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Chickenpox (Varicella)

Chickenpox (varicella) is a highly contagious primary infection caused by varicella-zoster virus (VZV), a member of the ... MRCPCH, RCPCH Progress Test exam pre

Updated 9 Jan 2025
Reviewed 17 Jan 2026
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Clinical reference article

Chickenpox (Varicella)

1. Clinical Overview

Summary

Chickenpox (varicella) is a highly contagious primary infection caused by varicella-zoster virus (VZV), a member of the Herpesviridae family (Human Herpesvirus 3). It is characterised by a generalised vesicular rash appearing in successive crops, with lesions at different stages of development — the pathognomonic "starry sky" appearance. [1,2]

The classic vesicular lesion is described as a "dewdrop on a rose petal" — a clear, superficial vesicle on an erythematous base. In immunocompetent children, chickenpox is typically a mild, self-limiting illness lasting 5-10 days. However, it can cause severe morbidity and mortality in high-risk populations including neonates, pregnant women, adults, and immunocompromised individuals. [2,3]

Following primary infection, VZV establishes lifelong latency in sensory dorsal root ganglia and cranial nerve ganglia. Reactivation, typically decades later or during immunosuppression, causes herpes zoster (shingles) — a dermatomal vesicular eruption with associated neuropathic pain. [1,4]

Prevention strategies include live attenuated vaccination (part of routine childhood immunisation in many countries) and post-exposure prophylaxis with varicella-zoster immunoglobulin (VZIG) for high-risk contacts. [5,6]

Key Facts

ParameterValue
Causative agentVaricella-zoster virus (VZV) — Human Herpesvirus 3 (HHV-3), Herpesviridae family
Transmission routesRespiratory droplets (airborne), direct contact with vesicle fluid, vertical (transplacental)
Incubation period10-21 days (median 14-16 days)
Infectious period2 days before rash onset until all lesions crusted (typically 5-7 days post-rash)
Attack rate> 90% in susceptible household contacts; 10-35% in school contacts
Classic lesion"Dewdrop on a rose petal" — clear vesicle on erythematous base
Rash distributionCentripetal: trunk predominant → spreads to face, scalp, limbs
Rash evolutionMacule → papule → vesicle → pustule → crust (24-48 hours per lesion)
Total lesion countTypically 250-500 (range 10 to > 1500)
Complication rate2-6% in immunocompetent children; significantly higher in high-risk groups
Latency siteDorsal root ganglia, cranial nerve ganglia
Reactivation diseaseHerpes zoster (shingles)
Vaccine typeLive attenuated (Oka strain)

Clinical Pearls

"Starry Sky Rash": The pathognomonic feature of chickenpox is crops of vesicles at multiple stages of evolution (macules, papules, vesicles, pustules, crusts) visible simultaneously — creating a "starry sky" or "pleomorphic" appearance. This distinguishes varicella from monomorphic rashes such as smallpox where all lesions are at the same stage. [1,2]

"No NSAIDs — Ever!": NSAIDs (particularly ibuprofen) are contraindicated in chickenpox due to a significant association with invasive Group A Streptococcal (GAS) infection and necrotising fasciitis. Case-control studies demonstrate a 4-10 fold increased risk. Use paracetamol only for fever and discomfort. [7,8]

"Adults Get Sicker": While typically benign in children, varicella in adults carries 15-25 times higher mortality. Adults have significantly increased rates of varicella pneumonitis (1 in 400), hepatitis, and encephalitis. All immunocompetent adults should receive oral aciclovir if presenting within 24 hours of rash onset. [2,9]

"Pregnancy: Double Danger": Varicella in pregnancy poses dual risks — severe maternal disease (particularly varicella pneumonitis with 10-15% mortality if untreated) and fetal effects (congenital varicella syndrome if infection occurs before 20 weeks; severe neonatal varicella if maternal infection occurs peripartum). [10,11]

"The Prodrome Precedes Contagion": Patients become infectious approximately 48 hours BEFORE the rash appears, during the non-specific prodromal phase (fever, malaise). This complicates infection control as transmission occurs before diagnosis. [1,2]

"Immunocompromised = IV Aciclovir": Any immunocompromised patient with varicella requires immediate hospitalisation and intravenous aciclovir (10 mg/kg TDS). Without treatment, mortality in leukaemic children with varicella approaches 7-10%. [3,12]

Why This Matters Clinically

Chickenpox remains a significant cause of morbidity despite its reputation as a "benign childhood illness." While 90% of healthy children recover uneventfully, serious complications occur in 2-6% of cases. Recognising high-risk patients (immunocompromised, pregnant, neonates, adults) and initiating appropriate antiviral therapy within 24-48 hours of rash onset significantly reduces morbidity and mortality. [2,3]

Key clinical priorities include:

