01OverviewDefinition, clinical context and the essential points that orientate the chapter.
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.
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.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Respiratory primary infection
Airborne particles and respiratory droplets from chickenpox reach susceptible mucosa, with transmission beginning before the rash becomes obvious.
Lesion contact
Virus within fresh vesicle fluid spreads through direct contact from chickenpox, disseminated zoster or uncovered localised shingles lesions.
Ganglionic latency
After primary infection, VZV genomes persist in cranial and dorsal-root sensory ganglia without producing continuous viraemia.
Reactivation triggers
Ageing, transplantation, malignancy, corticosteroids and other impairment of cell-mediated immunity permit latent virus to reactivate as zoster.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Primary viraemia
Respiratory replication seeds lymphoid tissue and blood, then secondary viraemia distributes virus to skin and sometimes visceral organs.
- 2Epidermal vesiculation
Viral cytolysis and inflammation separate epidermal cells, creating fragile fluid-filled lesions that crust as immune control develops.
- 3Sensory nerve spread
Reactivated virus travels from a ganglion along a sensory axon, producing dermatomal inflammation, pain and grouped vesicles.
- 4Vascular and neural injury
Direct infection and immune inflammation in arteries, meninges, brain, cord or nerve roots causes infarction, encephalitis, myelitis and radiculopathy.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Generalised itchy macules, papules, vesicles and crusts coexist because new lesions appear in successive crops, often beginning centrally.
Burning pain or allodynia precedes grouped vesicles in one or adjacent sensory dermatomes, usually stopping at the midline.
Forehead, upper-eyelid or nasal lesions with red eye, photophobia, pain or visual change indicate trigeminal involvement.
Painful auricular vesicles with ipsilateral facial weakness, hearing symptoms or vertigo suggests geniculate ganglion reactivation.
Lesions beyond the primary dermatome, haemorrhagic vesicles or systemic organ symptoms indicate viraemic spread, particularly during immunosuppression.
Segmental neuropathic pain or neurological disease can rarely occur without visible rash and requires virological and specialist correlation.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 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.
- 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.
- 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.
- 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.
- 05
Ophthalmic examination - Why
- Identify keratitis, uveitis, retinitis, raised pressure or optic involvement.
- 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.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Disseminated HSV
HSV produces clustered painful erosions and can disseminate during immune suppression; lesion PCR distinguishes it from VZV.
Bullous impetigo
Staphylococcal superficial bullae form honey-coloured crusts without dermatomal pain, crops of lesions or VZV PCR positivity.
Contact dermatitis
A sharply exposure-related pruritic vesicular eruption lacks systemic viraemia and follows the distribution of an external trigger.
Mpox
Firm deep lesions, lymphadenopathy and epidemiological exposure can mimic varicella, but lesions are often synchronous within one area.
Neuropathic pain
Radiculopathy, peripheral nerve entrapment and musculoskeletal pain can mimic pre-eruptive zoster, especially when no diagnostic rash subsequently appears.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01ISOLATEControl suspected chickenpoxFirst stepA generalised vesicular rash or disseminated zoster is suspected in a healthcare or shared setting.+
- 1Separate the patient from susceptible pregnant, neonatal and immunosuppressed people and apply airborne plus contact precautions in healthcare.
- 2Establish rash onset, lesion distribution, immune status, pregnancy, respiratory and neurological symptoms and every significant contact during the infectious interval.
- 3Obtain lesion PCR when confirmation affects management or contact action, but do not delay treatment of severe disease.
- 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.+
- 1Start 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.+
- 1Admit with appropriate isolation, collect lesion, blood, CSF and imaging studies selected by the involved organ and immediate safety.
- 2Start intravenous aciclovir 10 mg/kg every eight hours for encephalitis or severe immunocompromised infection, using a renal- and weight-appropriate protocol.
- 3Infuse over one hour with adequate hydration and daily renal review to reduce crystal nephropathy and neurotoxicity.
- 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.+
- 1Confirm that the index condition, contact intensity and timing meet UKHSA definitions, then assess susceptibility with documented history and VZV IgG as required.
- 2For susceptible pregnant and immunosuppressed contacts, use oral aciclovir or valaciclovir from day 7 to day 14 after the first exposure day.
- 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.
- 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.+
- 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.
- 2Offer targeted varicella vaccination to susceptible eligible contacts or workers under the Green Book, checking live-vaccine contraindications first.
- 3Offer recombinant shingles vaccine to eligible older and immunosuppressed adults according to the current age, interval and immune-status programme.
- 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+
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.
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.
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.
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.
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.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Varicella pneumonitis
Diffuse viral lung injury causes cough, dyspnoea and rapidly progressive hypoxaemia, particularly in adults, pregnancy and smokers.
CNS infection
Meningitis, encephalitis, cerebellitis, myelitis and vasculopathic stroke can cause seizures, ataxia, focal deficit and permanent disability.
Ocular injury
Keratitis, uveitis, retinitis, optic neuropathy and secondary glaucoma can permanently reduce visual acuity after untreated or severe ophthalmic zoster.
Post-herpetic neuralgia
Persistent sensory-nerve injury produces burning pain and allodynia beyond rash healing, with frequency increasing substantially with age.
Secondary bacterial infection
Scratching and skin-barrier loss permit streptococcal or staphylococcal cellulitis, abscess, sepsis and rarely necrotising soft-tissue infection.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- 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.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
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.
11Common pitfallsFrequent interpretation and management errors.
- 01
Do not call a generalised vesicular eruption shingles simply because the patient previously had chickenpox; consider recurrent primary-like dissemination.
- 02
Do not wait for lesion or CSF PCR before starting intravenous aciclovir in a severely ill patient with compatible disease.
- 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.
- 04
Do not dismiss ocular risk because the nose is spared when red eye, photophobia, pain or visual change is present.
- 05
Do not give a live varicella-containing vaccine during pregnancy or substantial immunosuppression; use the appropriate exposure pathway instead.
- 06
Do not use pre-2026 routine childhood vaccine timing; confirm cohort-specific MMRV and catch-up eligibility in the current Green Book.