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CASE REPORT
Year : 2018  |  Volume : 19  |  Issue : 4  |  Page : 369-370

Eczema herpeticum in a patient with atopic dermatitis, coxsackie B virus, and staphylococcal infection: A double skin damage


1 Department of Clinical and Experimental Medicine, Section of Pediatrics and Child Neuropsychiatry, University of Catania, Catania, Italy; Department of Psychiatry, Psychology and Neuroscience, Maurice Wohl Clinical Neuroscience Institute, King's College London, London, United Kingdom, Italy
2 Department of Clinical and Experimental Medicine, Section of Pediatrics and Child Neuropsychiatry, University of Catania, Catania, Italy

Date of Web Publication28-Sep-2018

Correspondence Address:
Dr. Andrea D Pratico
Department of Clinical and Experimental Medicine, Section of Pediatrics and Child Neuropsychiatry, University of Catania, Via Santa Sofia 7895123 Catania
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijpd.IJPD_70_17

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  Abstract 


Eczema herpeticum is a rare viral skin scattered infection whose main etiologic agents are HSV1–2 and coxsackievirus, but its association with atopic dermatitis suggests that different factors may play a role in this complex phenotype. When not promptly treated, it can spread to other organs, causing severe complications such as keratoconjunctivitis, encephalitis, and meningitis. We describe the case of a patient with atopic dermatitis who came to our observation presenting with diffuse purulent vesicular lesions, whose bacterial culture was positive for Staphylococcus aureus and whose serologic examinations showed IgM positivity for coxsackie B virus.

Keywords: Atopic dermatitis, eczema, infection – bacterial, infection – viral


How to cite this article:
Pratico AD, Fatuzzo V, Cucuzza ME, C La Mendola FM. Eczema herpeticum in a patient with atopic dermatitis, coxsackie B virus, and staphylococcal infection: A double skin damage. Indian J Paediatr Dermatol 2018;19:369-70

How to cite this URL:
Pratico AD, Fatuzzo V, Cucuzza ME, C La Mendola FM. Eczema herpeticum in a patient with atopic dermatitis, coxsackie B virus, and staphylococcal infection: A double skin damage. Indian J Paediatr Dermatol [serial online] 2018 [cited 2020 Oct 22];19:369-70. Available from: https://www.ijpd.in/text.asp?2018/19/4/369/220991




  Introduction Top


Eczema herpeticum (EH) is a rare viral infection of the skin, whose main etiologic agents are HSV1–2 and coxsackievirus.[1] It occurs more frequently in patients affected by atopic dermatitis (AD) or other conditions causing epidermal barrier dysfunctions (e.g., psoriasis, contact dermatitis, rosacea, lupus vulgaris, and burns).[2] If not treated, EH can cause severe complications, such as keratoconjunctivitis, encephalitis, and meningitis. Therefore, an early clinical recognition and laboratory confirmation are indispensable to perform a rapid and targeted treatment.[3]

We describe a patient with atopic dermatitis who presented a purulent diffuse vesicular rash, positive for Staphylococcus aureus, and whose blood tests were positive for coxsackie B virus IgM.


  Case Report Top


A 7-year-old patient affected by AD since the age of 6 months, came to our observation for the occurrence of vesicular lesions, initially localized at the right popliteal area, and subsequently spread to the trunk, the ventral surfaces of the elbows, and to the left labial commissure. In the preceding 2 days, she had presented fever and had been treated with cetirizine (10 mg, once/day) and clarithromycin (15 mg/kg, twice/day).

At admission, her general conditions were fair; her weight was 21 kg (10–25th percentile), height 122.5 cm (50th percentile), and head circumference 54 cm (>97th percentile). She presented vesicular purulent injuries localized in her knees [Figure 1], trunk, neck, ventral surface of the elbows, and in the left labial commissure. Body temperature was 38.1°C. The remaining of the physical examination, including neurological examination, was negative.
Figure 1: The patient, at admission. Severe painful vesicles are present in her right knee. A larger purulent lesion can be observed in the center. Left knee is less severely affected

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In the suspect of a EH caused by a viral infection, blood tests for HSV1, HSV2, and coxsackie were performed, and oral acyclovir (15 mg/kg, four times per day) added to the treatment. Because of a clinical worsening, after 24 h, acyclovir was administrated intravenously (10 mg/kg, three times/day), and clarithromycin replaced by intravenous ampicillin-sulbactam (1.5 g, twice a day).