  1. Identification of high-risk patients requiring antiviral therapy or hospitalisation
  2. Recognition of complications — particularly secondary bacterial infection, pneumonitis, and neurological involvement
  3. Appropriate supportive care — including avoidance of NSAIDs
  4. Post-exposure management — VZIG for high-risk contacts, vaccination for eligible exposures
  5. Infection control — isolation until all lesions crusted, contact tracing for vulnerable individuals

2. Virology and Microbiology

Varicella-Zoster Virus (VZV)

VZV is a double-stranded DNA virus belonging to the Alphaherpesvirinae subfamily of Herpesviridae. It is the smallest of the human herpesviruses with a genome of approximately 125,000 base pairs encoding at least 71 unique open reading frames. [1,4]

Structural Characteristics:

ComponentDescription
GenomeLinear double-stranded DNA (~125 kbp)
NucleocapsidIcosahedral symmetry, ~100 nm diameter
TegumentProteinaceous layer between capsid and envelope
EnvelopeLipid bilayer derived from host cell membrane
GlycoproteinsgB, gC, gE, gH, gI, gK, gL, gM, gN — essential for cell entry and cell-to-cell spread
Key glycoproteingE — most abundant; target of neutralising antibodies

Unique Features of VZV:

  1. Highly cell-associated: Unlike HSV, VZV is extremely cell-associated; cell-free virus is unstable and difficult to culture
  2. Strict human tropism: No animal reservoir; humans are the only natural host
  3. Neurotropism: Establishes latency specifically in sensory neurons of dorsal root and cranial nerve ganglia
  4. Single serotype: All VZV strains are antigenically similar; infection confers lifelong immunity

Viral Replication Cycle

Entry and Uncoating:

  • VZV enters cells via fusion of viral envelope with plasma membrane
  • Glycoproteins gB and gH/gL complex mediate membrane fusion
  • Mannose-6-phosphate receptor and insulin-degrading enzyme serve as cellular receptors
  • Nucleocapsid transported to nucleus via microtubule network

DNA Replication and Gene Expression:

  • Immediate-early genes (regulatory proteins) expressed first
  • Early genes (DNA replication machinery) follow
  • Late genes (structural proteins) expressed after DNA replication begins
  • Viral DNA replication occurs in nucleus using rolling circle mechanism

Assembly and Egress:

  • Nucleocapsids assembled in nucleus
  • Primary envelopment at inner nuclear membrane
  • De-envelopment at outer nuclear membrane
  • Re-envelopment at trans-Golgi network
  • Release via exocytosis or cell lysis

Comparison with Other Herpesviruses

FeatureVZV (HHV-3)HSV-1 (HHV-1)HSV-2 (HHV-2)
Primary diseaseChickenpoxOral herpes, encephalitisGenital herpes
Reactivation diseaseShinglesCold sores, keratitisGenital recurrence
Latency siteDorsal root/cranial gangliaTrigeminal ganglionSacral ganglia
Cell associationHighly cell-associatedCell-free virus stableCell-free virus stable
Lesion distributionGeneralised (primary)Localised (orolabial)Localised (genital)
TransmissionAirborne + contactDirect contactSexual contact
VaccineAvailable (live attenuated)Not availableNot available

3. Epidemiology

Global Burden

Chickenpox occurs worldwide, with distinct epidemiological patterns based on climate and vaccination status. [2,13]

Pre-Vaccination Era (Temperate Climates):

ParameterData
Lifetime infection risk> 95% by adulthood
Annual incidence3.5-4.0 million cases (UK); ~4 million (USA)
Peak age of infection4-10 years
Percentage infected by age 1580-90%
Hospitalisation rate2-3 per 1,000 cases (children); 8-10 per 1,000 (adults)
Mortality rate~1 per 60,000 cases (children); 1 per 4,000 (adults)

Post-Vaccination Era (Countries with Universal Vaccination):

In countries implementing universal childhood varicella vaccination (USA, Australia, Germany), significant reductions have been observed:

OutcomeReduction
Varicella incidence85-90% decline
Varicella-related hospitalisations88-93% decline
Varicella-related deaths87-92% decline
Disease in vaccinated (breakthrough)Milder; less than 50 lesions; rarely complicated

United Kingdom Epidemiology

The UK does not currently include varicella vaccine in the routine childhood immunisation schedule (targeted use only). [5,14]

ParameterUK Data
Estimated annual cases~600,000-650,000
Primary care consultations~450,000/year
Hospital admissions~2,000-2,500/year
Deaths~20-30/year (majority in adults/immunocompromised)
Peak age1-4 years (> 50% of cases); 90% occur in less than 14 years
SeasonalityLate winter to early spring peak (March-May)
Cyclical patternEpidemic peaks every 2-5 years

