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← Infectious diseases, microbiology and sexual health indexChapter sections
OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Varicella-zoster infection

Infectious diseases, microbiology and sexual health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

RapidFull
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Disseminated or neurological VZV

Widespread lesions, hypoxaemia, haemorrhagic rash, confusion, focal deficit, meningism, severe immunosuppression or visceral pain suggests disseminated varicella, pneumonitis, encephalitis, vasculopathy or organ involvement.

Action: Use ABCDE, institute airborne and contact precautions, involve infection specialists and critical care, obtain appropriate PCR samples and start renal-adjusted intravenous aciclovir promptly without waiting for every result.

Overview

Distinguish primary varicella from zoster reactivation, recognise ocular, neurological and disseminated disease, treat promptly, and deliver current UK exposure prophylaxis and vaccination.

Varicella-zoster virus is an alpha-herpesvirus. Primary respiratory or direct-contact infection produces viraemia and chickenpox; after recovery the virus remains latent in sensory ganglia. Reactivation years later travels along a sensory nerve to cause shingles, with risk increasing through age and impaired cell-mediated immunity.

Chickenpox is highly transmissible and often more severe in adults than children. A person exposed to shingles develops chickenpox if susceptible, not shingles. Localised covered shingles in an immunocompetent person presents much less transmission risk than chickenpox, disseminated shingles or exposed lesions.

The infectious-disease focus is severity triage, antiviral timing, isolation, exposure assessment and prevention. Morphological description and chronic post-herpetic pain procedures overlap with dermatology and pain services, while ocular disease is co-managed urgently with ophthalmology.

UK prevention changed in 2026. The routine childhood programme now uses two MMRV doses for eligible cohorts, and a separate shingles programme protects older and immunosuppressed adults according to current age and risk criteria.

Aetiology

01

Respiratory primary infection

Airborne particles and respiratory droplets from chickenpox reach susceptible mucosa, with transmission beginning before the rash becomes obvious.

02

Lesion contact

Virus within fresh vesicle fluid spreads through direct contact from chickenpox, disseminated zoster or uncovered localised shingles lesions.

03

Ganglionic latency

After primary infection, VZV genomes persist in cranial and dorsal-root sensory ganglia without producing continuous viraemia.

04

Reactivation triggers

Ageing, transplantation, malignancy, corticosteroids and other impairment of cell-mediated immunity permit latent virus to reactivate as zoster.

Pathophysiology

  1. 1
    Primary viraemia

    Respiratory replication seeds lymphoid tissue and blood, then secondary viraemia distributes virus to skin and sometimes visceral organs.

  2. 2
    Epidermal vesiculation

    Viral cytolysis and inflammation separate epidermal cells, creating fragile fluid-filled lesions that crust as immune control develops.

  3. 3
    Sensory nerve spread

    Reactivated virus travels from a ganglion along a sensory axon, producing dermatomal inflammation, pain and grouped vesicles.

  4. 4
    Vascular and neural injury

    Direct infection and immune inflammation in arteries, meninges, brain, cord or nerve roots causes infarction, encephalitis, myelitis and radiculopathy.

Clinical features and red flags

Chickenpox crops

Generalised itchy macules, papules, vesicles and crusts coexist because new lesions appear in successive crops, often beginning centrally.

Dermatomal shingles

Burning pain or allodynia precedes grouped vesicles in one or adjacent sensory dermatomes, usually stopping at the midline.

Ophthalmic zosterRed flag

Forehead, upper-eyelid or nasal lesions with red eye, photophobia, pain or visual change indicate trigeminal involvement.

Ramsay Hunt syndromeRed flag

Painful auricular vesicles with ipsilateral facial weakness, hearing symptoms or vertigo suggests geniculate ganglion reactivation.

Disseminated infectionRed flag

Lesions beyond the primary dermatome, haemorrhagic vesicles or systemic organ symptoms indicate viraemic spread, particularly during immunosuppression.

Zoster sine herpete

Segmental neuropathic pain or neurological disease can rarely occur without visible rash and requires virological and specialist correlation.

Red flags requiring action

  • Eye pain, photophobia, reduced vision, red eye or vesicles on the forehead or nose needs same-day ophthalmic assessment for sight-threatening zoster.
  • Confusion, seizure, meningism, focal weakness, ataxia or stroke-like symptoms requires urgent CNS investigation and intravenous aciclovir.

