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Staphylococcal Scalded Skin Syndrome
Introduction
Staphylococcal scalded skin syndrome (SSSS), also known as Ritter disease or pemphigus neonatorum, is a dangerous cutaneous infection caused by certain exotoxin-producing strains of Staphylococcus species (see Image. Staphylococcal Scalded Skin Syndrome).[1] The condition typically presents with superficial skin blistering and denudation and affects children more often than adults. In adults, SSSS is often associated with renal dysfunction or immunocompromise.[2][3]
Skin desquamation is typically caused by exotoxins from a distant location rather than a local infection spreading through the bloodstream.[4][5] In the pediatric population, SSSS can present as early as 48 hours after birth and occurs less frequently in children older than 6.[6] Staphylococcal scalded skin syndrome is primarily diagnosed clinically, with diagnostic evaluation aimed at detecting bacteremia, differentiating it from similar conditions such as bullous impetigo, and guiding appropriate treatment. Therapy includes antibiotics, specifically penicillinase-resistant penicillins, supportive care, and monitoring for possible sequelae, including hypothermia, hemodynamic instability, and relapse.
Etiology
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Etiology
Staphylococcus aureus, a gram-positive coccus, causes most cases of SSSS. Many individuals are colonized, particularly in areas such as the umbilicus, groin, buttocks, and the face, especially the nares.[7][8] Methicillin-sensitive S aureus is more commonly identified than methicillin-resistant S aureus.[9] Exfoliative or epidermolytic exotoxins A and B are serine proteases released by S aureus at the primary infection site. The primary infection source is often located away from the areas of skin denudation; however, in many cases, no specific source is identified. The bacteria may originate from sites such as the upper respiratory tract, ears, and eyes, or abscesses, fistulas, or joint infections.[10]
These toxins are produced by less than 5% of Staphylococcus species, although all species produce some form of toxin.[11][12][13] Phage group II types 3A, 3B, 3C, 55, and 71, along with the strain ST121, are the most likely S aureus species implicated in producing exotoxins A and B.[14][15][16] The accumulated toxins directly target cadherin desmoglein-1 at distant sites after hematogenous dissemination, leading to the loss of cellular adhesion among keratinocytes in the stratum granulosum. Notably, desmoglein-3, which predominates in the lower epidermis, is not affected by the exotoxins A and B produced by S aureus.[17][18][19] However, testing for the specific phage type is often not helpful or available.
Epidemiology
The incidence of SSSS is low. Results from a study in the Czech Republic reported an incidence of approximately 25 cases per 100,000 children younger than 1 year.[20] Most cases involve children younger than 5 years, with most cases occurring before 3 years. However, neonates are relatively protected from SSSS due to the predominance of desmoglein-3 in the epidermis, which is not targeted by staphylococcal exotoxins.[21][22] The disease is much less common in adults due to the presence of neutralizing antibodies and mature kidney function, which enable efficient clearance of exotoxins from the bloodstream.[23] Thus, SSSS in adults typically affects individuals with immunosuppression, including people with human immunodeficiency virus/acquired immunodeficiency virus and advanced malignancies or those with severe kidney impairment.[24] A predominance among men is observed, with a ratio of 2:1 in sporadic cases and 4:1 in epidemics.[25] SSSS may occur as an outbreak in daycares or nurseries. The frequent occurrence of prodromal symptoms resembling those of upper respiratory viral infections, such as fever and irritability, has led some authors to suggest a role for viral infections as promoters of the proliferation of exotoxin-producing strains of S aureus. Viral coinfection may explain the autumnal predominance of the condition and the prodromal upper respiratory infection symptoms observed in patients with SSSS.
Pathophysiology
The majority of SSSS cases are attributed to S aureus phage group II types 55 and 71, which may exhibit methicillin sensitivity or resistance. These organisms produce exfoliative, or epidermolytic, toxins. The 2 main types—one encoded on the bacterial chromosome and the other on a plasmid—are serine proteases that selectively bind to and cleave desmoglein-1 (Dsg1), a key protein in skin cell adhesion. This results in the separation of desmosomes, leading to the rupture of the epidermal layer and the creation of bullae. Dsg1 is also the target of autoantibodies in pemphigus foliaceus, which has histologic characteristics identical to those of SSSS. Young children possess a relatively low concentration of Dsg1 and exhibit diminished renal clearance of exfoliative toxins, which heightens their susceptibility to SSSS, whereas adults are more prone to harbor anti-exfoliative toxin antibodies.