Risk Factors for Severe Disease

Risk FactorRelative Risk/Odds RatioKey Complications
Age > 14 years15-25x mortality vs childrenPneumonitis, hepatitis
Age > 50 yearsFurther increased mortalityMulti-organ involvement
Pregnancy5x increased pneumonitis riskVaricella pneumonitis (10-15% mortality)
Trimester 1-2Risk of CVSCongenital varicella syndrome (0.5-2%)
Peripartum (5 days pre to 2 days post delivery)Severe neonatal diseaseNeonatal varicella (30% mortality untreated)
Neonates (less than 28 days)Very high mortalityDisseminated disease, pneumonitis
Primary immunodeficiencyMarkedly increasedProgressive varicella, visceral dissemination
Secondary immunodeficiency10-30% mortality (untreated)Fulminant hepatitis, DIC
Malignancy (esp. leukaemia)7-10% mortality (untreated)Disseminated disease, haemorrhagic varicella
Solid organ transplantSignificantly increasedProlonged disease, visceral involvement
HIV/AIDS (CD4 less than 200)Increased severityChronic varicella, VZV retinitis
High-dose corticosteroidsIncreased (> 2 mg/kg/day or > 20 mg/day for > 14 days)Severe disseminated disease
Chronic lung diseaseIncreased pneumonitis riskRespiratory failure
Chronic skin disease (eczema)More extensive cutaneous diseaseSecondary infection, scarring

Transmission Dynamics

Routes of Transmission:

  1. Airborne (respiratory droplets and aerosols): Primary route — virus shed from respiratory tract and aerosolised from vesicle fluid
  2. Direct contact: Contact with vesicle fluid; less efficient than airborne
  3. Vertical transmission: Transplacental (congenital varicella syndrome); perinatal (neonatal varicella)

Attack Rates by Setting:

SettingAttack Rate (Susceptible Contacts)
Household> 90%
Classroom/daycare10-35%
Hospital (shared room)70-90%
Casual contactLow (less than 5%)

Environmental Stability:

VZV is highly labile outside the human host:

  • Survives only minutes to hours on fomites
  • Rapidly inactivated by desiccation, heat, and detergents
  • Less stable than many other respiratory viruses
  • Fomite transmission rare but theoretically possible

4. Pathophysiology

Mechanism of Infection

The pathogenesis of chickenpox follows a well-characterised sequence of events from initial mucosal infection to systemic disease and eventual latency. [1,4,15]

Stage 1: Initial Infection (Day 0-4)

  • VZV enters via inhalation of respiratory droplets or aerosols
  • Initial viral replication occurs in nasopharyngeal mucosa and oropharyngeal lymphoid tissue (tonsils, adenoids)
  • Virus infects epithelial cells and local dendritic cells
  • Dendritic cells transport virus to regional lymph nodes

Stage 2: Primary Viraemia (Day 4-6)

  • Virus replicates in regional lymph nodes
  • First (primary) viraemia occurs — virus enters bloodstream
  • VZV spreads to reticuloendothelial system (liver, spleen, other lymphoid tissue)
  • Amplification of viral load in these organs
  • Virus infects T lymphocytes, which become major vehicles for dissemination

Stage 3: Secondary Viraemia (Day 10-14)

  • Massive secondary viraemia occurs as virus is released from reticuloendothelial organs
  • Infected T lymphocytes transport virus throughout body
  • VZV reaches skin and mucosal surfaces
  • Prodromal symptoms begin (fever, malaise) due to cytokine release
  • Peak viral load in blood correlates with symptom onset

Stage 4: Cutaneous Manifestations (Day 14-21)

  • VZV infects epidermal keratinocytes via infected T cells in dermal capillaries
  • Virus spreads cell-to-cell within epidermis
  • Cytopathic effects cause characteristic pathology:
    • "Ballooning degeneration: Intracellular oedema of infected cells"
    • "Acantholysis: Loss of intercellular adhesion"
    • "Intraepidermal vesicle formation: Unilocular vesicles form within epidermis"
    • "Multinucleated giant cells: Fusion of infected keratinocytes (Tzanck cells)"
    • "Intranuclear inclusions: Cowdry type A inclusions (eosinophilic)"

Vesicle Characteristics:

FeatureDescription
LocationIntraepidermal (within stratum spinosum)
TypeUnilocular (single cavity)
ContentsSerous fluid with high viral titre, inflammatory cells, epithelial cells
BaseErythematous due to dermal inflammation
EvolutionClouding (pustular) → umbilication → crusting

Stage 5: Immune Response and Resolution

  • Innate immune response (interferons, NK cells) begins early
  • Adaptive immunity develops:
    • "Humoral: VZV-specific IgM (acute), IgG (convalescent and long-term)"
    • "Cellular: VZV-specific CD4+ and CD8+ T cells (critical for clearance)"
  • Resolution of viraemia and cessation of new lesion formation
  • Crusting represents immune control and end of infectious period

Stage 6: Latency Establishment (Concurrent)

  • During primary infection, VZV travels via retrograde axonal transport to sensory neurons
  • Virus establishes latent infection in:
    • Dorsal root ganglia (thoracic > lumbar > cervical)
    • Trigeminal ganglion
    • Other cranial nerve ganglia
  • Latent VZV exists as circular episomal DNA
  • Limited gene expression during latency (latency-associated transcripts)
  • Lifelong persistence with potential for reactivation as herpes zoster

