Eczema herpeticum B00.0

Kaposi, 1887; Juliusberg, 1898

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.

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)

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.

Especially face, neck, neck, chest, arms.

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.

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.

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.

Eccema vaccinatum, acute exacerbation of atopic eczema, pyoderma,

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.

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.

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.

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

1. Cavalié M et al (2013) Kaposi's varicelliform eruption in a patient with pityriasis rubra pilaris (pityriasis rubra pilaris herpeticum). J Eur Acad Dermatol Venereol 27:1585-1586.
2. Bunce PA et al (2013) Grover's disease secondarily infected with herpessimplex virus and Staphylococcus aureus: case report and review. Australas J Dermatol 54:88-91
3. De Benedetto A et al (2011) Reductions in claudin-1 may enhance susceptibility to herpes simplex virus 1 infections in atopic dermatitis. J Allergy Clin Immunol 128: 242-246 e5.
4. Garg G et al.(2012) Psoriasis Herpeticum due to Varicella Zoster Virus: A Kaposi's Varicelliform Eruption in Erythrodermic Psoriasis. Indian J Dermatol 57:213-214
5. Gupta M et al (2012) Unusual complication of vemurafenib treatment of metastatic melanoma: exacerbation of acantholytic dyskeratosis complicated by Kaposi varicelliform eruption. Arch Dermatol 148:966-968
6. Howell MD et al (2006) Cathelicidin deficiency predisposes to eczema herpeticum. J Allergy Clin Immunol. 2006;117(4):836-41.
7. Juliusberg F (1898) On pustulosis acuta varioliformis. Arch Derm Syph 46: 21-28
8. Kaposi M (1887) Pathology and therapy of skin diseases. Urban & Schwarzenberg, Vienna & Leipzig, p. 483.
9. Mathes EF et al (2013) "Eczema coxsackium" and unusual cutaneous findings in an enterovirus outbreak. Pediatrics 132:149-157
10. Rappersberger K (1999) Infections with herpes simplex and varicella zoster viruses in pregnancy. Clinical manifestation in mother, fetus and newborn - therapeutic options. Dermatologist 50: 706-714
11. Sanderson IR et al (1987) Eczema herpeticum: a potentially fatal disease. Br Med J (Clin Res Ed) 294(6573):693-694.
12. Moustafa GA et al (2022) Facial Eczema Herpeticum. J Pediatr 248:126.
13. Walker D et al (2012) A painful eruption in a woman with Darier disease. J Am Acad Dermatol 67:1089-1990.
14. Wolf R, Tamir A, Weinberg M et al (1992) Eczema herpeticatum induced by sun exposure (letter). Int J Dermatol 31: 298-299.
15. Wollenberg A et al (2002) Plasmacytoid dendritic cells: a new cutaneous dendritic cell subset with distinct role in inflammatory skin diseases. J Invest Dermatol 119(5):1096-1102.
16. Wollenberg A et al (2003) Predisposing factors and clinical features of eczema herpeticum: a retrospective analysis of 100 cases. J Am Acad Dermatol 49: 198-205.
17. Wollenberg A (2012) Eczema herpeticum. Chemical immunology and allergy 96:89-95.
18. Yoon M et al (2002) Disruption of adherens junctions liberates nectin-1 to serve as receptor for herpes simplex virus and pseudorabies virus entry. J Virol 76:7203-7208.
19. Yoshida M et al. (2003) Close association of predominant genotype of herpes simplex virus type 1 with eczema herpeticum analyzed using restriction fragment length polymorphism of polymerase chain reaction. J Virol Methods 109:11-16.