Letter to the Editor.

Abstract

A previously well 10-year-old boy was seen at our clinic with generalised ulceration over his buttocks, legs and forearms (Fig. 1). He has a history of atopic eczema with recent flare up, which was treated with topical steroids, wet wraps and ultra-violet light therapy. There was no history of trauma, insect bites or recent travel. Investigations showed Erythrocyte sedimentation rate of 38 mm, C-reactive protein was mildly raised at 9 mg/d. Human immunodeficiency virus serology and Herpes simplex virus 1 and 2, which were negative. Protein C, protein S, ANA, ENA and ds DNA which were normal. Atypical mycobacterial culture was negative. The gram-negative bacillus Serratia ureilytica was the only micro-organism isolated from lesional skin biopsy specimen. The histopathologic findings showed focal ulceration with underlying granulation tissue and a moderate mixed inflammatory cell infiltrate including neutrophils, lymphocytes and occasional eosinophils. Spongiosis, viral inclusions and granulomas not identified. The patient was admitted into hospital and was treated with empirical antibiotic therapy: flucloxacillin 1650 mg every 6 hourly and acyclovir 325 mg every 8 hourly. He was commenced on daily wet wrap therapy with moisturisers and topical corticosteroids for the management of his eczema. Serratia species are opportunistic Gram-negative aerobic bacilli found in water, soil, plants and animals. They rarely cause of skin ulcerations and are infrequently reported in the immunocompetent paediatric patients.1, 2 Skin injuries, trauma and compromised skin integrity can act as a route of entry for the bacteria.1, 3 Our patient has moderate atopic eczema with compromised skin barrier, chronic topical steroid use, which increased his risk of skin infections. It is also possible that a combination of disturbed barrier from excoriation, maceration of the skin and contaminated water or wet dressings is the source for this opportunistic infection. There is a possibility that Serratia was a commensal on these ulcers. However, the lack of another cause of ulceration identified clinically or histopathologically, the rapid improvement following appropriate antibiotic therapy, suggest that it is more likely a pathogenic cause. It is important to consider possible underlying immune deficiency or chronic granulomatous disease in a child with recurrent serratia skin infections or invasive bacterial or fungal infection.4 We did not think that this was likely in our patient given that he is a well grown and healthy child with no history of recurrent infections. Clinicians should maintain a high index of suspicion in patients presenting with discrete punched out ulcers. Serratia species may be resistant to penicillins and third generation cephalosporins, usually susceptible to carbapenems, fluroquinolones and aminoglycosides,1 but susceptibility testing to determine antibiotic resistance and discussion with an infectious disease specialists are recommended. Our case highlights the possibility of Serratia species as a cause of ulceration, cellulitis and secondary skin infection in immunocompetent children with atopic eczema. We confirm that this manuscript contains original unpublished work that is not being considered for publication elsewhere at the same time. Our patient has provided written consent for the publication of this manuscript.