Immune Response

Innate Immunity:

ComponentRole in VZV Control
Type I interferons (IFN-α/β)Limit viral replication; activate antiviral state
NK cellsEarly cytotoxic response to infected cells
ComplementAntibody-dependent neutralisation
Pattern recognitionTLR detection of viral nucleic acids

Adaptive Immunity:

ComponentTimingFunction
VZV-specific IgMDay 3-5 post-rashAcute phase; wanes within months
VZV-specific IgGDay 5-7 post-rashLong-term protection; prevents reinfection
CD4+ T cellsWeek 1-2Helper function; cytokine production
CD8+ T cellsWeek 1-2Cytotoxic killing of infected cells; CRITICAL for clearance
Memory T cellsWeeks to monthsLong-term cellular immunity; prevents reactivation

Critical Role of Cell-Mediated Immunity (CMI):

CMI, particularly VZV-specific CD8+ T cell responses, is essential for:

  1. Clearance of primary infection
  2. Limitation of disease severity
  3. Prevention of reactivation (herpes zoster)
  4. Control of disseminated disease

This explains why immunocompromised patients (particularly those with T cell defects) experience:

  • Progressive primary varicella
  • Prolonged disease course
  • Visceral dissemination
  • Higher mortality
  • More frequent zoster reactivation

Histopathology

Skin Biopsy Findings:

FeatureDescription
Vesicle locationIntraepidermal (stratum spinosum)
Keratinocyte changesBallooning degeneration, acantholysis
Multinucleated giant cellsSyncytial formation (pathognomonic for herpesvirus)
Nuclear inclusionsCowdry type A bodies (eosinophilic intranuclear)
Dermal changesPerivascular lymphocytic infiltrate, oedema
Vessel involvementEndothelial infection, vasculitis (severe cases)

Tzanck Smear:

A rapid bedside diagnostic test involving:

  1. Unroofing a fresh vesicle
  2. Scraping the vesicle base
  3. Smearing on a glass slide
  4. Staining (Giemsa, Wright, or Diff-Quik)
  5. Identifying multinucleated giant cells

Sensitivity ~60-80%; not specific for VZV (positive in HSV infections also)


5. Clinical Presentation

Prodrome (1-2 Days Before Rash)

The prodrome is typically mild or absent in children but more pronounced in adolescents and adults. [1,2]

SymptomFrequencyNotes
Fever70-90%Low-grade (37.5-38.5°C) in children; higher in adults
Malaise60-80%General unwellness, fatigue
Headache30-50%More common in adolescents/adults
Anorexia40-60%Loss of appetite common in young children
Myalgia20-40%Muscle aches; more prominent in adults
Abdominal pain10-20%May precede rash; sometimes prominent

Important: Patients become infectious during the prodrome, approximately 48 hours before rash onset.

Rash Characteristics

The exanthem of chickenpox is highly characteristic and often allows clinical diagnosis. [1,2,16]

Evolution of Individual Lesions:

MACULE (2-4mm red spot)
    ↓ (hours)
PAPULE (raised, erythematous)
    ↓ (hours)
VESICLE ("dewdrop on rose petal")
    ↓ (24-48 hours)
PUSTULE (cloudy, umbilicated)
    ↓ (24-48 hours)
CRUST (dried, healing)
    ↓ (5-7 days)
RESOLUTION (± scarring)

Vesicle Description — "Dewdrop on a Rose Petal":

FeatureDescription
AppearanceClear, superficial, thin-walled vesicle
Size2-4 mm diameter (range 1-5 mm)
ShapeRound or ovoid; becomes umbilicated
BaseErythematous ("rose petal" — surrounding red halo)
ContentsClear serous fluid (initially); becomes cloudy/pustular
WallFragile; easily ruptured
TzanckPositive for multinucleated giant cells

Rash Distribution:

PatternDescription
OverallCentripetal — concentrated centrally with peripheral spread
Most denseTrunk (chest, back, abdomen)
ModerateFace, scalp
Least denseExtremities (arms, legs)
SparingPalms and soles typically spared (unlike hand, foot and mouth disease)
Mucosal involvementOral cavity (palate, buccal mucosa), conjunctiva, genitalia

Characteristic Features:

FeatureSignificance
CropsNew lesions appear in waves over 3-5 days
Pleomorphism ("Starry Sky")Lesions at ALL stages visible simultaneously
PruritusIntense itching is characteristic; main symptom in many children
NumberTypically 250-500 lesions (range 10 to > 1500)
Duration of new lesions3-5 days (healthy); prolonged in immunocompromised
Time to crusting4-7 days from vesicle formation
Crusts fall off1-3 weeks after formation

Disease Severity Grading

SeverityLesion CountClinical Features
Mildless than 50Minimal systemic symptoms; brief illness
Moderate50-250Typical presentation; fever, pruritus, full course
Severe> 250-500Higher fever; more systemic symptoms
Very severe> 500-1000+Confluent lesions; haemorrhagic; immunocompromised

