Relatively uncommon

Herpes Zoster

Introduction

Primary infection with varicella-zoster virus (VZV) is commonly referred to as chickenpox, a childhood disease that, prior to the advent of varicella vaccine use in 1995, infected 99.5% of the US population. After patient recovery from primary infection, the VZV lies dormant in sensory dorsal root or cranial nerve ganglia.1 Herpes zoster, also known as shingles, occurs when latent VZV reactivates and spreads down the sensory nerve to establish infection in the skin. Herpes zoster most commonly presents as an acute, vesicular, painful skin eruption that is distributed unilaterally in a dermatomal distribution.2 Children who get the varicella vaccine have a lower risk of herpes zoster compared with people who were infected with wild-type VZV, but reactivation from the vaccine itself may occur.4 Genital dermatomes are involved in up to 2% of herpes zoster cases.5

Etiology

The reasons that VZV reactivates and herpes zoster affects a particular nerve dermatome are not well understood. That said, the risk of developing herpes zoster increases as VZV-specific, cell-mediated immunity declines, whether from advancing age, certain medical condtitions, (cancer, HIV, bone marrow or organ transplant) or medications that suppress the immune system such as steroids, chemotherapy, or transplant-related drugs.

Symptoms and clinical manifestations

Typical localized herpes zoster, characterized by a painful, vesicular skin eruption distributed over one or two contiguous dermatomes, is the most common presentation. Less commonly, patients may develop “disseminated” zoster in which three or more dermatomes are affected. Disseminated zoster is more likely to occur in immunosuppressed patients. “Zoster sine herpete” describes infrequent cases in which the patient develops the dermtomal pain typical of herpes zoster, without the associated skin eruption.

Most patients with typical herpes zoster will initially notice unilateral, prodromal paresthesias, without any visible skin changes. Prodromal symptoms precede the onset of the skin eruption by a few days and may be described as tingling, burning, sharp or throbbing pain, or itch in the affected area. Some patients will also have early systemic symptoms such as fever, fatigue, and headache.

The morphology of the skin eruption evolves over the course of the illness, usually starting as crops of red papules and plaques on a dermatomal distribution. Over three to five days, groups of small, clustered vesicles (and sometimes pustules) develop on the red-based papule. In areas that are exposed to friction from clothing and activity, including the anogenital region, the vesicles and pustules may become unroofed and appear as erosions. Such erosions occurring in the anogenital region may trigger complaints of pain with urination and bowel movements.

Over the following two to four weeks, the lesions dry, become crusted, and heal. The inflammation from the skin eruption may leave residual pigmentary changes and scarring. Pain and other symptoms gradually improve as the skin eruption resolves. Prolonged pain localized to the affected area for more than 90 days after onset is known as post-herpetic neuralgia (PHN) and can last for months or even years.6

 

Herpes Zoster

 

Herpes Zoster

Herpes Zoster

Diagnosis

In general, the diagnosis of herpes zoster can be made clinically when the history and exam show typical findings of a unilateral, painful, vesibular eruption in a dermatomal distribution. However, herpes zoster occurring in the anogenital region can be difficult to distinguish from herpes simplex infection, and immunocompromised patients may present with atypical history and exam. If the clinical presentation is uncertain, and in all cases where clinical features overlap with genital herpes infection or recurrent herpes zoster is suspected, laboratory confirmatioin of the diagnosis is indicated.7

Pathology/Laboratory Findings

The real-time polymerase chain reaction (PCR) assays provide uniformly rapid and sensitive confirmation of VZV from clinical specimens obtained from skin lesions.8 When compared to viral culture zoster was isolated by culture in 15 samples (14%) and by PCR in 51 (46%) of 110 clinical specimens. 9 Viral culture is therefore insensitive and of low yield compared with PCR testing. 10

Rapid diagnosis of zoster infection can usually be made with direct fluorescent antibody testing (DFA) on scrapings from active vesicular skin lesions that have not yet crusted. The DFA test is widely available, is less expensive compared to culture, and is associated with more rapid turnaround time. 11 The DFA assay can simultaneously detect both HSV and VZV with a 1.5 hour turnaround time. 12

Histology of herpes zoster is identical to HSV. Keratinocytes swell and rupture. Epipthelial cells form giant cells with an associated leukocytoclastic vasculitis.

Differential diagnosis

Differential diagnosis includes herpes simplex, cellulitis, contact dermatitis, and pemphigoid.

Treatment/management

Non-specific care for the acute swollen vulva consists of the following:

  • A sitz bath or as a cool compress 2 to 3 times a day to decrease the swelling and to heal the blisters.
  • For pain use lidocaine-prilocaine cream (EMLA) applied in a thick layer under plastic wrap for 20 minutes for local anesthesia as needed.
  • Catheterization and sedation may be necessary.

