Eczema herpeticum has a sudden onset with eruptions of vesicles or pustules in areas affected by dermatitis. Vesicles are often very painful, edematous and crusted. The eruptions may be confused with the preexisting condition which may affect accurate diagnosis. The person may present with malaise, fever and lymphadenopathy. As the disease progresses, the vesiculopustules may develop into punched-out erosions. Eruptions are most commonly seen in the upper part of the body and the head. In some cases localized eruptions are also seen [11]. The eruptions may become hemorrhagic and crusted. Fusion of lesions produces large denuded areas which often bleed and increase the chance of secondary bacterial infections. Periorbital infection may manifest in the form of keratoconjuctivitis. This may lead to scarring of stroma and sometimes blindness. Secondary infections by Staphylococcus aureus or β-hemolytic streptococci are characterized by high fever and other systemic symptoms.

Laboratory observation of the infected cells obtained from scrapings by direct fluorescent antibody (DFA) staining is one of the definitive diagnostic test for this condition. Viral cultures from vesicular fluid is also useful in diagnosis. DFA helps in differentiating the different causative viruses including HSV-1, HSV-2, and varicella zoster virus. A Tzank smear of the vesicles or eruptions is one of the quickest method and is used to observe the multinucleated giant cells and acantholytic balloon cells, both of which are characteristic of eczema herpeticum. But Tzank smear is not virus specific and hence difficult to differentiate the causative agent. Atypical or old lesions are subjected to biopsy or PCR. PCR helps to amplify viral DNA for easy diagnosis. Secondary infections by Staphylococcus or Streptococcus are identified through bacterial cultures. Tissue biopsy of eczema herpeticum shows characteristics that resemble herpes virus infection.

Treatment should be started immediately if Tzank test is positive or if there is a suspicion of eczema herpeticum. The first step of treatment is the antiviral, acyclovir. If the disease is severe and the patient is immunocompromised, 15 mg/kg of acyclovir is given for five days intravenously. Oral acyclovir is given 400 mg five times daily for 5 days for outpatients. For pediatric patients the dose is 25 mg/kg/day for five days. Adequate hydration is essential as there are chances of acyclovir being precipitated in the kidneys.

If the eruptions are diffused and painful in nature, pain medications are recommended. They are given intravenously for extensive erosions while oral medications are suggested in an outpatient setting. Oral antibiotics are used to treat bacterial superinfection, if present. Infections can be prevented by topical application of antibiotic creams. Those who are at a risk of recurrent infection, prophylactic antiviral therapy is recommended. This may be used in patients with chronic skin diseases if the risk of eczema herpeticum is high. If the patient is acyclovir resistant or is severely immunocompromised, foscarnet is suggested. Consultation with ophthalmologist is suggested if eye is involved.

Antiviral treatment has reduced the rate of mortality associated with eczema herpeticum. The average duration of illness due to this condition is reported to be around 16 days, when appropriate treatment is initiated. In some cases, the disease condition may last for as long as 6 weeks. Recurrence of eczema herpeticum is noted in certain cases, but the symptoms are milder when compared to the initial episode. Recurrent episodes of this disease may not have systemic symptoms. Lesions leave a scar after healing in severe cases of eczema herpeticum.

Eczema herpeticum is primarily caused by HSV-1 infection, but may also be caused by HSV-2, coxsackievirus A16, and vaccinia virus. It is a superinfection on dermatosis, commonly atopic dermatitis. Infection can be from autoinoculation or due to contact with an infected person. Apart from atopic dermatitis, eczema herpeticum may also be associated with neurodermatitis, irritant contact dermatitis, pemphigus foliaceus, skin grafts, burns, cowpox, cutaneous T-cell lymphomas, seborrheic dermatitis, ichthyosis vulgaris, and rosacea [2]. Medications or diseases that lead to immunosuppression increase the risk of developing superinfection. Other etiological factors include conditions that precipitate herpes simplex.

Epidemiological data on this disease is negligible. Some studies show an increase in the number of people being treated for the condition. In the US, the incidence of eczema herpeticum has increased since 1980 [3]. Incidence is equally common among men and women. Earlier, this condition was thought to be a disease of childhood. But, this disorder occurs in children of all age and also in adults. In a study conducted in Germany, about half of the patients with eczema herpeticum were in the age group of 15-24 years [4]. Onset of the disease may occur at any time from infant to 70 years of age. Atopic dermatitis, one of the most common predisposing factors of eczema herpeticum, affects about 12% to 26% of the children. The incidence of atopic dermatitis is also increasing over the years.

