|Year : 2016 | Volume
| Issue : 8 | Page : 66-68
Staphylococcal scalded skin syndrome in a neonate following prolong labor
Zarak Hassan Khan, Haider Ghazanfar, Hamza Hassan Khan
Department of Pediatrics, Shifa College of Medicine, Islamabad, Pakistan
|Date of Web Publication||3-Jan-2017|
House Number 19, Askari Villas, Chaklala Scheme 3, Rawalpindi
Source of Support: None, Conflict of Interest: None
Staphylococcal scalded skin syndrome (SSSS) encompasses a spectrum of superficial blistering skin disorders caused by the exfoliative toxins (ETs) of some strains of Staphylococcus aureus. In this case report, we present a case of SSSS in an 8-day-old neonate. Furthermore, we tried to highlight the importance of early diagnosis by history and physical examination and isolation of the infected neonates because of the risk of spread of infection to other neonates in the Neonatal Intensive Care Unit.
Keywords: Mortality, newborn, staphylococcal scalded skin syndrome
|How to cite this article:|
Khan ZH, Ghazanfar H, Khan HH. Staphylococcal scalded skin syndrome in a neonate following prolong labor. N Niger J Clin Res 2016;5:66-8
| Introduction|| |
Staphylococcal scalded skin syndrome (SSSS) encompasses a spectrum of superficial blistering skin disorders caused by the exfoliative toxins (ETs) of some strains of Staphylococcus aureus.  Mortality in children with SSSS is approximately 4%.  The data about SSSS on neonate are limited. Inadequate immunity and immature renal clearance of exotoxin can increase the chance of development of SSSS in neonates.  The severity of SSSS varies from a few localized blisters to severe exfoliation affecting the entire body.  In this case report, we present a case of SSSS in a neonate. Furthermore, we tried to highlight the importance of early diagnosis by history and physical examination because of the risk of spread of infection to other neonates in the Neonatal Intensive Care Unit (NICU). 
| Case Report|| |
An 8-day-old male neonate presented with erupted skin lesions since birth with bullous formations. He was born at full term through spontaneous vaginal delivery after 9 h of ruptured membranes in a local clinic. Initially, there was a small vesicular lesion on one foot that later on appeared on both the legs, and it eventually spread to the rest of the body. There was no family history of similar skin lesions. On examination, the child was toxic looking and irritable and had a fever of 103 F. Respiratory rate was 33 breaths/min while pulse rate was 124 beats/min. His weight was 3.2 kg while his length was 50 cm. The patient had conjunctivitis in both his eyes. Diffuse erythematous lesions were present all over the body [Figure 1] and [Figure 2].
There was perioral crusting but the oral mucosa was normal. Nikolsky's sign was positive.  Provisional diagnosis of SSSS was made. The baby was admitted to isolation in the NICU and placed in an incubator. X-ray was done to rule out pneumonia as a source of infection. Complete blood count, electrolytes, urine routine examination, urine culture/sensitivity (C/S), and blood C/S were done and the child was started on ceftriaxone, cloxacillin, and intravenous fluids. Strict temperature regulation was done to prevent the development of hypothermia. Daily dressings with Vaseline and Bactroban were done. Blood and conjunctival C/S yielded growth of S. aureus which was sensitive to ceftriaxone. The lesions started to heal after 7 days. The child became afebrile on the 8 th day and was tolerating oral feed. The child was discharged on the 10 th day on syrup cephalexin (125 mg/5 ml) 2.5 ml two times a day for 5 days and was advised daily dressing with Vaseline and Bactroban until the lesions completely disappear. The child was advised on follow-up after a week time. The parents were counseled about the child disease and were advised to come to pediatric emergency room in case the condition of the child worsened. The patient recovered completely after 3 weeks from the onset of the symptoms.
| Discussion|| |
The epidermolytic toxin produced by the S. aureus causes separation of the epidermis beneath the granular cell layer of the skin, which leads to bullae formation and diffuse desquamation of the skin. The severity of the disease depends on the amount of toxin produced and whether the toxin was released locally or systemically.  Ritter's disease of the newborn is the most severe form of SSSS. Phage lytic Group II is the most common strain of S. aureus isolated from patients suffering from SSSS.  Exfoliative toxin acts as proteases which target desmogein-1 (DG-1), an important keratinocyte cell to cell attachment protein in the superficial epidermis.  The increased frequency of SSSS in neonates can be explained due to relatively increased quantity of DG-1, immature renal function in this age group, and absence of antibodies specific for exotoxins. , Bullous impetigo differs from SSSS because in bullous impetigo the infection is restricted to the area of infection.
