Staphylococcal scalded skin syndrome (SSSS) is a generalized, fused, superficial, exfoliative skin disease caused by the exfoliative toxin (ET) produced by Staphylococcus aureus. The causative organisms are phage group II Staphylococcus aureus, including methicillin-susceptible and methicillin-resistant Staphylococcus aureus. Epidermolytic toxin, also known as epidermolytic toxin, is mainly produced by phage group II type 71 strains and is a serine protease that specifically cleaves pontine core glycoprotein-1 (a protein that is the target antigen of autoantibodies in deciduous aspergillosis), leading to disruption of keratin-forming cell adhesion and loosening of the epidermis. ssss is produced by S. aureus The epidermal exfoliating toxin produced is caused by hematogenous dissemination and is considered to be one of the components of the spectrum of staphylococcal toxin-mediated infections, which also includes pustular impetigo (limited form) and staphylococcal scarlet fever-like dermatitis (tonoplast). SSSS occurs mainly in neonates and children under 6 years of age, and occasionally in adults with chronic renal insufficiency and immunosuppression, possibly due to impaired renal clearance of exfoliative toxins or low titers of exfoliative toxin-specific antibodies. There are gender differences, with a male to female ratio of 2 to 4:1. Clinical manifestations Most often occur in infants 1 week to 5 weeks after birth. Before the onset of the disease, there are often foci of purulent infections in the skin or oral mucosa, such as impetigo, pharyngitis, conjunctivitis, otitis media, etc. The onset of the disease is sudden, with erythema occurring on the face, especially around the mouth or eyelids, then spreading rapidly to the trunk and proximal extremities, or even all over the body, with obvious tenderness on the skin. 1 to 2 days later, loose blisters appear on the basis of the erythema, with oozing and crusting around the mouth and eyes, and large scabs may fall off, leaving radiating chaps around the mouth. The blisters are commonly found on the back of the chest and less frequently on the extremities, and the skin has a wrinkled paper appearance due to the presence of relaxed blisters in the superficial layer of the epidermis. If rubbed hard, the epidermis is peeled off, revealing a bright red edematous erosion, which is positive for Nikolsky’s sign, resembling a burn, and positive for the appearance of uninvolved skin. The epidermal peeling usually occurs first at the flexural site, while the palmoplantar and mucous membranes are not involved. 5-7 d later, the skin of the vesicle dries and flakes, gradually changing from bright red to purplish red, dark red, and no longer peeling. The course of the disease is self-limiting, generally about 7 to 14 d healed, the lesions healed without scarring. Children have fever, anorexia, vomiting, irritability, drowsiness and other systemic symptoms. Individuals with severe disease or weak and young children may die from sepsis, cellulitis, pneumonia, etc. The mortality rate is 3% in children and up to 50% in adults. Laboratory tests 1. Bacterial culture and drug sensitivity test: SSSS is a toxin-mediated disease, therefore, the pathogen cannot be obtained from the culture at the skin lesion. Epidermal exfoliative toxin-producing Staphylococcus aureus can be cultured from sites external to the lesion, most commonly the conjunctiva, nasopharynx, umbilicus, rectum, and blood. Blood cultures are often negative in children, but can be positive in adults. Screening of S. aureus carriers is performed. 2, histopathology: rapid diagnosis can be made by taking frozen sections of the epidermis of the top of the herpes, no epidermal necrosis, epidermal loosening fissures above the granular layer; minimal dermal inflammation. 3, other examinations: blood routine shows that the white blood cell count may be increased or normal; urine routine may show proteinuria; blood biochemical examination of liver and kidney function, electrolytes, C-reactive protein, etc. Differential diagnosis 1.Desquamative erythroderma: It occurs mostly in infants from 2 months to 4 months after birth, with seborrheic dermatitis, erythema often starts on the scalp and trunk, and then progresses to reddish skin all over the body, with fine grayish white scales on the basis of erythema. 2, toxic epidermal necrolysis loosening disease (TEN): mainly caused by drugs, other viruses or vaccines, etc.. The pathogenesis is mainly metamorphic reaction. Mainly occurs in adults, early damage with polymorphic erythema damage, lesions are light to the touch, only the lesions at the Nisei sign positive, mucosal involvement is serious, the course of the disease is generally 1 to 3 weeks. Histology shows total epidermal necrosis and subepidermal blisters located at the epidermal-dermal junction. The mortality rate is high. Treatment Treatment includes antibacterial drugs, supportive therapy, water and electrolyte balance, thermoregulation, nutrition, pain relief and skin care. 1. Systemic treatment: With appropriate treatment, SSSS can subside in 1 to 2 weeks and often leaves no sequelae. Patients with extensive, systemic SSSS should be treated with intravenous β-lactamase-resistant penicillins, such as benzocillin, cloxacillin, dicloxacillin, flucloxacillin; limited SSSS can be treated with oral flucloxacillin (500 mg, 4 times/d) for at least 1 week. This is followed by the use of glycopeptide antibiotics, such as vancomycin. Other drugs include quinolones, tetracyclines, cephalosporins, and aminoglycosides. Also strengthen supportive therapy, pay attention to supplemental fluid and electrolyte balance, and transfuse immunoglobulin, fresh frozen plasma, etc. if necessary. 2.Local treatment: moist, exposed areas should be treated with mild lubricants to reduce friction and unconscious loss of body fluids. Non-adherent dressing is covered on the stripped bare surface to avoid direct contact of the tape with the skin. Topical mupirocin ointment, fusidic acid cream, or compounded polymyxin B ointment may be applied topically. Prevention Nasal Staphylococcus aureus carriers may lead to outbreaks of infection in boils among infants and among postoperative patients, and can also lead to severe infections in immunosuppressed individuals. Carriage rates are higher in patients with renal failure, diabetes, and a history of drug use than in normal subjects, so it is important to remove nasal carriage of S. aureus colonization, which patients apply topically twice daily and family members apply once every 4 weeks. Outbreaks in neonatal nurseries often arise from asymptomatic caregivers and parents carrying virulence-producing strains of S. aureus. Strict infection control measures, including patient isolation, isolation care, and hand washing, are required. Screening procedures can identify carriers of S. aureus among patient contacts, including health care workers. Carriers require topical disinfectants such as chlorhexidine, while nasal carriers are eradicated by topical antimicrobial agents.