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Eczema Herpeticum

Editor: Arline Tsuchiya Updated: 8/8/2023 1:20:26 AM


Eczema herpeticum (EH) is a disseminated cutaneous infection with herpes simplex virus that develops in a patient with atopic dermatitis.[1] EH typically presents as a sudden onset eruption of monomorphic vesicles and "punched-out" erosions with hemorrhagic crusts over eczematous areas. Patients may have systemic symptoms, such as fever, lymphadenopathy, or malaise.[2] Presentation ranges from mild and self-limiting in healthy adults to life-threatening in children, infants, and immunocompromised patients. Early treatment with antiviral therapy can shorten the duration of mild disease and prevent morbidity and mortality in severe cases.[3]


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Eczema herpeticum is due to cutaneous superinfection with herpes simplex virus (HSV), usually HSV-1, in patients with atopic dermatitis. Cases due to reactivation of HSV are more common than primary infection.[4] Patients with atopic dermatitis are prone to recurrent bacterial and viral skin infections due to impaired epidermal barrier function and immune dysregulation.[5] Disseminated cutaneous HSV infection can also occur in patients with other forms of dermatitis that impair the skin barrier and is known as Kaposi varicelliform eruption (KVE). KVE has been reported in patients with Darier disease, Hailey–Hailey disease, immunobullous diseases, burns, irritant contact dermatitis, mycosis fungoides, Sézary syndrome, ichthyoses, and pityriasis rubra pilaris.[6][7] 

Risk factors associated with the development of EH are more severe atopic skin disease, decreased epidermal expression of filaggrin, and decreased production of cathelicidin and other antimicrobial peptides.[8] EH patients exhibit biomarkers associated with T-helper type 2 (Th2) cell responses, such as reduced interferon levels, elevated eosinophil count, and increased serum IgE levels.[5] EH patients are more likely to have food and environmental allergies, asthma, early onset of atopic dermatitis before age five, and history of Staphylococcus aureus and molluscum contagiosum infections.[5] The HLA-B7 allele has been found to be associated with an increased risk of EH.[9] Increased interleukin-10 (IL-10) and local IL-25 expression is found in EH patients and may play a role in the development of EH.[10] The Th2 shift of the immune system in EH patients is associated with decreased antimicrobial peptides in the epidermis and reduced defense against cutaneous HSV infection.


Eczema herpeticum occurs in less than 3% of atopic dermatitis patients, affecting infants and children more than adults.[5] Atopic dermatitis is the most common chronic inflammatory skin disease in the world, affecting 10 to 20% of children in developed countries and 7 to 10% of adults in the United States.[11][12] Given the prevalence of HSV exposure, the comparative rarity of EH in atopic dermatitis patients suggests many host factors play an important role in the development of EH. A study of pediatric EH patients in Canada found that predictors of hospitalization included male sex, age less than one year, fever, and systemic symptoms at presentation.[13] 

Another study in the United States found that the average age of hospitalized pediatric patients with EH was 3.26 +/- 0.1 years, and 41.8% of patients were female.[13] This study also reported higher prevalence, length of hospital stay, and cost of care occurring in Asian pediatric patients.[13] The epidemiology of EH in non-hospitalized and adult patients is not well defined.

History and Physical

Eczema herpeticum presents as a sudden onset eruption of monomorphic, dome-shaped, grouped, 2 to 3 mm vesicles on an erythematous base. Lesions are superimposed on areas of pre-existing atopic dermatitis, most commonly on the face, neck, and upper trunk. The lesions are pruritic, painful, and may spread to involve normal skin over seven to 10 days.[14] Within two weeks, the vesicles rupture and form characteristic "punched-out" erosions with the hemorrhagic crust. Small erosions may coalesce to form a larger erosion or ulceration with a scalloped border.

Numerous vesicles may appear in successive crops, and multiple morphologies may be present at the same time. Lesions that are secondarily impetiginized may have an overlying honey-colored crust. In patients with severe or poorly-controlled atopic dermatitis, the characteristic morphology may be difficult to recognize and can be misdiagnosed as an exacerbation of eczematous dermatitis.[15] Patients may have systemic symptoms, such as fever, malaise, and lymphadenopathy.[3] EH lesions generally heal without scarring within six weeks.[16]


The diagnosis of eczema herpeticum can be made clinically if characteristic morphology is present. Viral polymerase chain reaction (PCR) can be performed on vesicle fluid to confirm the diagnosis and determine the type of herpesvirus with high sensitivity and specificity.

