After a symptom-free interval, a relapse was noted on day of life 120, when she developed rapidly expanding skin lesions with diffuse flaccid bullae and epidermal peeling on the lower extremities (Fig. 1c and d). Antibiotics (teicoplanin and amikacin) were administered again for 10 days, together with analgesics and aseptic care. No systemic features was observed. Staphylococcus aureus was cultured only from the skin cultures. Genetic test for epidermolysis bullosa was negative. Skin biopsy showed splitting at the granular layer of the epidermis without inflammatory infiltrates. Skin lesions did not increase and resolved after 10 days.At discharge, the child had intact skin without scarring. No relapses were reported during the six-month follow-up period.In the present case, clinical symptoms (diffuse blanching erythema, blisters, epidermal peeling and Nikolsky sign positive), microbiological features (isolation of Staphylococcus aureus) and histopathologic findings (intraepidermal acantolysis without inflammatory infiltrate) suggested the diagnosis of SSSS. 2 The clinical course of the first episode and the recurrence could be related to prematurity. The vulnerable skin in a preterm neonate can facilitate the breakdown of both the immunological barrier function and consequent spread of Staphylococcus aureus, and the liquid-liquid barrier causing transepidermal water loss and dehydration.The recurrence could be due both to a low antibody response to toxin, as reported in adults and term neonates with recurrent SSSS, 4 and to a lower excretion of epidermolytic toxins due to impaired renal function. 5
AcknowledgementNone.
Author ContributionsSC, MPDC, RI, GP, ET, MLP and GV participated in the design of the study. SC and MPDC wrote the discussion and reviewed the results. All authors read and approved the final manuscript.
