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Pediatrics · Chapter 12. Infectious and parasitic diseases

Shingles

Herpes zoster

Herpes zoster (shingles) is a sporadic viral disease representing the endogenous reactivation of a latent infection caused by Varicella Zoster Virus. The disease is accompanied by pronounced pain syndrome and unilateral vesicular eruptions located strictly along the affected nerves within a dermatome.

PathogenHuman herpesvirus type 3 (HHV-3 / Varicella Zoster Virus).
Virus LocalizationSensory nerve ganglia (spinal roots, Gasserian ganglion).
SeasonalityA predominant increase in incidence is observed during the cold season.
Frequent ComplicationSecondary bacterial infection of the vesicular rash elements.
3 min readFor medical studentsUpdated Sep 20, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Etiology and pathogenesis

The disease occurs exclusively sporadically and is not the result of a primary infection. It is the result of endogenous reactivation of human herpesvirus type 3 (HHV-3), which persists in the body for life after a primary episode of chickenpox. The main triggering factor for the development of the disease is a decrease in immunological reactivity (immunosuppression).

In its latent state, the virus resides in sensory nerve ganglia. The most frequent localizations are the dorsal root spinal ganglia (predominantly in the thoracic region) and the trigeminal Gasserian ganglion. Upon reactivation, the pathogen spreads via neurogenic pathways — centrifugally along nerve fibers. This determines the appearance of skin rashes strictly within the boundaries of the dermatome innervated by the affected ganglion.

Clinical presentation

The acute onset of the disease (prodromal period) is characterized by fever and intense, burning pain in the area of the future rash. At this stage, the pronounced pain syndrome can mimic acute therapeutic or surgical pathology: pleuritis, acute cholecystitis, or renal colic.

Approximately 1–3 days after the onset of pain, a characteristic exanthema appears. It goes through clearly defined stages of development:

  1. Appearance of erythema and closely grouped red papules.
  2. Transformation of papules into vesicles filled with clear exudate.
  3. Clouding of the vesicle contents.
  4. Drying of the elements (in about a week) with the formation of crusts.
  5. Sloughing of the crusts, after which mild residual hyperpigmentation forms on the skin.

A key diagnostic sign is the strict localization of the rash and pain syndrome along the course of the affected nerve.

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Clinical features in children

In pediatric practice, herpes zoster is rarely recorded in patients under 10 years of age. The process is always strictly unilateral and predominantly affects the innervation zones of the trigeminal and intercostal nerves (involvement of the limbs is atypical).

Unlike adults, postherpetic neuralgia and severe pain syndrome are rare in children. A mild (abortive) course is often noted, while severe atypical forms (bullous, hemorrhagic, gangrenous, generalized) develop only as exceptions.

Diagnostic Principles

The basis of diagnosis is the clinical method: assessment of vesicle morphology and the strict sequential stages of rash development. To confirm the infection in the laboratory, the following are used:

  • Virological and molecular methods: study of vesicle contents using PCR and immunofluorescence assay (IFA), as well as virus isolation on cell culture (human fibroblasts).
  • Cytological method (Tzanck smear): microscopy of a scraping from the base of the vesicle to detect specific multinucleated giant cells.
  • Immunological and serological methods: indication of viral antigens in the material and detection of specific antibodies in blood serum.

Management and Prevention

The basis of etiotropic treatment for herpes zoster is the administration of systemic antiviral drugs — acyclovir or famciclovir. To relieve pain (symptomatic therapy), analgesics, physiotherapy procedures, and local procaine (novocaine) blocks are used. If bacterial complications occur, antibiotics and local agents with mupirocin or bacitracin are prescribed.

Anti-epidemic measures include isolation of the patient until the 5th day after the appearance of the last rash elements. Non-immune contacts among children are subject to quarantine for 21 days (or from the 11th day if the exact date of contact is established). Terminal disinfection in the focus is not carried out due to the low persistence of the virus. Specific prophylaxis using a vaccine exists for individuals over 60 years of age.

How to memorize

To memorize the classical evolution of herpetic rash, the sequence E-P-V-C can be used (Erythema → Papule → Vesicle → Crust).

Class and exam questions

What is the isolation period for a patient with herpes zoster?

The patient is isolated until the 5th day from the moment the last rash elements appear, as they are most contagious during this period.

How is quarantine applied to contact children?

Children who have not previously had chickenpox are subject to quarantine for 21 days from the moment of contact. If the date of contact is precisely established, quarantine is introduced from the 11th day.

What diseases can herpes be confused with in the early period?

Before the appearance of typical exanthema, severe pain can mimic surgical or therapeutic pathology: renal colic, pleuritis, acute cholecystitis.

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What else to study on this topic

  • Clinical differences between chickenpox and herpes zoster.
  • Differential diagnosis of vesicular eruptions (impetigo, HSV types 1 and 2).
  • Severe atypical forms of herpetic infection (bullous, gangrenous, generalized).
  • Features of the development and relief of postherpetic neuralgia.

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