Blood tests showed positivity for HSV1 IgG (1:20) and for IgM (1:256) and IgA (1:8) for Group B coxsackievirus. There was also a high serum level of IgE antibodies (420 kU/L), an increased erythrocyte sedimentation rate (40 mm/h), and the cutaneous bacterial culture resulted positive for S. aureus. Specific RAST IgE tests were positive for strawberry, peach, banana, and lettuce.

After 10 days of intravenous antibiotic and antiviral therapy, the patient was discharged in good conditions, with an almost total regression of the skin lesions.


  Discussion Top


EH consists on an eruption of monomorphic-shaped vesicles associated with the fever, malaise, and lymphadenopathy. The regions more frequently involved are head, neck, and thorax; moreover, despite EH usually starts in skin affected by atopic dermatitis, the lesions usually involve the normal skin in about 7–10 days. Vesicles transform into pustules and scabs, forming erosions that often result a scar in about 2–6 weeks, and lesions involving the eyes can lead to keratoconjunctivitis.[1] Viral dissemination can, however, lead to meningitis and encephalitis with mortality that can be up to 75% in the absence of targeted antiviral treatment.

EH is a rare skin disease occurring in 3%–6% of patients affected by atopic dermatitis. This frequent association is probably due to an impaired immune response or to the alteration of the skin barrier, typically observed in DA patients. These patients have recently been considered as affected by “atopic dermatitis with a history of EH” (ADEH+).[1],[2],[3]

Initially, EH was thought to be caused by bacterial superinfections, but recently, it has been shown that the majority of cases are due to viral infections:[4] inhibition of interferon regulatory factor-3 and 7 innate immune pathways has been related to ADEH+, and this is a known causative mechanism for increased susceptibility to disseminated viral infection.[5] Moreover, these patients often present significantly low plasma cells and an overall increased susceptibility to Th2 response, which can cause viral invasion and replication [1].

As pointed out by a multicenter study,[6] the most important risk factors for the occurrence of ADEH + are predominant Th2 helper cells' immune response (with relative deficit of Th1 response), a decreased production of epidermal filaggrin (a filament-associated protein that binds to keratin fibers in epithelial cells), and other antimicrobials peptides, as well as a history of food allergies, bronchial asthma, and increased levels of serum IgE and eosinophils, as well as early-onset AD.

This report highlights the importance of suspecting a viral – not only bacterial – infection when individuals affected by DA present an abrupt worsening and spreading of their lesions. A targeted antiviral treatment, in such cases, can avoid the risk of potentially lethal systemic complications.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Wollenberg A, Zoch C, Wetzel S, Plewig G, Przybilla B. Predisposing factors and clinical features of eczema herpeticum: A retrospective analysis of 100 cases. J Am Acad Dermatol 2003;49:198-205.  Back to cited text no. 1
    
2.
Leung DY. Why is eczema herpeticum unexpectedly rare? Antiviral Res 2013;98:153-7.  Back to cited text no. 2
    
3.
Wollenberg A, Wetzel S, Burgdorf WH, Haas J. Viral infections in atopic dermatitis: Pathogenic aspects and clinical management. J Allergy Clin Immunol 2003;112:667-74.  Back to cited text no. 3
    
4.
Luca NJ, Lara-Corrales I, Pope E. Eczema herpeticum in children: Clinical features and factors predictive of hospitalization. J Pediatr 2012;161:671-5.  Back to cited text no. 4
    
5.
Bin L, Edwards MG, Heiser R, Streib JE, Richers B, Hall CF, et al. Identification of novel gene signatures in patients with atopic dermatitis complicated by eczema herpeticum. J Allergy Clin Immunol 2014;134:848-55.  Back to cited text no. 5
    
6.
Beck LA, Boguniewicz M, Hata T, Schneider LC, Hanifin J, Gallo R, et al. Phenotype of atopic dermatitis subjects with a history of eczema herpeticum. J Allergy Clin Immunol 2009;124:260-9, 269.e1-7.  Back to cited text no. 6
    


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