Unlike bullous impetigo, in which the effects of the exotoxins are confined to the infection site, in SSSS, the toxin disseminates from the infection nidus and distributes hematogenously, resulting in extensive consequences. In infants, the site of infection is typically located in the nasopharynx or conjunctivae, while adults may exhibit staphylococcal pneumonia or bacteremia.[26] Neonates during the initial weeks of life possess a degree of protection against SSSS, according to the widespread presence of Dsg3 in the epidermis. In contrast, Dsg3 is exclusively found in the deep epidermis of adult skin. By the conclusion of the neonatal period and during infancy, infants face a heightened risk when the relative concentration of Dsg1 in the upper layers of the epidermis starts to shift towards that of adult skin.[1]
Histopathology
SSSS is primarily diagnosed based on clinical presentation and rarely requires further testing; however, a skin biopsy may be helpful in uncertain cases to support the diagnosis. Histopathological evaluation of a skin biopsy from a patient with SSSS typically reveals superficial intraepidermal cleavage beneath the stratum corneum.[27] Cleavage at the stratum granulosum may show sparse neutrophils or a mixed inflammatory infiltrate, complicating the diagnosis in adult patients with coexisting conditions, such as malignancy, where toxic erythema of chemotherapy may present similarly.[28] However, inflammatory cells are usually absent in the bullae, and the upper dermis is devoid of inflammatory infiltrate. No organisms are observed on the Gram stain of biopsy specimens.
History and Physical
A prodrome to SSSS frequently includes malaise, fever, agitation, and skin tenderness. The patient may exhibit purulent rhinorrhea or conjunctivitis as a manifestation of the underlying staphylococcal infection. Erythema typically initially manifests on the head, commonly accompanied by varying degrees of facial edema, and in intertriginous areas, frequently spreading to other areas within 48 hours. The skin subsequently acquires a wrinkled look due to the production of flaccid, sterile bullae inside the superficial epidermis. A positive Nikolsky sign is present. Traditionally, the flexural regions are the initial sites of exfoliation, resulting in moist skin and a delicate, varnish-like crust. Patients exhibit distinctive periorificial (eg, perioral, periocular) crusting and radial fissuring. Intraoral lesions are absent. Scaling and desquamation persist for 3 to 5 days, followed by re-epithelialization without scarring. Adults exhibit findings similar to those seen in children.[29]
Evaluation
SSSS is primarily diagnosed clinically, though additional evaluation may be useful in select cases where diagnostic uncertainty exists. As with other systemic illnesses, clinicians may perform routine blood tests, including a complete blood count, urinalysis, comprehensive metabolic profile, and blood cultures. Blood cultures typically provide limited information since the toxins, not the organisms, spread hematogenously. Although blood and blister fluid cultures are typically negative, they may yield positive results in adults, particularly in cases complicated by sepsis due to bacteremia.
Despite negative cultures from complete bullae, S aureus may be isolated from the conjunctiva, nasopharynx, perianal region, or pyogenic foci on the skin. Adults with severe disease may require additional evaluation to identify a source of infection, such as infected fistulae in patients with renal failure, bacteremia, or septic arthritis. The leukocyte count may be either elevated or within the normal range. The analysis of frozen sections is sometimes beneficial in verifying the location of the split within the bullae. Slide latex agglutination, double immunodiffusion, or enzyme-linked immunosorbent assay tests can detect the toxins responsible for SSSS.
Treatment / Management
Patients exhibiting severe, generalized manifestations of SSSS necessitate hospitalization and intravenous antibiotics. Admission to an intensive care unit may be necessary, as saline-soaked gauze and wound care may be required.[30] Emollients and nonadherent dressings should be applied to denuded areas to promote healing and reduce heat loss. Supportive care, including management of dehydration, temperature regulation, and nutrition, proves essential. Patients with significant skin involvement are prone to hypothermia and fluid deficits due to epidermal loss. Intravenous fluids become necessary for patients showing signs of dehydration or sepsis. Some children may require intravenous immunoglobulin or fresh frozen plasma to address volume loss. The identification and decontamination of S aureus carriers are crucial, particularly in instances of hospital-acquired infections.[31](B2)
Oral administration of a β-lactamase-resistant penicillin or first-generation cephalosporin for at least one week is typically adequate for milder cases. Antibiotics effective against methicillin-sensitive Staphylococcus aureus, such as cefazolin, nafcillin, and oxacillin, should be administered promptly. In children, nafcillin or oxacillin should be initiated at 100 to 150 mg/kg daily, divided every 6 hours. Cefazolin should be administered at 50 to 100 mg/kg daily, divided every 8 hours. Oral alternatives, such as cephalexin or dicloxacillin, at 500 mg every 6 hours, or trimethoprim/sulfamethoxazole at 160/800 mg every 12 hours, may be used for mild infections.
SSSS may occasionally be attributed to methicillin-resistant Staphylococcus aureus (MRSA). Vancomycin should be administered if MRSA is suspected, particularly in patients with recent healthcare exposure, including those residing in a skilled nursing facility, recently hospitalized, or living in areas with a high MRSA prevalence.[32] Treatment should continue for 10 days unless clinical judgment dictates a longer course. Additional antibiotics with Pseudomonas coverage should be initiated if concern arises for a secondary bacterial skin infection.