SSSS clinical presentation includes fever, tenderness to palpation, facial edema, conjunctivitis, perioral crusting with mucous membranes being spared, dehydration, Nikolsky's sign, and diffuse erythematous rash which begins centrally, is sandpaper like in appearance and accentuated in flexor crease. Patient with SSSS have impaired temperature control, can lose an extensive amount of fluids, and are vulnerable to secondary infection. These complications significantly contribute to high mortality associated with SSSS. 
The diagnosis of SSSS is made on a clinical basis.  It is further confirmed by demonstration of staphylococcal infection. In our case, the conjunctiva and blood culture came out to be positive for S. aureus. A chest radiograph should be considered to rule out pneumonia as the focus of infection. The result of chest radiograph in our patient was unremarkable.
Parental anti-staphylococcal antibiotics, fluid and electrolyte balance, temperature regulation, nutritional management, and skin care are the fundamental treatment for patients with SSSS. Topical antibiotics are advised for conjunctivitis. Incubator should be used to maintain temperature. Sterile wrapping and minimal handling of the neonate is advised to decrease the chance of secondary complications associated with SSSS. Neonates affected with SSSS should be isolated from other neonates to decrease the chance of spread of infection.
Early diagnosis and prompt treatment remarkably improve the outcome of patients with SSSS. The mortality of SSSS in neonates who are treated properly is less than 5%.  The erythroderma usually decreases within 7-10 days with complete resolution in 3 weeks' time. Our case followed a similar course.
| Conclusion|| |
SSSS is a life-threatening condition and is associated with high mortality if not managed properly. Early diagnosis and prompt treatment remarkably improve the outcome of patients with SSSS. Isolating neonates are imperative to prevent transmission of SSSS.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Murono K, Fujita K, Yoshioka H. Microbiologic characteristics of exfoliative toxin-producing Staphylococcus aureus
. Pediatr Infect Dis J 1988;7:313-5.
Li MY, Hua Y, Wei GH, Qiu L. Staphylococcal scalded skin syndrome in neonates: An 8-year retrospective study in a single institution. Pediatr Dermatol 2014;31:43-7.
Kadam S, Tagare A, Deodhar J, Tawade Y, Pandit A. Staphylococcal scalded skin syndrome in a neonate. Indian J Pediatr 2009;76:1074.
Jeyakumari D, Gopal R, Eswaran M, Maheshkumar C. Staphylococcal scalded skin syndrome in a newborn. J Glob Infect Dis 2009;1:45-7.
Duijsters CE, Halbertsma FJ, Kornelisse RF, Arents NL, Andriessen P. Recurring staphylococcal scalded skin syndrome in a very low birth weight infant: A case report. J Med Case Rep 2009;3:7313.
Moss C, Gupta E. The Nikolsky sign in staphylococcal scalded skin syndrome. Arch Dis Child 1998;79:290.
Patel GK, Finlay AY. Staphylococcal scalded skin syndrome: Diagnosis and management. Am J Clin Dermatol 2003;4:165-75.
Hanakawa Y, Stanley JR. Mechanisms of blister formation by staphylococcal toxins. J Biochem 2004;136:747-50.
Ladhani S. Understanding the mechanism of action of the exfoliative toxins of Staphylococcus aureus
. FEMS Immunol Med Microbiol 2003;39:181-9.
Ladhani S, Joannou CL, Lochrie DP, Evans RW, Poston SM. Clinical, microbial, and biochemical aspects of the exfoliative toxins causing staphylococcal scalded-skin syndrome. Clin Microbiol Rev 1999;12:224-42.
Johnston GA. Treatment of bullous impetigo and the staphylococcal scalded skin syndrome in infants. Expert Rev Anti Infect Ther 2004;2:439-46.
Kouakou K, Dainguy ME, Kassi K. Staphylococcal scalded skin syndrome in neonate. Case Rep Dermatol Med 2015;2015:901968.
[Figure 1], [Figure 2]