Clinical Dermatology Review

: 2020  |  Volume : 4  |  Issue : 1  |  Page : 50--52

Kaposi varicelliform eruption caused by varicella virus in a case of tinea corporis et cruris

Mudita Gupta, Saru Thakur, Reena Kumari Sharma 
 Department of Dermatology, Venereology and Leprosy, I.G.M.C, Shimla, Himachal Pradesh, India

Correspondence Address:
Mudita Gupta
Department of Dermatology, Venereology and Leprosy, I.G.M.C, Shimla, Himachal Pradesh


Kaposi varicelliform eruption (KVE) is a disseminated vesiculopustular lesion occurring over a preexisting cutaneous lesion. Although initially thought to be caused by herpes virus 1 and 2, other viruses have also been known to provoke the disease. There are no reports of human herpes virus 3 over tinea infections causing KVE.

How to cite this article:
Gupta M, Thakur S, Sharma RK. Kaposi varicelliform eruption caused by varicella virus in a case of tinea corporis et cruris.Clin Dermatol Rev 2020;4:50-52

How to cite this URL:
Gupta M, Thakur S, Sharma RK. Kaposi varicelliform eruption caused by varicella virus in a case of tinea corporis et cruris. Clin Dermatol Rev [serial online] 2020 [cited 2020 Aug 12 ];4:50-52
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Kaposi varicelliform eruption (KVE), also known as eczema herpeticum (EH), was first described by Moritz Kaposi in 1884. Clinically, it presents as vesicles and pustules localized over damaged skin and is associated with fever. Disseminated lesions may be occasionally present. It is most commonly caused by human herpes virus 1 and 2. Other viruses such as smallpox virus and Coxsackie have been reported as causative agents.[1] There is a study reporting EH secondary to herpes virus 1 and 2 infection over tinea corporis lesions.[2] There is no report of KVE caused by human herpes virus 3 on tinea lesions to the best of our knowledge.

 Case Report

A 30-year-old male presented to the dermatology outpatient department with complaints of high-grade fever and fluid-filled lesions over the whole body. The patient was apparently well 5 days prior to presentation when he developed itchy vesicular lesions, with cephalocaudal spread. The lesions on the groins, trunk, and hands had burning pain. The evolution of lesion was in the form of a red papule, leading to the formation of a vesicle followed by central crusting. He was diagnosed to have superficial fungal infection 2 months before presentation for which he took treatment, but showed no response. His wife had suffered from chickenpox about 15 days prior to the onset of his disease. On examination, the patient was febrile with significant lymphadenopathy in both axilla and groin. There was generalized body involvement with discrete vesicular lesions on the erythematous base, giving the clinical impression of varicella [Figure 1]. We also observed that, localized over the tinea plaques, there was clustering of vesicular lesions which were monomorphic [Figure 2]. These were the lesions which had burning pain also.{Figure 1}{Figure 2}

Routine hematological and biochemical parameters were normal. Scrapings from the plaques which dissolved in 10% potassium hydroxide showed fungal hyphae, and fungal culture showed growth of Trichophyton rubrum. A Tzanck smear was prepared from lesions on the face, groin, and forearm, all smears showed multinucleated giant cells. With a tentative diagnosis of EH, serology for herpes simplex 1 and 2 was done which was negative. Facilities for varicella culture and polymerase chain reaction are not available at our institute.

The patient was prescribed a course of acyclovir 800 mg five times a day for 7 days. Tablet terbinafine 250 mg daily was prescribed for 3 weeks to treat the underlying fungal infection. A 5-day course of amoxicillin with clavulanic acid was given along with antipyretics. The vesicular lesions had subsided in 2 weeks.


KVE was first described by Moritz Kaposi in the 19th century. However, in the 20th century, Freun demonstrated cytoplasmic inclusions, confirming the viral etiology.[3] KVE is popularly known as eczema herpeticum. Initially, it was thought that infection by herpes virus 1 or 2 is the only causative agent, and hence the name eczema herpeticum was given. However, now, it is known that, in addition to these viruses, it can also be caused by other viruses such as Vaccinia, Coksackie A 16, and molluscum virus, hence the name kaposi varicelliform eruption is more appropriate.[4]

Most commonly, KVE has been reported in association with atopic dermatitis, but it can be seen in areas of skin damage due to varied causes. Atopic dermatitis is the most common dermatosis associated with KVE, though there are case reports of KVE in other dermatological diseases with compromised epidermal barrier.[5] There is a case report describing EH in patients with tinea corporis lesions.[2] In addition to damaged skin, altered innate or acquired immunity can also predispose to the development of KVE lesions.

In superficial fungal infections which are caused by Trichophyton rubrum, one-fifth develop a chronic state. This is because the organism invades the deeper layers of skin, thus suppressing immune response and switching the immunity from Th1 to a Th2 response. In addition to this, patients of chronic dermatophytosis also have 20%–30% lower levels of nitric oxide and free radicals.[6] Overall, the anti-inflammatory cytokines increase and pro-inflammatory cytokines decrease. Garcia-Madrid et al. and Oliveira et al. demonstrated that certain dermatophytes such as T. rubrum can downmodulate receptors (such as toll-like receptors and human β-defensins) that are crucial in activating the appropriate immune response.[7],[8] This altered immune response in tinea lesions in addition to the breached epidermis could play a key role in predisposing the lesions to localize at these sites. In addition to this, exposure of sites to which virus binds and a lack of plasmacytoid dendritic cells may favor the multiplication of virus. This is because plasmacytoid cells produce type 1 interferons (IFNs) – IFN-α and IFN-β, which have antiviral activity.[9]

Infection by human herpes virus 3 causes a primary viremia 4–6 days after infection with dissemination into various organs of reticulo-endothelial system where the virus multiplies. After 2–3 weeks, a secondary viremia occurs with the onset of cutaneous lesions. The decreased pro-inflammatory and increased anti-inflammatory cytokines in areas of tinea plaques allow increased multiplication of virus at this site. It is not due to direct inoculation because nerve endings and sensory ganglia are usually not involved.

KVE is self-resolving without scarring within an average period of 16 days. Occasionally, it may disseminate to the liver, brain, etc. Adjuvant antibiotics should be added to cover superadded bacterial infections.


KVE can be a life-threatening generalized vesicular eruptive disease. Damaged cutaneous barrier and altered immune response are predisposing factors for the development of KVE. Early detection and timely treatment prevents morbidity and mortality associated with the disease.

Declaration of patient consent

The informed consent was obtained for participation in the study and publication of data and images for research and educational purposes.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


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