Investigations

  1. 01
    Vesicle or lesion PCRFirst step
    Why
    Confirm VZV in atypical, severe, disseminated or epidemiologically important rash.
    Interpretation and limitations
    PCR from vesicle fluid, base swab or crust distinguishes VZV from HSV; a poor superficial sample can be falsely negative.
  2. 02
    VZV IgG
    Why
    Assess susceptibility after significant exposure in selected high-risk contacts.
    Interpretation and limitations
    IgG evidence supports previous immunity but does not diagnose the current rash; immunosuppressed contacts require laboratory assessment because history alone is unreliable.
  3. 03
    CSF cell count and VZV PCR
    Why
    Investigate meningitis, encephalitis, myelitis or vasculopathy when lumbar puncture is safe.
    Interpretation and limitations
    Lymphocytic inflammation and detectable VZV DNA support CNS infection, but treatment should start before results when suspicion is high.
  4. 04
    MRI brain or spine
    Why
    Define encephalitis, vasculopathic infarction, myelitis and competing structural causes.
    Interpretation and limitations
    Imaging may show temporal or multifocal abnormalities, infarcts or cord lesions; normal early imaging does not exclude VZV CNS disease.
  5. 05
    Ophthalmic examination
    Why
    Identify keratitis, uveitis, retinitis, raised pressure or optic involvement.

Differential diagnosis

01

Disseminated HSV

HSV produces clustered painful erosions and can disseminate during immune suppression; lesion PCR distinguishes it from VZV.

02

Bullous impetigo

Staphylococcal superficial bullae form honey-coloured crusts without dermatomal pain, crops of lesions or VZV PCR positivity.

03

Contact dermatitis

A sharply exposure-related pruritic vesicular eruption lacks systemic viraemia and follows the distribution of an external trigger.

04

Mpox

Firm deep lesions, lymphadenopathy and epidemiological exposure can mimic varicella, but lesions are often synchronous within one area.

05

Neuropathic pain

Radiculopathy, peripheral nerve entrapment and musculoskeletal pain can mimic pre-eruptive zoster, especially when no diagnostic rash subsequently appears.

Management

01ISOLATEControl suspected chickenpoxFirst stepA generalised vesicular rash or disseminated zoster is suspected in a healthcare or shared setting.+
  1. 1Separate the patient from susceptible pregnant, neonatal and immunosuppressed people and apply airborne plus contact precautions in healthcare.
  2. 2Establish rash onset, lesion distribution, immune status, pregnancy, respiratory and neurological symptoms and every significant contact during the infectious interval.
  3. 3Obtain lesion PCR when confirmation affects management or contact action, but do not delay treatment of severe disease.
  4. 4Inform infection prevention and health protection when exposure occurred in healthcare, care, maternity or another high-risk setting.
02TREATTreat localised zosterA patient has a compatible unilateral dermatomal eruption without visceral or neurological disease.+

Complications

01

Varicella pneumonitis

Diffuse viral lung injury causes cough, dyspnoea and rapidly progressive hypoxaemia, particularly in adults, pregnancy and smokers.

02

CNS infection

Meningitis, encephalitis, cerebellitis, myelitis and vasculopathic stroke can cause seizures, ataxia, focal deficit and permanent disability.

03

Ocular injury

Keratitis, uveitis, retinitis, optic neuropathy and secondary glaucoma can permanently reduce visual acuity after untreated or severe ophthalmic zoster.

04

Post-herpetic neuralgia

Persistent sensory-nerve injury produces burning pain and allodynia beyond rash healing, with frequency increasing substantially with age.

05

Secondary bacterial infection

Scratching and skin-barrier loss permit streptococcal or staphylococcal cellulitis, abscess, sepsis and rarely necrotising soft-tissue infection.

Monitoring and follow-up

  • During intravenous aciclovir, monitor creatinine, urine output, hydration and neurological state at least daily, with renal-adjusted intervals.
  • Review ophthalmic zoster according to eye findings because keratitis, uveitis, pressure change and retinal disease can emerge after the skin presentation.
  • Reassess immunosuppressed patients for new lesions or organ symptoms until dissemination is excluded and a response to therapy is clear.
  • Follow pregnant infection or exposure through the designated maternity and fetal-medicine pathway rather than arranging unsupervised serology alone.
  • Document PEP start and stop dates relative to exposure and tell the patient that breakthrough rash still requires isolation and urgent review.
  • For post-herpetic neuralgia, review pain, sleep, function and neuropathic treatment toxicity after the acute rash has healed.

Special situations

Shingles transmits chickenpox

A susceptible contact exposed to VZV from shingles develops primary varicella rather than acquiring shingles directly.

Rash can be absent

VZV vasculopathy, meningitis or radiculitis occasionally occurs without vesicles, requiring CSF and clinical correlation.

Nasal lesions matter

Involvement of the nasociliary branch increases ocular risk, but any eye symptom deserves urgent assessment regardless of rash location.

