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PubMed2004

Defining the pathogenic involvement of desmoglein 4 in pemphigus and staphylococcal scalded skin syndrome.

Desmogleins (Dsgs), cadherin-type cell adhesion molecules, are targeted in skin-blistering diseases such as pemphigus and staphylococcal scalded skin syndrome (SSSS). The role of Dsg4, a new isoform, was investigated in these diseases. Dsg4 was recognized by 30 (77%) of 39 pemphigus sera containing anti-Dsg1 IgG but not by 16 pemphigus sera containing no anti-Dsg1 IgG or by 34 normal control sera. The Dsg4 immunoreactivity of these sera was abolished by removal of anti-Dsg1 IgG. Conversely, the removal of anti-Dsg4 IgG from pemphigus sera reduced the immunoreactivity against Dsg1 only 13.8% +/- 8.8% (n = 23) and did not affect its ability to induce blisters in neonatal mice. IgG that was affinity-purified on Dsg4 recognized Dsg1 but failed to induce blisters, while IgG purified on Dsg1 from the same pemphigus foliaceus sera induced blisters. Thus, pemphigus sera show Dsg4 reactivity due to cross-reactivity of a subset of anti-Dsg1 IgG, and the Dsg4/Dsg1-cross-reacting IgG has no demonstrable pathogenic effect. In addition, Dsg4 was not cleaved by exfoliative toxins that induce blisters in SSSS. These findings suggest that Dsg4 may play a role other than adhesion and that the cross-reactivity of desmoglein autoantibodies should be factored into the framework of future studies of autoimmune mechanisms in pemphigus.

Amino Acid Sequence↗
PubMed2004

Treatment of staphylococcal scalded skin syndrome.

Humans are a natural reservoir for Staphylococcal aureus. Colonization begins soon after birth and predisposes to infection. S. aureus is one of the most common causes of skin infection, giving rise to folliculitis, furunculosis, carbuncles, ecthyma, impetigo, cellulitis and abscesses. In addition, S. aureus may cause a number of toxin-mediated life-threatening diseases, including staphylococcal scalded skin syndrome (SSSS). Epidermolytic toxins released by certain S. aureus strains cause SSSS by cleaving the epidermal cell adhesion molecule, desmogelin-1, resulting in superficial skin erosion. Recent experiments have revealed similarities in the pathophysiology of SSSS and pemphigus foliaceus, an autoimmune disorder that is characterized by antibodies targeting the same epidermal attachment protein. SSSS typically affects neonates and infants but may also occur in predisposed adults. It is painful and distressing for the patient and parents, although most cases respond to antibiotic treatment. Mortality is low in infants but can be as high as 67% in adults, and is dependent on the extent of skin involvement and the comorbid state. Thus, the management of adults who develop SSSS remains a major therapeutic challenge. The antibody response against the toxins neutralizes their effect and prevents recurrence or limits the effects to the area of infection, which is known as bullous impetigo.

Animals↗
PubMed2000

Staphylococcal scalded skin syndrome with prosthetic valve endocarditis.

We report staphylococcal scalded skin syndrome (SSSS) in a 67-year-old man. He showed diffuse erythema with erosion on his face and erythema with giant desquamation on his neck, axilla, genitalia, chest and abdomen 39 days after a coronary artery bypass graft and aortic valve replacement. He died of cardiac rupture caused by myocardial necrosis, and autopsy findings demonstrated prosthetic valve endocarditis due to a strain of exfoliative toxin-B producing methicillin-resistant Staphylococcus aureus. To the best of our knowledge, this is the first case of SSSS caused by prosthetic valve endocarditis.

Aged↗
PubMed2003

Neonatal Staphylococcal scalded skin syndrome complicating ileal atresia.

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.

Anti-Bacterial Agents↗
PubMedDate not supplied

The management of staphylococcal scalded skin syndrome in infants.

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).

Analgesia↗
PubMed2004

Congenital staphylococcal scalded skin syndrome in a premature infant.

UNLABELLED: A case of congenital staphylococcal scalded skin syndrome (SSSS) with fatal outcome in a premature infant is reported. An intrauterine infection with Staphylococcus aureus was probably the cause for the fulminant course of the disease. Despite adequate antibiotic treatment, the infant died within 24 h after birth because of respiratory failure. CONCLUSION: Although rare, infection may occur in the perinatal period and SSSS may present within the first 24 h of life. In this situation, early administering of appropriate antibiotics is essential.

Fatal Outcome↗
PubMed1990

Concomitant disseminated varicella and generalized staphylococcal scalded skin syndrome in a leukemic patient.

We report a case of nosocomial fatal varicella infection in a 13-year-old boy with acute lymphoblastic leukemia complicated with staphylococcal scalded skin syndrome. His underlying leukemia, immunosuppressive drugs, disseminated varicella, S. aureus colonization, and acute renal insufficiency were all contributing factors that were pathogenetically linked in the development of his generalized SSSS.

Adolescent↗
PubMed1989

Staphylococcal scalded skin syndrome mimicking acute graft-vs-host disease in a bone marrow transplant recipient.

A 33-year-old man with mild acute graft-vs-host disease after an allogeneic bone marrow transplant for chronic myelogenous leukemia developed a necrolytic rash 90 days after transplant. A diagnosis of staphylococcal scalded skin syndrome was made when a skin biopsy specimen revealed a split in the granular layer and phage group 2, type 71 Staphylococcus aureus was cultured from the blood.

Acute Disease↗
PubMed1989

[Staphylococcal scalded skin syndrome in 2 adults with acute kidney failure].