If PCR is not available, a Tzank smear, direct fluorescent antibody (DFA) testing, and viral cultures can confirm HSV infection. Bacterial culture should be done if there is a concern for impetiginization. If the clinical presentation is atypical, a skin biopsy may be indicated. Laboratory tests may reveal lymphopenia and an increased erythrocyte sedimentation rate.[14]

Treatment / Management

Eczema herpeticum patients should be treated promptly with systemic acyclovir or valacyclovir to minimize the risk of complications and prevent progression to severe disease.

  • Mild cases can be treated with oral acyclovir or valacyclovir for 7-21 days or until all lesions are crusted over.[17] The recommended dosage for oral acyclovir is 30-60 mg/kg/d divided into three doses per day in children and 400 mg 3 times per day in adults.[16][18] The dosage for oral valacyclovir is 20 mg/kg/d in children and 500 mg 3 times per day in adults.[4]
  • Severe cases or immunocompromised patients should be hospitalized for intravenous acyclovir 5-10 mg/kg every 8 hours. Patients can be transitioned to oral acyclovir once there is clinical improvement, and the lesions start to crust over.[15] Supportive care with gentle emollients and cool compresses can provide symptomatic relief.
  • Critically ill patients may need intravenous fluids, electrolyte repletion, wound care, pain control, and nutritional support. Patients should be counseled about the risk of autoinoculation, and frequent handwashing should be encouraged. EH lesions are considered infectious until crusted over.
  • Contact precautions should be initiated for hospitalized patients, including patient isolation and the use of face masks and gowns for healthcare providers.[18] Patients should be monitored for the development of secondary bacterial infections and treated with systemic antibiotics according to culture and susceptibility results.[18]
  • (B2)

Differential Diagnosis

The differential diagnosis for eczema herpeticum includes impetigo, hand-foot-and-mouth disease, eczema coxsackium, primary varicella infection, disseminated herpes zoster, disseminated molluscum contagiosum, acute generalized exanthematous pustulosis, dermatitis herpetiformis, cellulitis, and erysipelas. Misdiagnosis of EH can lead to delayed initiation of antiviral treatment and subsequent complications. Diagnostic clues that favor EH are painful lesions, monomorphic size of the lesions, and characteristic "punched-out" erosions in areas of pre-existing atopic dermatitis. Unlike herpes zoster, EH does not respect dermatomal boundaries.


Eczema herpeticum is a potentially life-threatening disease with mortality risk due to complications of systemic viremia, bacteremia, and fungal infection leading to multi-organ failure.[19] Prior to the use of acyclovir, mortality rates in EH patients were reportedly 10% to 50% [20] Since the widespread implementation of systemic antiviral treatment, mortality rates have decreased significantly.

A 2011 study of 1331 hospitalized pediatric EH patients in the United States found no deaths and concluded that the mortality rate of hospitalized patients is low. The median length of hospital stay was three days, with 9.2% of patients requiring hospitalization longer than one week, and 3.8% required ICU admission.[21] A study in 2018 of 4655 hospitalized children with EH found a mortality rate of 0.1%, with 98.1% of patients classified as minor mortality risk. Only 4.5% of patients were classified as having major loss of function, while 33.1% had moderate, and the majority had a minor loss of function.[13]


Potential complications of EH include cutaneous superinfection with Staphylococcus aureus (S. aureus), Streptococcus pyogenes, and molluscum contagiosum virus.[22][23] The study by Aronson et al. found S. aureus infection in 30.3% of hospitalized pediatric EH patients with 9.2% due to methicillin-resistant S aureus and 3.9% with bacteremia. 86.4% of patients were treated with oral or intravenous antibiotics.[21] Additional complications include meningoencephalitis and herpetic keratoconjunctivitis, which can result in scarring and blindness.[4] Disseminated systemic infections of HSV leading to bone marrow suppression, disseminated intravascular coagulation, and death has been reported.[15]

Deterrence and Patient Education

Patients with eczema herpeticum should be counseled that they are infectious until all lesions have crusted over and thus avoid close contact with others until then. Encourage patients to avoid scratching and wash hands frequently due to the risk of autoinoculation. Patients diagnosed with mild EH and treated as outpatients should be cautioned to seek emergency care if they develop systemic symptoms or worsening rash, as they may require hospitalization, intravenous acyclovir treatment, or antibiotic coverage.