The application of silver sulfadiazine should be avoided due to the potential for increased systemic absorption and resultant toxicity.[33] Acetaminophen and opioids may be needed for pain control, but nonsteroidal anti-inflammatory drugs, such as ibuprofen, should be avoided due to the risk of kidney impairment. Clindamycin administration may diminish bacterial toxin production; however, up to 50% of strains associated with SSSS have clindamycin resistance, rendering monotherapy with this medication inadvisable. Topical antimicrobial therapies are generally ineffective, though they may be used for decolonization at the primary site of infection.[34](B2)
Differential Diagnosis
A thorough clinical investigation and judicious diagnostic testing can differentiate SSSS from similar conditions, guide therapeutic strategies, and improve outcomes. The differential diagnosis should include:
- Drug reaction
- Viral exanthem
- Sunburn
- Graft-versus-host disease
- Pemphigus foliaceus
- Bullous impetigo is typically seen in newborns and also results from cleavage of desmoglein-1. However, this condition features a large dermal inflammatory infiltrate and demonstrates a negative Nikolsky sign.[35]
- Stevens-Johnson syndrome and toxic epidermal necrolysis present with dusky areas that show necrotic keratinocytes. As opposed to clinical patterns associated with SSSS, Stevens-Johnson syndrome and toxic epidermal necrolysis are commonly linked to medications and affect older children and adults.[36]
- Acute generalized exanthematous pustulosis occurs more frequently in women. This disorder is characterized by nonfollicular pustules on flexural sites, exhibiting subcorneal pustules with eosinophilic and neutrophilic inflammation on biopsy.[37][38]
- Toxic shock syndrome may be caused by S aureus, by a mechanism involving the toxic shock syndrome toxin-1, or by Streptococcus pyogenes. This condition presents with necrolysis of keratinocytes, fever, hypotension, and involvement of multiple organ systems.[39][40]
- Kawasaki disease affects a similar age group and is diagnosed based on criteria that include a fever lasting 5 days and at least 4 minor criteria, one of which is acral desquamation.[41][42]
- Scarlet fever, caused by S pyogenes, typically affects older children. This condition presents with flu-like symptoms followed by a characteristic sandpaper rash.[43]
Prognosis
With appropriate therapy, SSSS typically disappears within 1 to 2 weeks, generally without complications. Pediatric patients generally do well with minimal to no scarring. The mortality rate is less than or equal to 4% for children but may reach 50% in adults, attributable to underlying comorbidities.[30] The recurrence of SSSS is very rare, with only a few cases documented in the literature. Relapse can be prevented through the use of appropriate hygiene practices, including the use of barrier methods, regular hand washing, and meticulous equipment cleaning.[1]
Complications
Potential complications of SSSS include:
- Dehydration
- Secondary infections
- Electrolyte imbalance
- Sepsis
- Acute kidney injury
- Scarring [44]
Consultations
If the diagnosis is uncertain, consultation with a dermatologist is recommended. In severe cases, involving burn centers, specialized burn units, or critical care clinicians is essential for comprehensive management.
Deterrence and Patient Education
Preventing SSSS in children and adults involves practicing good hygiene, including regular handwashing and proper wound care. Parents and caregivers should keep the skin clean and monitor for any signs of infection, especially in children with cutaneous disorders such as eczema. Additionally, limiting exposure to infected individuals and maintaining good sanitation can help minimize the risk of transmission. Strict adherence to infection control protocols is critical to prevent outbreaks in healthcare settings.
Enhancing Healthcare Team Outcomes
SSSS cases should be approached as a team, particularly with complex cases. Expert consultation with dermatologists can help eliminate alternative diagnoses and guide treatment. Colonized caregivers and individuals with patient contact require treatment with chlorhexidine. Nasal carriers should be treated with topical mupirocin. The mortality is relatively low in children when appropriate treatment is initiated, but it is much higher in adults, even with appropriate antibiotics and supportive therapy.[45][46] In severe cases, referral to a burn center with wound care experts should be strongly considered to reduce fluid losses and prevent scarring.
Effective management of SSSS requires the timely identification and coordination of efforts across an interprofessional healthcare team. Initial recognition typically begins with primary care clinicians and nurses, who should be trained to spot characteristic symptoms like skin redness, blistering, and peeling, especially in pediatric or immunocompromised individuals. If SSSS is suspected, the clinician should quickly refer the patient to appropriate specialists, such as dermatologists and infectious disease experts, for further diagnostic support, including skin biopsies or cultures to confirm the presence of S aureus. Lab technicians also play a crucial role in analyzing samples, while infectious disease specialists may help guide the choice of antibiotics. Immediate referral to an emergency department is appropriate for the rapid stabilization and treatment of severe cases.
In cases requiring hospitalization, collaboration among the inpatient nursing team, pharmacists, and nutritionists is crucial to managing symptoms, administering antibiotics, and addressing hydration and nutritional needs resulting from potential fluid loss due to damaged skin. All team members should maintain thorough documentation in electronic health records throughout the process to support clear communication and effective care coordination. Once the patient stabilizes, discharge coordinators help arrange follow-up care and provide guidance on wound care and infection prevention. This team-based approach, supported by structured referral pathways and regular interdisciplinary communication, ensures comprehensive care for patients with SSSS, optimizing recovery and reducing the risk of complications.
Media
(Click Image to Enlarge)
Staphylococcal Scalded Skin Syndrome. This young patient exhibits signs and symptoms of staphylococcal scalded skin syndrome.
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