Many preexisting dermatological conditions are associated with eczema herpeticum, but the pathophysiology of the condition is not clearly defined [5]. Theories have been proposed to explain the development of superinfection in patients with atopic dermatitis. One of the theories suggests that immune dysfunction, including both cellular and humoral immunity, results in IgE sensitization and impaired cutaneous responses. This affects the mechanical, protective properties of the skin in a person with preexisting conditions like atopic dermatitis. As the serum immunoglobulin levels increase due to immune dysfunction, expression of antimicrobial peptide cathelicidin decreases. This is presumed to be one of the reasons for increased replication of HSV-2 [3].

Th-2 cytokine is considered to play a key role in the development of this condition. Higher levels of this cytokine increases allergen sensitivity, frequency of food allergy, and also chances of infections by Staphylococcus aureus and fungi [6]. It is also found to increase inflammatory response that elevate the risk of erosive lesions, and satellite lesions. Th-2 inflammatory reaction amplifies the expression of interleukins which increases the frequency of replication of vaccinia virus [7]. Another factor that enhances the replication of HSV-1 and vaccinia virus is the decrease in the levels of specificity protein 1 (SP-1) [8]. Certain genetic conditions are also known to favor an increase in the rate of replication of viruses. For example, polymorphisms of certain genes lead to an increased expression of interleukins that enhance the replication of viruses [9].

Patients with atopic dermatitis have mutations in the protein filaggrin that aids in the formation of an effective skin barrier. One of the mutations increases the risk of developing superinfections in patients with atopic dermatitis [10]. Certain other genetic changes, as in mutations of interferon regulatory factor 2, affect the levels of interferon gamma that is characteristic of patients with herpetic superinfection of atopic dermatitis.

As eczema herpeticum is a viral superinfection of a preexisting dermatitis, prevention of infection is very important. Patients with high risk of the disease should avoid direct contact with people who have HSV infections. Those who have chronic skin diseases may be offered prophylactic antiviral therapy, if the risk of developing this condition is high.

Eczema herpeticum, also known as Kaposi varicelliform eruption, is a potentially life threatening usually herpetic, cutaneous superinfection. It is marked by cutaneous vesicular eruptions arising from a preexisting skin infection, commonly atopic dermatitis. Eruptions may be caused by herpes simplex virus (HSV) type 1, HSV type 2, coxsackievirus A 16, or vaccinia virus. HSV infection is the most common cause of eczema herpeticum.

If left untreated, this infection may develop into a severe disseminated form, and even lead to death [1]. This viral infection can affect people of any age. Eczema herpeticum can involve multiple organs like lungs, liver, brain, eyes, adrenal glands and gastrointestinal tract. Progression of the disease ca be prevented by treating with antiviral medications.

Eczema herpeticum is a potentially dangerous viral infection that affect people with atopic dermatitis. It may involve any other organs like lungs, liver, and/or brain. It can affect people of any age group and gender. The condition is most commonly caused by herpes simplex virus (HSV), but may also be caused by other viruses like vaccinia virus and coxsackie virus. With the advent of antiviral therapy, treatment of this disease is more successful and death rate due to eczema herpeticum has reduced.

A number of disorders of the skin like pemphigus, burns or eczema may become infected. The virus gains access into the skin when the protective barrier of the skin is weak or nonexistent due to preexisting condition. People with this viral infection may have flu-like symptoms including fever, tiredness and chills. Symptoms start appearing 5-12 days after exposure to the virus. Small pustules develop which expands over a period of 7 days. This gradually form painful, crusted, erosions which may fuse to form large areas. These areas may further be infected by Sterptococcus or Staphylococcus. Affected areas usually include the areas of dermatitis, particularly in the upper parts of the body. A person usually gets the infection by direct contact with another person with viral infection.

Viral culture and direct fluorescent antibody staining helps in identification of the virus. Tznak test helps to view the characteristic multinucleated giant cells in the infected cells, but is unable to distinguish the causative virus. Tissue biopsy also helps to observe the changes characteristic of HSV infection. Antiviral medications should be started immediately when there is a suspicion of this infection or when the infection is confirmed through tests. The most common medications used are acyclovir and valacyclovir. If the patient is resistant to acyclovir, foscarnet is recommended. If the eruptions have secondary bacterial infections, antibiotics are used. Even when bacterial infection is not present, topical antibiotics should be applied to prevent further infection. Since the lesions are very painful, analgesics are recommended. Analgesics are given intravenously if the pustules are diffused and very painful. If the treatment is on outpatient basis, oral pain killers are useful. If eye is infected, ophthalmologists should be consulted. Antiviral therapy has reduced death rate due to eczema herpeticum. The disease may usually last for about 16 days, but may extend to 6 weeks in some cases. Starting the treatment immediately is very important in controlling the symptoms.

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