type. However, the neonatal mice born to a high-responder mother immunized with ETA were resistant to the subcutaneous challenge of ETA, but those born to an immunized low-responder mother were susceptible to the challenge. 3) The relationship between susceptibility and immune response to ETA in some mammalians could be divided into three groups: the possession of resistant skin and high production of antibody to ETA (rabbits and rats); the possession of resistant skin and low production of antibody to ETA (golden hamsters and guinea pigs); the possession of sensitive skin and various titers of antibody to ETA (humans and mice). 4) The incidence of ET producing strains of Staphylococcus aureus in various clinical specimens obtained from patients without SSSS was 12% (50 out of 418 strains) in our epidemiological investigation. The percentages of antibody to ETA in sera obtained from healthy males and females were 23% and 29%, respectively. Eventually, ET-producing strains of Staphylococcus aureus seem to be spread out wider than the microbiological result obtained from clinical specimens. 5) The mitogenic responses of lymphocytes isolated from patients with the first impetigo could be measured by using PHA, and the five-of them were in the low range, whereas lymphocytes from patients with recurrent impetigo were in the normal range on this survey. Maybe this results suggest the T lymphocyte functions of some patients with impetigo are deteriorated.(ABSTRACT TRUNCATED AT 400 WORDS)
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.
Staphylococcal scalded skin syndrome (SSSS) is a disease that usually affects infants and young children who lack the antibodies to Staphylococcus aureus toxins that adults have. It is caused by bacterial infection by group II S. aureus that produces toxins that cause exfoliation, bullae (blister) formation and redness of skin. In children mortality is low, but can be high in adults, who will usually have a serious underlying disease that makes them susceptible to infection (Kim, 2002; Ladhani and Joannu, 2000).
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.
Staphylococcal scalded skin syndrome is a toxin mediated Staphylococcal infection, the toxin produced by staphylococcus aureus type 2 phage types (55,71,3A,3B,3C). There is a generalized tender erythema which commences on the head and neck, accompanied by fever, irritability, continuous cry and miserable look. The erythema is followed by cleavage of the upper epidermis in a large sheets mainly in the head, neck and the flexures, with formation of bullae (Nikolsky sign). It is most common in infants and children under 5 years. Most cases respond to antibiotics with other supportive measures. The prognosis is good, and the skin lesions disappear without a residual scar.
Staphylococcal scalded skin syndrome (SSSS) is a common disorder that is usually seen in infants and children and rarely seen in adults. SSSS usually presents with a prodrome of sore throat or conjunctivitis. Extremely tender flaccid bullae, which are Nikolsky sign-positive, develop within 48 hours and commonly affect the flexures; occasionally, large areas of the skin may be involved. The bullae enlarge and rupture easily to reveal a moist erythematous base, which gives rise to the scalded appearance. SSSS in adults is a rare disorder, though there are now over 50 documented cases. Usually SSSS occurs in predisposed individuals, but not all adults have an underlying illness. Whereas mortality in childhood SSSS is approximately 4%, the mortality rate in adults is reported to be greater than 60%. SSSS is caused by an infection with a particular strain of Staphylococcus aureus, which leads to blistering of the upper layer of the skin, by the release of a circulating exotoxin. It has recently been demonstrated that the exfoliative exotoxin responsible for SSSS leads to the cleavage of desmoglein 1 complex, an important desmosomal protein. The same toxins that are responsible for causing SSSS also cause bullous impetigo. There appears to be a relationship between the disease extent, the amount of toxin produced and whether the toxin is released locally or systemically. As a result there is likely to be a spectrum of disease and there are likely to be a number of milder cases of adult SSSS that go undiagnosed. Social improvements and hygiene have led to a dramatic fall in the number of cases of SSSS. Treatment is usually straightforward, when there is no coexistent morbidity and the presentation is mild, but can be demanding if the patient is particularly ill. SSSS is still associated with mortality, particularly when it occurs in adults.
Staphylococcal scalded skin syndrome, a generalized exfoliative dermatitis complicating infections by exfoliative toxin-producing strains of Staphylococcus aureus, is rarely observed in adults. In contrast to mortality in infants, mortality in adults is usually high. A case of generalized staphylococcal scalded skin syndrome in an immunocompromised woman is reported. Culture of skin biopsy and pleural fluid yielded identical strains of staphylococcus aureus belonging to phage group II. Exfoliative toxins A and B were detected in both isolates. As far as can be determined, this is the first reported case of generalized staphylococcal scalded skin syndrome in an adult with detection of exfoliate toxins A and B in which the patient was treated successfully.
In order to study the differences between staphylococcal scalded skin syndrome (SSSS) and bullous impetigo, the anti exfoliatin level was assessed in the sera from both groups of patients, and no significant difference in the level was found. However a significant difference was noted in the anti alpha-toxin levels in sera from both group of patients; that of SSSS patients was much lower than that of impetigo patients and of children in a control group. Five out of 6 patients with SSSS showed an unchaged level of anti alpha-toxin at the second examination, while an increased anti exfoliatin level was noted in 4 out of 6 SSSS patients.
Prevention of progression of staphylococcal scalded skin syndrome by molluscum contagiosum indicated a possible interference by viral anti-cytokine molecule such as interleukin-18 binding protein.
The diagnosis of staphylococcal scalded skin syndrome is usually made upon the bases of characteristic skin lesions and the isolation of toxin-producing staphylococci. However, these criteria are not always reliable. An adult patient with characteristic skin lesions was colonized with phage group 2 staphylococci. The patient was subsequently found to have a drug-induced toxic epidermal necrolysis. The criteria necessary for the diagnosis of staphylococcal scalded skin syndrome are reviewed.
The production of staphylococcal exfoliative toxin A (ETA) and toxin B (ETB), toxic shock syndrome toxin (TSST-1), and enterotoxins A-E was analyzed in 60 Staphylococcus aureus strains isolated from children with scalded skin syndrome (15 with generalized exfoliative syndrome, 28 with bullous impetigo, and 17 with staphylococcal scarlet fever). All strains isolated from patients with generalized exfoliative syndrome or bullous impetigo produced ETA and/or ETB and caused a Nikolsky's sign when injected subcutaneously into newborn mice. In contrast, exfoliative toxin was detected in an S. aureus strain from only one of 17 case of staphylococcal scarlet fever; the 16 other S. aureus strains produced TSST-1 and/or an enterotoxin. In conclusion, enterotoxins or TSST-1 are more frequently associated with staphylococcal scarlet fever than are exfoliative toxins. Hence staphylococcal scarlet fever may well represent an abortive form of toxic shock syndrome rather than a milder form of staphylococcal scalded skin syndrome.