Enhancing Healthcare Team Outcomes

Eczema herpeticum is considered a medical emergency and should be treated promptly with systemic antivirals, as misdiagnosis and delay in treatment can result in serious complications. An ophthalmologic evaluation is warranted in cases of EH involving the face and eyelids. A dermatology consult may be beneficial to confirm the diagnosis. Clinicians should be aware of the risk factors associated with EH, including severe or poorly controlled atopic dermatitis, food and environmental allergies, asthma, the onset of atopic dermatitis before age five, and history of S. aureus and molluscum contagiosum infections.

Patients with systemic symptoms or widespread involvement should be promptly referred to the Emergency Department. To improve patient outcomes and prevent morbidity and mortality, healthcare providers should have a high index of suspicion for EH in patients with a history of atopic dermatitis presenting with a sudden onset, vesicular, monomorphic rash in areas of pre-existing dermatitis.


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Eczema, Herpeticum

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Micali G, Lacarrubba F. Eczema Herpeticum. The New England journal of medicine. 2017 Aug 17:377(7):e9. doi: 10.1056/NEJMicm1701668. Epub     [PubMed PMID: 28813215]


Seegräber M, Worm M, Werfel T, Svensson A, Novak N, Simon D, Darsow U, Augustin M, Wollenberg A. Recurrent eczema herpeticum - a retrospective European multicenter study evaluating the clinical characteristics of eczema herpeticum cases in atopic dermatitis patients. Journal of the European Academy of Dermatology and Venereology : JEADV. 2020 May:34(5):1074-1079. doi: 10.1111/jdv.16090. Epub 2020 Jan 30     [PubMed PMID: 31733162]

Level 2 (mid-level) evidence


Vera-Kellet C, Hasbún C. Eczema herpeticum: A medical emergency in patients with atopic dermatitis. IDCases. 2020:19():e00663. doi: 10.1016/j.idcr.2019.e00663. Epub 2019 Nov 6     [PubMed PMID: 32226756]

Level 3 (low-level) evidence


Wollenberg A, Wetzel S, Burgdorf WH, Haas J. Viral infections in atopic dermatitis: pathogenic aspects and clinical management. The Journal of allergy and clinical immunology. 2003 Oct:112(4):667-74     [PubMed PMID: 14564342]


Leung DY. Why is eczema herpeticum unexpectedly rare? Antiviral research. 2013 May:98(2):153-7. doi: 10.1016/j.antiviral.2013.02.010. Epub 2013 Feb 22     [PubMed PMID: 23439082]


Lehman JS, el-Azhary RA. Kaposi varicelliform eruption in patients with autoimmune bullous dermatoses. International journal of dermatology. 2016 Mar:55(3):e136-40. doi: 10.1111/ijd.13091. Epub 2015 Oct 24     [PubMed PMID: 26500144]


Walker K, Martini A, Philips H, Sharp L, Thomas K, Tarbox M. Darier disease with disseminated herpes simplex virus type 2 infection. Dermatology online journal. 2019 Apr 15:25(4):. pii: 13030/qt4qg8s971. Epub 2019 Apr 15     [PubMed PMID: 31046908]


Hata TR, Kotol P, Boguniewicz M, Taylor P, Paik A, Jackson M, Nguyen M, Kabigting F, Miller J, Gerber M, Zaccaro D, Armstrong B, Dorschner R, Leung DY, Gallo RL. History of eczema herpeticum is associated with the inability to induce human β-defensin (HBD)-2, HBD-3 and cathelicidin in the skin of patients with atopic dermatitis. The British journal of dermatology. 2010 Sep:163(3):659-61. doi: 10.1111/j.1365-2133.2010.09892.x. Epub 2010 Jun 9     [PubMed PMID: 20545685]

Level 3 (low-level) evidence


Mathias RA, Weinberg A, Boguniewicz M, Zaccaro DJ, Armstrong B, Schneider LC, Hata TR, Hanifin JM, Beck LA, Barnes KC, Leung DY. Atopic dermatitis complicated by eczema herpeticum is associated with HLA B7 and reduced interferon-γ-producing CD8+ T cells. The British journal of dermatology. 2013 Sep:169(3):700-3. doi: 10.1111/bjd.12382. Epub     [PubMed PMID: 23600999]