Mucosal Involvement

SiteManifestationClinical Significance
Oral cavityVesicles → shallow ulcers on palate, buccal mucosa, gingiva, tonguePain; decreased oral intake; dehydration risk
OropharynxPharyngeal ulcerationOdynophagia
ConjunctivaConjunctival vesicles, conjunctivitisUsually self-limiting; rarely corneal involvement
GenitaliaVulvar/scrotal vesicles → ulcersPainful; secondary infection risk
LarynxLaryngeal lesions (rare)Stridor; airway compromise (very rare)

Special Populations

Neonatal Varicella:

The timing of maternal infection relative to delivery determines neonatal risk:

Maternal Infection TimingNeonatal PresentationMortality (Untreated)
> 7 days before deliveryMild disease (passive maternal antibodies transferred)Low
5 days before to 2 days after deliverySevere disseminated varicella (no passive antibodies)20-30%
Congenital (in utero, weeks 1-20)Congenital varicella syndromeVariable

Congenital Varicella Syndrome (CVS):

Occurs with maternal infection in first 20 weeks (highest risk 13-20 weeks):

FeatureDescription
CutaneousCicatricial (zigzag) skin scarring in dermatomal distribution
LimbLimb hypoplasia, limb shortening
NeurologicalMicrocephaly, cortical atrophy, mental retardation
OphthalmologicalChorioretinitis, cataracts, microphthalmos, Horner syndrome
OtherLow birth weight, IUGR
Risk0.5% (weeks 1-12); 2% (weeks 13-20); rare after 20 weeks

Immunocompromised Patients:

FeaturePresentation
Lesion countOften > 1500; continuous crops for > 7 days
Lesion typeHaemorrhagic (purpuric), necrotic, umbilicated, confluent
DurationProlonged (weeks without treatment)
Visceral involvementPneumonitis, hepatitis, encephalitis, DIC common
New lesion developmentBeyond day 7-10 indicates progressive disease
Mortality7-10% (leukaemia); 10-30% overall (without treatment)

Red Flags — Urgent Assessment Required

[!CAUTION] Red Flags in Chickenpox — Require Immediate Assessment:

Bacterial Superinfection:

  • High fever (> 39°C) persisting or recurring after day 4
  • Rapidly spreading erythema, warmth, or tenderness around lesions
  • Lesions becoming very painful, indurated, or necrotic
  • Systemic toxicity (tachycardia, hypotension, confusion)
  • Concern: Cellulitis, invasive GAS, necrotising fasciitis

Respiratory Involvement:

  • Cough, dyspnoea, tachypnoea
  • Hypoxia (SpO2 less than 94% on air)
  • Chest pain
  • Haemoptysis
  • Concern: Varicella pneumonitis

Neurological Involvement:

  • Ataxia, unsteady gait
  • Altered consciousness, drowsiness
  • Seizures
  • Severe headache, neck stiffness
  • Concern: Encephalitis, cerebellar ataxia, meningitis

Haematological:

  • Purpuric or haemorrhagic lesions
  • Bleeding from mucosae
  • Petechiae beyond lesion sites
  • Concern: Thrombocytopenia, haemorrhagic varicella, DIC

High-Risk Patients with Chickenpox:

  • Immunocompromised patient (any cause)
  • Pregnant woman (any gestation)
  • Neonate (less than 28 days)
  • Very young infant (less than 1 month if mother not immune)

Progressive Disease:

  • New lesion formation beyond day 7
  • Failure of lesions to crust by day 10
  • Worsening despite supportive care

6. Clinical Examination

Systematic Examination Approach

General Inspection:

FindingSignificance
AlertnessDrowsiness may indicate encephalitis
Toxic appearanceSuggests secondary bacterial infection
Respiratory distressSuggests pneumonitis
Hydration statusOral intake often reduced

Skin Examination:

AssessmentMethodFindings
Lesion descriptionSystematic description"Dewdrops on rose petals" — vesicles on erythematous base
Lesion stagesIdentify all stages presentMacules, papules, vesicles, pustules, crusts (simultaneously)
DistributionMap body involvementCentripetal: trunk > face/scalp > limbs
Density estimationCount sample area, extrapolateMild (less than 50), Moderate (50-250), Severe (> 250)
Mucosal examinationInspect mouth, conjunctivaeOral vesicles/ulcers, conjunctivitis
Signs of superinfectionLook for bacterial infectionSpreading erythema, honey crusting, warmth, tenderness
Staging of lesionsAssess if all crustedAll crusted = no longer infectious
ScarringDocument any already presentScratching, secondary infection increase risk

Secondary Bacterial Infection Signs:

FindingConcern
Enlarging erythema around lesionsCellulitis
Honey-coloured crustingImpetigo (S. aureus, GAS)
Warmth, fluctuanceAbscess formation
Pain disproportionate to appearanceNecrotising fasciitis
CrepitusGas-forming organism; necrotising infection
Rapid spreadInvasive GAS
Systemic toxicityBacteraemia, sepsis

Systems Examination (If Complications Suspected)

Respiratory Examination:

FindingSuggests
TachypnoeaPneumonitis, respiratory distress
HypoxiaSignificant pneumonitis
Cough (dry)Early pneumonitis
Crackles (bilateral)Varicella pneumonitis
Reduced air entryConsolidation, effusion

Neurological Examination:

FindingSuggests
Ataxia (truncal)Cerebellar ataxia (most common CNS complication)
NystagmusCerebellar involvement
DysarthriaCerebellar involvement
Altered GCSEncephalitis
SeizuresEncephalitis
Neck stiffnessMeningitis, meningoencephalitis
Focal neurological signsFocal encephalitis, stroke (VZV vasculopathy)

Abdominal Examination:

FindingSuggests
HepatomegalyHepatitis (common subclinically)
Tender hepatomegalySignificant hepatic involvement
SplenomegalyHaematological involvement
Abdominal tendernessVisceral dissemination

7. Investigations

Uncomplicated Chickenpox

No investigations required. Diagnosis is clinical based on characteristic rash, history, and epidemiological context (exposure to varicella or shingles in preceding 10-21 days).

Investigations for Specific Indications

1. Confirmation of Diagnosis (When Uncertain):

InvestigationSpecimenMethodNotes
VZV PCRVesicle fluid/swabPCRGold standard; highly sensitive and specific
VZV DFAVesicle scrapingDirect fluorescent antibodyRapid (hours); less sensitive than PCR
Tzanck smearVesicle scrapingCytologyRapid bedside; multinucleated giant cells; non-specific (also positive in HSV)
Viral cultureVesicle fluidCell cultureSlow (7-14 days); low sensitivity; rarely used
VZV IgM/IgG serologyBloodELISA/EIAIgM = acute; IgG = past infection/immunity

Preferred test: VZV PCR from vesicle fluid (sensitivity > 95%, specificity > 99%)

2. Assessing Immunity (Pre-Exposure):

TestUse
VZV IgGConfirms immunity (past infection or vaccination)
InterpretationPositive = immune; Negative = susceptible

3. Investigations for Complications:

ComplicationInvestigations
Bacterial superinfectionFBC, CRP, blood culture, wound swab M/C/S
Varicella pneumonitisCXR, SpO2, ABG, VZV PCR (BAL if intubated)
Encephalitis/cerebellar ataxiaLP (CSF analysis, VZV PCR), MRI brain, EEG
HepatitisLFTs (ALT, AST often mildly elevated subclinically)
Haemorrhagic varicellaFBC (thrombocytopenia), coagulation screen, film
Reye syndromeLFTs, ammonia, glucose, coagulation, lactate

4. Expected Findings:

InvestigationUncomplicatedComplicated
FBCNormal or mild lymphocytosisLeukocytosis (bacterial); leukopenia (severe); thrombocytopenia
CRPNormal or mildly elevatedMarkedly elevated (bacterial superinfection)
LFTsOften mildly elevated AST/ALTSignificant elevation (hepatitis)
CXRNormalBilateral nodular/reticulonodular infiltrates (pneumonitis)
CSFN/ALymphocytic pleocytosis, normal glucose, VZV PCR positive (encephalitis)

Chest X-Ray Findings in Varicella Pneumonitis:

FindingDescription
PatternBilateral, diffuse, nodular or reticulonodular infiltrates
DistributionPerihilar and basal predominance
EvolutionMay develop rapidly; can progress to ARDS
ResolutionTypically resolves over weeks with treatment
CalcificationSmall calcified nodules may persist (late finding)

