Atypical Wounds - varicella virus

The varicella virus (both herpes simplex and herpes zoster) causes skin disorders that require early detection, diagnosis, and treatment in order to achieve optimal resolution and to prevent long-term complications.
Atypical Wounds - varicella virus

Unlike the coronavirus with which we are all dealing in one way or another, the varicella virus manifests itself in distinct skin changes. Varicella is a virus that presents in three different ways: herpes simplex Type 1 (oral or cold sores), herpes simplex Type 2 (genital herpes) and herpes zoster (varicella-zoster or shingles).  The herpes simplex virus (HSV) persists in an individual for a lifetime due to the presence of a latent virus pool in terminally differentiated neurons, usually the peripheral ganglion.[1] HSV is a DNA virus that invades the cell nucleus and replicates, thereby producing partial thickness wounds on the mouth and lips.  Herpes simplex Type 1 activation is commonly referred to as “cold sores” that occur on the lips and mouth.  Herpes simplex Type 2 is recognized as a sexually transmitted disease that results in lesions on the genital skin.  Both can be reactivated, and in immune-compromised individuals can lead to local infection, chronic herpetic ulcers, and mucous membrane damage, as well as systemic infections in the central and peripheral nervous systems, the gastrointestinal tract, and the ocular system.[2]

Chicken pox is a childhood disorder caused by the varicella-zoster virus (VZV).  The virus enters through the respiratory system and infects the tonsillar T cells.  The infected T cells carry the virus to the reticuloendothelial system where the major replication occurs and to the skin where the rash appears[3]

The VZV can remain latent in the nerve ganglion and reactivate in later years, usually during a period of stress or immunosuppression, as herpes varicella-zoster or “shingles.”   (See photo)   Vesicles can involve the corium and dermis, with degenerative changes characterized by ballooning, multinucleated giant cells and eosinophilic intra-nuclear inclusions.  Infection may involve localized dermal blood vessels, resulting in necrosis and epidermal hemorrhage.  Individuals who are immunosuppressed can have more severe cases of herpes, with the incidence of herpes zoster more than 14 times higher in adults with HIV.[4] 


Clinical Presentation

       Herpes simplex usually occurs initially in childhood and progresses through the stages of prodrome, erythema, papule, vesicle, ulcer, hard crust, and residual dry flaking and swelling.  Lesions can become secondarily infected by staphylococcus or streptococcus.  Individuals tend to have recurrent eruptions.  Non-ulcerative lesions tend to last 3 days; full-blown ulcerative lesions may last 7-10 days.

       Chicken pox usually presents with prominent fever, malaise, and a pruritic rash that starts on the face, scalp, and trunk and spreads to the extremities.  The rash is initially maculopapular and rapidly progresses to vesicles, then pustules that rupture, and then to crusts. 

       Herpes varicella-zoster presents as an eruption of grouped vesicles on an erythematous base usually limited to a single dermatome.   Initial symptoms include dermatologic tingling or pain in the affected dermatome 48-72 hours before the onset of lesions, which can appear for 3-5 days.  Lesions develop quickly into vesicles, then rupture, ulcerate, and dry out.  They usually resolve in 10-15 days, although the pain may remain as post-herpatic neuralgia.  In patients with advanced HIV, the herpetic infection may develop into chronic ulcers and fissures with a substantial degree of edema.  The patient in the photograph was being seen for lymphedema and came into clinic complaining of pain in the thigh under her compression bandages.  Upon removal, the blistering rash was observed on the anterior thigh, the patient’s referring physician was notified, and she was started immediately on medication.

Differential diagnosis

       History and clinical presentation are often all that is necessary to establish the diagnosis of herpes; therefore, confirmatory tests such as the Tzanck smear preparation, biopsy, or viral culture are rarely necessary.  Other differential diagnoses include:

       Small pox - lesions are deeper and painful; all lesions occur at the same stage.

       Disseminated HSV – usually occurs in the setting of a skin disorder

       Meningococcemia – presents with petechiae, purpura, sepsis

       Atopic dermatitis – usually in children and localized to one area (e.g. forehead or chest)

       Atypical measles – presents with diffuse rash, not dermatomal, usually in younger children

                      who have not been vaccinated

       Poison ivy – limited to area of contact with the plant

       Spinal nerve compression (pain) – also dermatomal but without skin changes


Medical Management

       Chicken pox will usually heal in less than 2 weeks without medical intervention.

       Uncomplicated herpes varicella-zoster is treated for 7 -10 days with acyclovir ( Zovirax), famciclovir (Famvir) or valacyclovir( Valtrex).[5] These oral antiviral medications reduce the duration and severity of adult symptoms. Oral prednisone may decrease the risk of post-herpetic neuralgia.  VariZIG may prevent complications in immunocompromised and pregnant patients, as well as decrease the severity of the HZV symptoms.[6]  As of October 2017, a new vaccine (Shingrix) is recommended to be administered twice, 2-6 months apart, and is considered 90% effective in preventing shingles and post-herpetic pain.[7] Antihistamines may help reduce the itching, and Zostix may help reduce severe neuralgia.  If the lesions have not healed in 3-4 weeks, the patient may have a drug-resistant virus that may require treatment with IV foscarnet.

Wound Management

       Herpes simplex can be treated with topical acyclovir and mild corticosteroid ointment[8]  or with a thin hydrocolloid dressing.3 Moisture retentive dressings such as hydrogels, hydrocolloids, transparent films or alginates may be helpful to facilitate autolytic debridement of necrotic tissue and healing of herpes-varicella wounds, as well as reduce pain by protecting the lesions from friction caused by clothing. 

       In summary, the varicella virus (both herpes simplex and herpes zoster) causes skin disorders that require early detection, diagnosis, and treatment in order to achieve optimal resolution and to prevent long-term complications.


[1] Suzich JB, Cliffe AR. Strength in adversity: Understanding the pathways to herpes simplex virus reactivation. Virology. 2018;52(2):81-91.

[2] Staikov IN, Neykov NV, Kazandjieva JS, Tsankov NK.  Is herpes implex a systemic disease? Clin Dermatol.  2015;33(5):551-555.

[3] Karlsmark T, Goodman JJ, Drouault Y, Lufrano L, Pledger GW, Cold Sore Study Group.  Randomized clinical study comparing Compeed cold sore patch to acyclovir cream 5% in the treatment of herpes simplex labialis.  J Eur Acad Dermatol Venereol.  2008;22(10):1184-1192.

[4] Hamm R, Shah JB.  Atypical Wounds. In Hamm R (Ed.) Text and Atlas of Wound Diagnosis and Treatment, 2nd Ed. New York: McGraw Hill Education.  2019;235-268.

[5] Junior HP, de Oliveira MB, Gambero S, Amazonas RB, Randomized clinical trial of famcicloviror acyclovir for the treatment of herpes zoster in adults.  Int J Infec Dis. 2018;72:11-15.

[6] Updated recommendations for the use of VariZIG – United States 2013.  Available at Accessed July 30, 2018.

[7] What everyone should know about shingles vaccine (Shingrix).  Available at  Accessed July 30, 2018.

[8] Harmenberg J, Oberg B, Spruance S.  Prevention of ulcerative lesions by episodic treatment of recurrent herpes labialis: A literature review.  Acta Derm Venereol.  2010;90(2):122-130.


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