Level 2 (mid-level) evidence


Damour A, Garcia M, Seneschal J, Lévêque N, Bodet C. Eczema Herpeticum: Clinical and Pathophysiological Aspects. Clinical reviews in allergy & immunology. 2020 Aug:59(1):1-18. doi: 10.1007/s12016-019-08768-3. Epub     [PubMed PMID: 31836943]


Lyons JJ, Milner JD, Stone KD. Atopic dermatitis in children: clinical features, pathophysiology, and treatment. Immunology and allergy clinics of North America. 2015 Feb:35(1):161-83. doi: 10.1016/j.iac.2014.09.008. Epub 2014 Nov 21     [PubMed PMID: 25459583]


Silverberg JI, Hanifin JM. Adult eczema prevalence and associations with asthma and other health and demographic factors: a US population-based study. The Journal of allergy and clinical immunology. 2013 Nov:132(5):1132-8. doi: 10.1016/j.jaci.2013.08.031. Epub 2013 Oct 4     [PubMed PMID: 24094544]


Hsu DY, Shinkai K, Silverberg JI. Epidemiology of Eczema Herpeticum in Hospitalized U.S. Children: Analysis of a Nationwide Cohort. The Journal of investigative dermatology. 2018 Feb:138(2):265-272. doi: 10.1016/j.jid.2017.08.039. Epub 2017 Sep 18     [PubMed PMID: 28927889]


Wollenberg A, Zoch C, Wetzel S, Plewig G, Przybilla B. Predisposing factors and clinical features of eczema herpeticum: a retrospective analysis of 100 cases. Journal of the American Academy of Dermatology. 2003 Aug:49(2):198-205     [PubMed PMID: 12894065]

Level 2 (mid-level) evidence


Zhuang K, Wu Q, Ran X, Ran Y, Ding L, Xu X, Lei S, Lama J. Oral treatment with valacyclovir for HSV-2-associated eczema herpeticum in a 9-month-old infant: A case report. Medicine. 2016 Jul:95(29):e4284. doi: 10.1097/MD.0000000000004284. Epub     [PubMed PMID: 27442669]

Level 3 (low-level) evidence


Luca NJ, Lara-Corrales I, Pope E. Eczema herpeticum in children: clinical features and factors predictive of hospitalization. The Journal of pediatrics. 2012 Oct:161(4):671-5. doi: 10.1016/j.jpeds.2012.03.057. Epub 2012 May 9     [PubMed PMID: 22575249]

Level 2 (mid-level) evidence


Atherton DJ, Harper JI. Management of eczema herpeticum. Journal of the American Academy of Dermatology. 1988 Apr:18(4 Pt 1):757-8     [PubMed PMID: 3372774]

Level 3 (low-level) evidence


Sohail M, Khan FA, Shami HB, Bashir MM. Management of eczema herpeticum in a Burn Unit. JPMA. The Journal of the Pakistan Medical Association. 2016 Nov:66(11):1357-1361     [PubMed PMID: 27812048]


Wollenberg A. Eczema herpeticum. Chemical immunology and allergy. 2012:96():89-95. doi: 10.1159/000331892. Epub 2012 Mar 13     [PubMed PMID: 22433376]


Wheeler CE Jr, Abele DC. Eczema herpeticum, primary and recurrent. Archives of dermatology. 1966 Feb:93(2):162-73     [PubMed PMID: 4159394]

Level 3 (low-level) evidence


Aronson PL, Yan AC, Mittal MK, Mohamad Z, Shah SS. Delayed acyclovir and outcomes of children hospitalized with eczema herpeticum. Pediatrics. 2011 Dec:128(6):1161-7. doi: 10.1542/peds.2011-0948. Epub 2011 Nov 14     [PubMed PMID: 22084327]

Level 2 (mid-level) evidence


Beck LA, Boguniewicz M, Hata T, Schneider LC, Hanifin J, Gallo R, Paller AS, Lieff S, Reese J, Zaccaro D, Milgrom H, Barnes KC, Leung DY. Phenotype of atopic dermatitis subjects with a history of eczema herpeticum. The Journal of allergy and clinical immunology. 2009 Aug:124(2):260-9, 269.e1-7. doi: 10.1016/j.jaci.2009.05.020. Epub 2009 Jun 27     [PubMed PMID: 19541356]


Narla S,Silverberg JI, Association between atopic dermatitis and serious cutaneous, multiorgan and systemic infections in US adults. Annals of allergy, asthma     [PubMed PMID: 29273131]