PEP starts later

High-risk oral antiviral prophylaxis starts on day 7 because suppressing viral replication during the incubation phase is the intended strategy.

History fails in immune suppression

Previous chickenpox recall is insufficient for immunosuppressed contacts, for whom urgent antibody assessment guides prophylaxis.

Scope boundary

Systemic complications, isolation and exposure prevention are central here; detailed rash morphology overlaps with dermatology teaching.

Common pitfalls

  1. 01

    Do not call a generalised vesicular eruption shingles simply because the patient previously had chickenpox; consider recurrent primary-like dissemination.

  2. 02

    Do not wait for lesion or CSF PCR before starting intravenous aciclovir in a severely ill patient with compatible disease.

  3. 03

    Do not use aciclovir 800 mg five times daily as the PEP schedule; UKHSA adult PEP uses four daily doses from day 7 to day 14.

  4. 04

    Do not dismiss ocular risk because the nose is spared when red eye, photophobia, pain or visual change is present.

  5. 05

    Do not give a live varicella-containing vaccine during pregnancy or substantial immunosuppression; use the appropriate exposure pathway instead.

  6. 06

    Do not use pre-2026 routine childhood vaccine timing; confirm cohort-specific MMRV and catch-up eligibility in the current Green Book.

Practice

Two practice questions

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Question 1 of 2
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Infectious diseases, microbiology and sexual healthOriginal SBA

Pregnant contact prophylaxis timing

A VZV-IgG-negative pregnant adult reports significant household chickenpox exposure two days ago and remains well. What oral antiviral timing follows current UKHSA guidance?

Choose one answer, then submit
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Sources and review status3 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • Varicella: the green book chapter
  • Guidelines on post-exposure prophylaxis (PEP) for varicella or shingles
  • Shingles | CKS | NICE

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom

Key points

  • Primary VZV causes chickenpox with crops of pruritic lesions at different stages; reactivation causes unilateral dermatomal shingles that usually does not cross the midline.
  • Chickenpox spreads by respiratory and lesion contact from about 48 hours before rash until all lesions crust; uncovered or disseminated shingles can also transmit VZV.
  • Adults, pregnant people, neonates and immunosuppressed patients have greater risk of pneumonitis, encephalitis and disseminated disease.
  • Lesion-vesicle PCR is the preferred laboratory confirmation when appearance is atypical, disease is severe or public-health consequences are important.
  • Treat uncomplicated shingles promptly, ideally within 72 hours, using oral aciclovir 800 mg five times daily for seven days or a suitable equivalent regimen.
  • Use intravenous aciclovir 10 mg/kg every eight hours for encephalitis or severe immunocompromised VZV, with renal adjustment, hydration and one-hour infusion.
  • UKHSA recommends oral aciclovir or valaciclovir as preferred PEP for susceptible high-risk contacts from day 7 through day 14 after exposure.
  • From January 2026, eligible children in England receive routine MMRV at 12 and 18 months, with cohort-specific catch-up; use current Green Book eligibility rather than an old schedule.
Dyspnoea, cough, hypoxaemia or chest pain during chickenpox suggests varicella pneumonitis and requires hospital admission.
  • Widespread, haemorrhagic or necrotic lesions in an immunosuppressed patient may mark disseminated infection with visceral involvement.
  • Pregnancy with chickenpox or significant exposure requires urgent maternity and infection advice because maternal and fetal risks and PEP are time dependent.
  • A neonate exposed to maternal chickenpox from seven days before to seven days after delivery needs immediate specialist risk assessment under the current UKHSA pathway.
    • Interpretation and limitations
    Visual acuity, fluorescein, slit-lamp and fundal findings determine topical and systemic specialist treatment; skin distribution alone cannot grade ocular injury.
  • 06
    Respiratory and organ assessment
    Why
    Detect pneumonitis or visceral dissemination in severe chickenpox.
    Interpretation and limitations
    Check oxygen saturation, chest imaging, FBC, liver and renal tests; respiratory symptoms can precede rapidly progressive bilateral pneumonitis.
  • 07
    Pregnancy and immune-status review
    Why
    Determine severity, PEP eligibility and fetal or neonatal pathways.
    Interpretation and limitations
    Document gestation, exposure date, rash onset, vaccine or infection history and immunosuppressive therapy, then use urgent VZV IgG and specialist advice where indicated.
    • 1
    Start oral antiviral therapy ideally within 72 hours when age, pain, site, new vesicles or immune status meets treatment criteria.
  • 2Consider treatment beyond 72 hours when new vesicles continue, ophthalmic involvement exists, the patient is immunosuppressed or severe complications remain possible.
  • 3Provide graded analgesia, protect lesions, advise hand hygiene and avoid contact with susceptible high-risk people until all vesicles crust.
  • 4EscalationEscalate eye, ear, motor, disseminated or CNS findings rather than managing them as routine shingles.
    • 03ESCALATETreat severe or complicated VZVEscalationDissemination, pneumonitis, encephalitis, vasculopathy, severe immune suppression or inability to absorb oral therapy is present.+
    1. 1Admit with appropriate isolation, collect lesion, blood, CSF and imaging studies selected by the involved organ and immediate safety.
    2. 2Start intravenous aciclovir 10 mg/kg every eight hours for encephalitis or severe immunocompromised infection, using a renal- and weight-appropriate protocol.
    3. 3Infuse over one hour with adequate hydration and daily renal review to reduce crystal nephropathy and neurotoxicity.
    4. 4Define duration and oral step-down with infection, neurology, respiratory or ophthalmology specialists according to disease site and virological response.
    04PEPProtect a susceptible high-risk contactA pregnant, immunosuppressed or qualifying neonatal person has significant exposure to infectious chickenpox or shingles.+
    1. 1Confirm that the index condition, contact intensity and timing meet UKHSA definitions, then assess susceptibility with documented history and VZV IgG as required.
    2. 2For susceptible pregnant and immunosuppressed contacts, use oral aciclovir or valaciclovir from day 7 to day 14 after the first exposure day.
    3. 3If presentation occurs after day 7, a seven-day antiviral course may start up to day 14; use the detailed neonatal exceptions in current guidance.
    4. 4Arrange intravenous varicella immunoglobulin only for the restricted groups and circumstances specified by UKHSA, including defined highest-risk neonatal exposure.
    05VACCINATEPrevent primary and reactivated diseaseRoutine childhood, catch-up, occupational, contact or shingles-vaccine eligibility is reviewed.+
    1. 1Use the 2026 cohort table: eligible children receive combined MMRV at 12 and 18 months, with date-of-birth-specific transitional and catch-up arrangements.
    2. 2Offer targeted varicella vaccination to susceptible eligible contacts or workers under the Green Book, checking live-vaccine contraindications first.
    3. 3Offer recombinant shingles vaccine to eligible older and immunosuppressed adults according to the current age, interval and immune-status programme.
    4. 4Record product, batch, route and next dose, and avoid assuming that previous shingles removes all need for scheduled vaccination.
    Key medicines and prescribing safety5 treatments · regimens, roles and cautions+
    Reduces viral replication and acute disease burden in treated herpes zoster, including selected later presentations with ongoing risk.