Specific treatment includes:

  • Acyclovir (Zovirax) 800 mg orally at 7:00 and 11:00 AM and 3:00, 7:00, and 11:00 PM x 7 days
  • Famciclovir (Famvir) 500 mg orally 3 times a day x 7 days
  • Valacyclovir (Valtrex) 1g orally 3 times a day x 7 days if renal function is normal

For severe disease, prescribe:

  • Acyclovir (Zovirax) 10 mg/kg IV q8h x 7 days

For immunosuppressed patients, prescribe:

  • Foscarnet (Foscavir) 40 mg/kg IV q8h x 7 to 10 days (only if intolerant to acyclovir)

For pain control, prescribe:

  • Acetaminophen and codeine 15 to 30 mg orally q3- 4h
  • Gabapentin 300 mg at bedtime. Increase by 300 mg every two days to 1000 mg OR
  • Pregabalin 50 mg at bedtime. Increase by 50 mg every three days to 150-300 mg if needed.

Herpes zoster of the vulva and the dermatomes S1 through S4 can be incapacitating and ultimately depressing. Early institution of gabapentin or pregabalin may reduce the zoster-associated pain complex. Usually the lesions settle in three to four weeks with some degree of scarring and, in the elderly, post-herpetic neuralgia may result. The use of prednisone to prevent the neuralgia is controversial.

Prescribe the herpes zoster vaccine for prevention.

For more on herpes zoster, see the CDC website: http://www.cdc.gov/shingles/index.html

References

  1. Centers for Disease Control and Prevention, 2022. https://www.cdc.gov/vaccines/vpd-vac/shingles/downloads/vzv_clinical_slideset_jul2010.pdf
  2. Fisher BK, Margesson, LJ. Genital Skin Disorders: Diagnosis and Treatment. Mosby, Inc., 1998. 133-134.
  3. Center for Disease Controls and Prevention, 2022.  https://www.cdc.gov/vaccines/vpd-vac/shingles/downloads/vzv_clinical_slideset_jul2010.pdf In this topic, we will review herpes zoster generally and devote specific attention to diagnosing and treating herpes zoster occurring in the anogenital region.

    Epidemiology

    Anyone who has had primary varicella infection or varicella vaccination can develop herpes zoster. The United States Centers for Disease Control and Prevention (CDC) estimates that approximately 30% of persons in the United States will experience herpes zoster during their lifetime. The epidemiology is similar worldwide. It is more common in females than in males and approximately 50% less common in blacks than in whites. Most will have only one episode of herpes zoster, but recurrences can occur.3Centers for Disease Control and Prevention, 2022. Shingles: Clinical Overview. https://www.cdc.gov/shingles/hcp/clinical-overview.html

  4. Magdaleno-Tapial J, et al. Genital Herpes Zoster: A rare location that can mimic genital herpes. Sex Transm Dis. 2022. Jan 1;49(1):e34-e36.
  5. Centers for Disease Control and Prevention, 2022. Shingles: Clinical Overview. https://www.cdc.gov/shingles/hcp/clinical-overview.html
  6. Birch CJ, Druce JD, Catton MC, et al. Deection of varicella zoster virus in genital specimens using a mutiplex polymerase chain reaction. Sex Transm Infect. 2003 Aug:79(4):298-300
  7. Stránská R, Schuurman R, de Vos M, van Loon AM. Routine use of a highly automated and internally controlled real-time PCR assay for the diagnosis of herpes simplex and varicella-zoster virus infections. J Clin Virol 2004; 30:39.
  8. Schmutzhard J, Merete Riedel H, Zweygberg Wirgart B, Grillner L. Detection of herpes simplex virus type 1, herpes simplex virus type 2 and varicella-zoster virus in skin lesions. Comparison of real-time PCR, nested PCR and virus isolation. J Clin Virol 2004; 29:120.
  9. Gnann JW Jr, Whitley RJ. Clinical practice. Herpes zoster. N Engl J Med 2002; 347:340.
  10. Chan EL, Brandt K, Horsman GB. Comparison of Chemicon SimulFluor direct fluorescent antibody staining with cell culture and shell vial direct immunoperoxidase staining for detection of herpes simplex virus and with cytospin direct immunofluorescence staining for detection of varicella-zoster virus. Clin Diagn Lab Immunol 2001; 8:909.
  11. Chan EL, Brandt K, Horsman GB. Comparison of Chemicon SimulFluor direct fluorescent antibody staining with cell culture and shell vial direct immunoperoxidase staining for detection of herpes simplex virus and with cytospin direct immunofluorescence staining for detection of varicella-zoster virus. Clin Diagn Lab Immunol 2001; 8:909.