8. Management

Management Algorithm

                          CHICKENPOX PRESENTATION
                                   ↓
┌──────────────────────────────────────────────────────────────────────────────┐
│                          INITIAL ASSESSMENT                                  │
│                                                                              │
│   1. Confirm clinical diagnosis (characteristic rash)                        │
│   2. Assess for red flags (complications)                                    │
│   3. Identify if HIGH-RISK or LOW-RISK patient                              │
│   4. Assess for high-risk contacts requiring protection                      │
└──────────────────────────────────────────────────────────────────────────────┘
                                   ↓
         ┌─────────────────────────┴────────────────────────────┐
         ↓                                                      ↓
┌─────────────────────────────┐            ┌──────────────────────────────────┐
│       LOW-RISK PATIENT      │            │        HIGH-RISK PATIENT          │
│                             │            │                                    │
│ • Healthy child (1-14 years)│            │ • Adults (> 14 years)              │
│ • No chronic disease        │            │ • Immunocompromised (any)         │
│ • Immunocompetent           │            │ • Pregnant women                  │
│ • No complications          │            │ • Neonates (less than 28 days)             │
│                             │            │ • Chronic lung/skin disease       │
│                             │            │ • Current/recent high-dose steroids│
│                             │            │ • Smokers (increased pneumonitis) │
└──────────────┬──────────────┘            └───────────────┬──────────────────┘
               ↓                                           ↓
┌──────────────────────────────────────────────────────────────────────────────┐
│                     SUPPORTIVE CARE (ALL PATIENTS)                           │
├──────────────────────────────────────────────────────────────────────────────┤
│                                                                              │
│   ANTIPYRETIC:                                                               │
│   ✓ Paracetamol for fever and discomfort (15 mg/kg QDS PRN)                │
│   ✗ AVOID NSAIDs (ibuprofen) — increased necrotising fasciitis risk        │
│                                                                              │
│   ANTI-PRURITIC:                                                            │
│   • Chlorphenamine (antihistamine): 1-2 years: 1mg BD; 2-5 years: 1mg TDS; │
│     6-12 years: 2mg TDS-QDS; > 12 years: 4mg TDS-QDS                         │
│   • Calamine lotion applied to lesions PRN                                  │
│   • Cooling preparations (e.g., Eurax lotion)                               │
│   • Cool compresses, tepid baths                                            │
│                                                                              │
│   GENERAL MEASURES:                                                         │
│   • Keep nails short (prevent excoriation and secondary infection)          │
│   • Consider mittens at night for young children                            │
│   • Loose, cool cotton clothing                                             │
│   • Maintain adequate oral fluid intake                                     │
│   • Oatmeal baths may soothe pruritus                                       │
│                                                                              │
│   ISOLATION AND EXCLUSION:                                                  │
│   • Exclude from school/daycare until ALL lesions crusted (~5-7 days)       │
│   • Avoid contact with high-risk individuals                                │
│   • Advise regarding infectious period and contact tracing                  │
│                                                                              │
└──────────────────────────────────────────────────────────────────────────────┘
               ↓                                           ↓
┌──────────────────────────────┐           ┌───────────────────────────────────┐
│    NO ANTIVIRALS NEEDED      │           │   ANTIVIRAL THERAPY INDICATED     │
│                              │           │                                   │
│ • Typical healthy child      │           │ Start within 24 hours of rash     │
│ • Uncomplicated disease      │           │ onset for maximum benefit         │
└──────────────────────────────┘           └──────────────┬────────────────────┘
                                                          ↓
┌──────────────────────────────────────────────────────────────────────────────┐
│                        ANTIVIRAL REGIMENS                                    │
├──────────────────────────────────────────────────────────────────────────────┤
│                                                                              │
│ ORAL ACICLOVIR (Immunocompetent High-Risk):                                 │
│                                                                              │
│   Adults/Adolescents:                                                       │
│   • Aciclovir 800 mg 5 times daily for 7 days                               │
│                                                                              │
│   Children (if indicated):                                                  │
│   • less than 2 years: 200 mg QDS                                                    │
│   • 2-5 years: 400 mg QDS                                                   │
│   • 6-12 years: 800 mg QDS                                                  │
│   • Duration: 5-7 days                                                      │
│   OR weight-based: 20 mg/kg (max 800 mg) QDS for 5 days                     │
│                                                                              │
│   Alternative:                                                              │
│   • Valaciclovir (adult): 1g TDS for 7 days (better bioavailability)        │
│                                                                              │
├──────────────────────────────────────────────────────────────────────────────┤
│                                                                              │
│ INTRAVENOUS ACICLOVIR (Immunocompromised/Severe Disease):                   │
│                                                                              │
│   Indications:                                                              │
│   • Immunocompromised patients (ANY)                                        │
│   • Varicella pneumonitis                                                   │
│   • Encephalitis/CNS involvement                                            │
│   • Disseminated/haemorrhagic varicella                                     │
│   • Neonatal varicella                                                      │
│   • Severe disease in pregnancy                                             │
│   • Unable to tolerate oral therapy                                         │
│                                                                              │
│   Dosing:                                                                   │
│   • Neonates: 10-20 mg/kg IV TDS (every 8 hours)                           │
│   • Children: 10 mg/kg IV TDS (max 500 mg/dose)                            │
│   • Adults: 10 mg/kg IV TDS                                                │
│   • Immunocompromised: 10-15 mg/kg IV TDS                                  │
│                                                                              │
│   Duration:                                                                 │
│   • Continue until no new lesions for 48 hours                              │
│   • Minimum 7 days; often 10-14 days                                        │
│   • Can switch to oral when clinically improving                            │
│                                                                              │
│   Monitoring:                                                               │
│   • Renal function (aciclovir is nephrotoxic)                               │
│   • Ensure adequate hydration                                               │
│   • Adjust dose for renal impairment                                        │
│                                                                              │
└──────────────────────────────────────────────────────────────────────────────┘
                                   ↓
┌──────────────────────────────────────────────────────────────────────────────┐
│                        HOSPITAL ADMISSION CRITERIA                           │
├──────────────────────────────────────────────────────────────────────────────┤
│                                                                              │
│   ADMIT:                                                                    │
│   • Immunocompromised patient with varicella                                │
│   • Respiratory symptoms (suspected pneumonitis)                            │
│   • Neurological symptoms (encephalitis, severe cerebellar ataxia)          │
│   • Signs of bacterial superinfection/sepsis                                │
│   • Haemorrhagic varicella                                                  │
│   • Neonatal varicella                                                      │
│   • Pregnant woman with severe disease                                      │
│   • Severe disease (> 500 lesions, high fever, toxic appearance)             │
│   • Dehydration/unable to maintain oral intake                              │
│   • Social concerns/inability to return if deterioration                    │
│                                                                              │
│   INFECTION CONTROL:                                                        │
│   • Airborne + contact precautions                                          │
│   • Negative pressure isolation room (if available)                         │
│   • Only immune staff should provide care                                   │
│                                                                              │
└──────────────────────────────────────────────────────────────────────────────┘