    Aciclovir for uncomplicated shingles

    Give 800 mg orally five times daily for seven days, started ideally within 72 hours of rash onset when treatment criteria are met.

    Adjust dose or frequency for renal impairment, maintain hydration, review nephrotoxins and recognise confusion or tremor as possible accumulation-related neurotoxicity.

    Provides systemic antiviral treatment with fewer daily doses than aciclovir for localised zoster.

    Valaciclovir for uncomplicated shingles

    Give 1 g orally three times daily for seven days as a simpler-bioavailability alternative when oral therapy is appropriate.

    Renally adjust, maintain hydration and review neurological toxicity, thrombotic microangiopathy risk at extreme exposure and significant medicine interactions.

    Immediate therapy for CNS, disseminated, visceral or otherwise life-threatening varicella-zoster infection.

    Intravenous aciclovir for severe VZV

    Give 10 mg/kg intravenously every eight hours by one-hour infusion for encephalitis or severe immunocompromised VZV, using renal and obesity-adjusted specialist dosing.

    Check creatinine before and during therapy, hydrate, adjust interval to renal function and investigate new confusion for aciclovir accumulation as well as encephalitis.

    Preferred oral PEP for susceptible pregnant or immunosuppressed adults and other defined high-risk contacts.

    Aciclovir for VZV post-exposure prophylaxis

    Give 800 mg orally four times daily from day 7 through day 14 after exposure to a susceptible qualifying adult under UKHSA guidance.

    Use is off-label for PEP, confirm exposure and susceptibility, renally adjust and follow separate neonatal timing and immunoglobulin rules.

    Preferred PEP alternative with fewer daily doses and improved oral bioavailability for eligible susceptible contacts.

    Valaciclovir for VZV post-exposure prophylaxis

    Give 1 g orally three times daily from day 7 through day 14 after exposure when selected by the UKHSA high-risk-contact pathway.

    This PEP use is off-label; adjust for kidney function, document the first exposure day and extend or restart only under the published repeated-exposure rules.