We report on two cases of staphylococcal scalded skin syndrome (SSSS) in adults. In contrast to the previously reported cases our patients were neither immunosuppressed nor haemodialysed, nor did they have cancer. In both cases, acute renal failure in the presence of a rather banal staphylococcal infection preceded the SSSS. The pathogenic role of acute renal failure in the development of SSSS is discussed.

Acute Kidney Injury↗
PubMed1995

[Immunological investigations on pathogenesis of staphylococcal scalded skin syndrome].

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)

Adult↗
PubMed1996

Staphylococcal scalded skin syndrome in an HIV-1 seropositive man.

The staphylococcal scalded skin syndrome (SSSS) is very rare in adults. Renal impairment and immunocompromise are predisposing causes. We report a 38-year-old HIV-1 seropositive intravenous drug abuser who developed SSSS due to staphylococcal pneumonia. An exfoliating toxin-releasing Staphylococcus aureus, phage type II type 3C, was isolated from the sputum and from blood cultures. This is the third case of adult SSSS to be reported in the context of HIV disease.

AIDS-Related Opportunistic Infections↗
PubMed1998

Staphylococcal scalded skin syndrome in an immunocompetent adult: possible implication of low-dosage prednisone.

Staphylococcal scalded skin syndrome (SSSS) mainly affects infants and young children. Very few cases of adult SSSS have been reported. Adult SSSS is usually associated with immunosuppression, overwhelming sepsis, and kidney failure. We report the case of an immunocompetent 51-year-old woman without renal failure who sustained SSSS after a 7-day course of oral prednisone administered postoperatively.

Administration, Oral↗
PubMed1977

Staphylococcal scalded skin syndrome. Clinical features, pathogenesis, and recent microbiological and biochemical developments.

The essential clinical features of staphylococcal scalded skin syndrome (SSSS) and otherforms of toxic epidermal necrolysis (TEN) are contrasted. Whereas TEN is a devastating disease of multiple causes and of high fatality affecting all age groups, SSSS comprises many clinical entitles that occur primarily in early childhood and is caused by certain phage group 2 staphylococci. Because of the high cleavage plane, the barrier is only translently perturbed, and rapid recovery is the rule. Although the early stages of SSSS may resemble other widespread dermatoses clinically, the correct diagnosis is suggested, even prior to frank exfoliation, by the presence of cutaneous tenderness and a positive Nikolski sign. However, rapid bedside confirmation is now possible with exfoliative cytology and frozen sections. Recent availability of in vivo and in vitro animal models of SSSS have advanced the knowledge of the disease: the responsible epidermolytic toxin has been characterized, and the purely extracellular pathogenesis of SSSS has been established. The epidermolytic toxin is strikingly species and tissue specific, attacking only certain keratinizing epithelia of mice, hamsters, monkeys, and man. The lower incidence of SSSS in adults is primarily due to a supreior capacity to metabolize and excrete the toxin, as well as more efficient immune capabilities. The mechanisms of epidermolytic toxin action and the molecular site of action are still the focus of active investigation.

Animals↗
PubMed1993

Metabolic changes in cimetidine treatment for scald injury on the peritoneo-serosal surface in far-advanced gastric cancer patients treated by intraperitoneal hyperthermic perfusion.

Since pretreatment with cimetidine results in the prevention of scald injury on the peritoneo-serosal surface caused by intraperitoneal hyperthermic perfusion (IPHP) for advanced gastric cancer, the diverse influence of IPHP on patients who were either given or not given cimetidine was studied both during and after IPHP treatment. Cimetidine 50 mg/kg was injected intravenously into 12 patients immediately prior to IPHP. There were no statistical background differences between the cimetidine and control groups (those not given cimetidine). The inflow and outflow temperatures of the hyperthermic perfusate in the control and cimetidine groups were 46.1 +/- 0.1 degree C and 44.1 +/- 0.1 degree C and 46.3 +/- 0.1 degree C and 44.2 +/- 0.04 degree C, respectively. Either the pre-IPHP hypothermia or IPHP in the control group resulted in a considerable increase in serum noradrenaline and adrenaline. The intravenous administration of cimetidine led to a stransient but moderate drop in the mean blood pressure as well as a delayed appearance of high concentrations of noradrenaline and adrenaline, induced by high concentrations of circulating histamine released with cimetidine. These results suggest that the sympathetic nervous responses were activated either by hypothermia or hyperthermia. The transient hypotension and delayed increases of both serum catecholamines were attributed to a marked increase in circulating histamine, released with the intravenous cimetidine.

Blood Pressure↗
PubMed1977

Abnormal neutrophil chemotaxis and T-lymphocyte function in staphylococcal scalded skin syndrome in an adult patient.

Staphylococcal scalded skin syndrome, a disease rarely reported in adults, developed in a 38-year-old male while on steroid therapy for chronic active hepatitis. Studies of immunologic parameters important in staphylococcal host defense revealed normal opsonic activity and phagocytic function but marked defects in neutrophil chemotaxis and T-lymphocyte function. Compromised host defense appears to play a significant role in the pathogenesis of the syndrome in adults.

Adult↗
PubMed1978

[Deadly scald or Lyell syndrome? (author's transl)].

The changes of skin of the Lyell Syndrome have an extreme likeness with those of a 2nd degree scald. As this illness is more frequently observed as of late, it may get forensic importance. Based on the case of a man, 48 years of age, who suddenly died without previous diagnosis and therapy the aetiologic and morphological problems are discussed.

Burns↗