Eczema herpeticum B00.0

Author: Prof. Dr. med. Peter Altmeyer

Co-Autors: Dr. Elisabeth Hanf, Hadrian Tran

All authors of this article

Last updated on: 13.06.2023

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Eccema herpetiforme Kaposi; Eccema herpetiformis; eczema herpeticatum; eczema herpeticum; Eruption Kaposi varizelliforme; Kaposi's varicelliform eruption; Kaposis varicelliform eruption; Kaposi varicelliform eruption; pustulosis acuta varicelliformis; Pustulosis acuta varioliformis Juliusberg; Pustulosis herpetica infantum; pustulosis vacciniformis acuta; Varicelliform eruption Kaposi

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Kaposi, 1887; Juliusberg, 1898

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Eczema herpeticum is an acute, febrile, severe, regionally localized or generalized herpes simplex infection (HSV infection) that occurs in people with extensive atopic dermatitis (AD). Severe viral infection is manifested by disseminated, monomorphic papules and vesicles. It is generally accompanied by lymphadenopathy or fever (Wollenberg A 2012). Before the introduction of aciclovir, the disease was fatal, with a mortality rate of up to 70% ( Sanderson IR et al 1987). It took an average of 4.2 ± 3.4 days to reach diagnosis (Seegräber M et al. 2020).

Generalized herpes simplex infections have also been described in M.Darier, pityriasis rubra pilaris, mycosis fungoides, erythrodermic psoriasis, M. Grover .

Some cases have been observed during treatment with vemurafenib and other biologics.

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The gender distribution was almost equal in a larger study with 122 male and 102 female patients. The mean age of patients at the onset of EH was 27.3 ± 11.9 years. The mean age at onset of underlying atopic dermatitis was 9.5 ±10.1 years (Seegräber M et al. 2020)

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Several risk factors influence the likelihood of developing EH, such as lesional atopic skin in which deficiencies of nectin-1 play a role, allowing the virus to enter the cell (Yoon M et al 2002; De Benedetto A et al 2011). The antiviral immune response in atopic dermatitis is inadequate due to a lack of plasmacytoid dendritic cells. This results in insufficient IFN- γ production (Wollenberg A et al 2002), which is associated with a generally higher risk of viral skin infections. In addition, AD-associated cathelicidin deficiency is a predisposing factor for eczema herpeticum (Howell MD et al 2006). Triggering by UV exposure has been described.

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Especially face, neck, neck, chest, arms.

Clinical features
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Usually fulminant, progressing in a single acute episode, generalized, symmetrical exanthema of 0.1-0.2 cm, red or brown-red, crusty, uniform erosions. Vesicles are often not (no longer) found. The punctate lesions, typically grouped, even once linearly arranged, occur at a nearly harmonized, uniform spacing from one another. They are all in an identical stage of development (apparently, in contrast to the relapsing varicella -starry sky-, usually only 1 single disease relapse takes place).

Less commonly, more densely staggered erosions confluence to form larger, pyodermatized wound areas. Bacterial superinfections typically accompany these generalized herpes simplex infections. There is a marked feeling of illness, high fever, headache. Regional painful lymphadenopathy.

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Usually only mild leukocytosis, inconstant lymphopenia. Significantly elevated CRP. In a larger cohort of patients with eczema herpeticum, 66.1% reported a history of rhinoconjunctivits allergica, and 37.5% reported a history of asthma (Seegräber M et al. 2020). The mean total serum IgE level was 976.64 kU/l, with a minimum of 17 kU/l and a maximum of 37,940 kU/l.

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See below Herpes simplex. Cultivation of the virus from vesicle contents (gold standard; specific and safest, but laborious method).

In the Tzanck test from the base of the blister, detection of multinuclear epidermal giant cells.

Electron microscopy: virus detection from vesicle contents using negative contrast.

Differential diagnosis
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Eccema vaccinatum, acute exacerbation of atopic eczema, pyoderma,

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Spread of HSV (viremia) to other organs. The most common complications occur in the CNS (aseptic meningitis and encephalitis). Cave! HSV encephalitis is lethal in 55-70% of cases if untreated.

Other rare systemic complications with possible lethal outcome: rhabdomyolysis, bronchopneumonia.

Ocular involvement in the form of keratitis herpetica.

External therapy
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Drying measures, antiseptic and antibiotic dry brushings: Lotio alba, possibly with addition of 0.5-2.0% Clioquinol R050. In case of very painful skin tension, careful cream treatment (e.g. Ungt. emulsif. aq.), but no ointments or fatty ointments (reapplication of cream after treatment with Clioquinol lotio).

Externals with antiviral additives such as idoxuridine solution(Zostrum, apply 4 times/day to affected skin, do not use for longer than 4 days) are used especially in the first 48 hours after the appearance of the vesicles.

Internal therapy
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Aciclovir (e.g. Zovirax) i.v. (dose: 5 mg/kg Kg/day, in immunosuppressed patients 10 mg/kg Kg/ every 8 h) for 5-8 days. For less extensive findings, oral therapy with aciclovir 5 times/day 200 mg at 4 h intervals may be sufficient. Alternatively, famciclovir (Famvir Filmtbl.) 3 times/day 250 mg.

Pregnancy: According to studies, no evidence of a fertility-damaging effect of aciclovir could be demonstrated. Therefore, despite the lack of approval, therapy in pregnancy is advocated after individual risk assessment ( off-label use!).

In case of existing aciclovir therapy resistance or immunosuppressive disease Foscarnet (Foscavir) 3 times/day 40 mg/kg bw as 1-hour drip infusion.

In case of bacterial superinfection (mostly Staphylococcus aureus) antibiotics such as flucloxacillin (e.g. Staphylex) 3-4 times/day 0.5-1.0 g p.o. or i.m. or dicloxacillin (e.g. InfectoStaph) 4 times/day 0.5-1.0 g p.o. or erythromycin (e.g. Erythromycin Wolff) 4 times/day 500 mg/day. As soon as possible antibiosis according to antibiogram.

Possibly try therapy with immunoglobulins (see IVIG) or immunostimulants (e.g. Isoprinosine, dose: 6-8 tbl./day p.o.), especially for prophylaxis.

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The mortality of Eccema herpeticatum, caused by viremia and multiple organ failure, was 10-50% before the introduction of acyclovir in 1977.

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