Management of Specific Complications

Bacterial Superinfection:

ScenarioManagement
Mild impetigoTopical fusidic acid or mupirocin
Extensive impetigo/cellulitisOral flucloxacillin (or co-amoxiclav if GAS suspected)
Severe infection/systemic toxicityIV antibiotics (flucloxacillin + clindamycin for toxin suppression)
Necrotising fasciitisUrgent surgical debridement + IV broad-spectrum antibiotics

Varicella Pneumonitis:

ActionDetails
AdmitHigh-dependency or ICU setting
AntiviralIV aciclovir 10 mg/kg TDS
OxygenSupplemental O2 to maintain SpO2 > 94%
Respiratory supportNIV or mechanical ventilation if required
SteroidsRole controversial; sometimes used in severe cases
MonitoringClose respiratory monitoring; ABGs

Encephalitis/Cerebellar Ataxia:

FeatureEncephalitisCerebellar Ataxia
TimingDays 3-8 post-rashDays 2-6 post-rash
PresentationAltered consciousness, seizuresAtaxia, nystagmus, dysarthria
CSFLymphocytic pleocytosisOften normal
ImagingMRI may show changesUsually normal
TreatmentIV aciclovir + supportiveSupportive (± aciclovir)
PrognosisVariable; mortality ~5-10%Excellent; usually self-limiting

Post-Exposure Prophylaxis (PEP)

Significant Exposure Definition:

Contact with varicella or herpes zoster (exposed lesions) in a susceptible person:

  • Face-to-face contact for ≥5 minutes
  • Same room for ≥15 minutes
  • Direct contact with vesicle fluid
  • Household contact

Varicella-Zoster Immunoglobulin (VZIG):

IndicationTimingNotes
Immunocompromised (susceptible)Within 10 days of exposureHighest priority
Pregnant (susceptible)Within 10 days of exposureReduces maternal severity
Neonate — maternal varicella -7 to +7 days of deliveryASAP after birthHigh-risk period
Neonate — VZV-exposed less than 7 days if mother non-immuneWithin 10 daysDepends on maternal status
Infants of mothers with varicella at deliveryASAPRegardless of maternal timing

VZIG Dosing:

  • UK: 250 mg per 10 kg body weight (minimum 250 mg, maximum 3 doses)
  • Given IM; can be given up to 10 days post-exposure

Post-Exposure Vaccination:

IndicationTimingEfficacy
Healthy susceptible contacts (≥12 months)Within 3-5 days of exposure70-100% prevention; reduces severity if infection occurs
Not indicatedImmunocompromised, pregnant, infants less than 12 months

Pregnancy Management

ScenarioManagement
Susceptible pregnant woman exposedCheck VZV IgG urgently; if negative → VZIG within 10 days
Pregnant with chickenpox (less than 20 weeks)Oral aciclovir if presenting within 24h; counsel re: CVS risk (0.5-2%); fetal medicine referral
Pregnant with chickenpox (≥20 weeks)Oral aciclovir recommended; lower CVS risk
Pregnant with severe varicella (any gestation)Admit; IV aciclovir; monitor for pneumonitis
Maternal varicella at deliveryPaediatric alert; neonatal VZIG ± IV aciclovir

Why Avoid NSAIDs in Chickenpox?

Epidemiological studies have demonstrated an association between NSAID use (particularly ibuprofen) in children with chickenpox and:

  • Invasive Group A Streptococcal (GAS) infection (OR 4.9-10.2)
  • Necrotising fasciitis (OR 2.7-5.4)
  • Severe soft tissue infections [7,8]

Proposed mechanisms:

  1. Masking of early signs of bacterial superinfection (anti-inflammatory effect)
  2. Impaired neutrophil function and chemotaxis
  3. Enhanced bacterial virulence (streptococcal toxin production)
  4. Selection bias (sicker children more likely to receive NSAIDs)

Recommendation: Paracetamol only for fever and discomfort in chickenpox. [5,7,8]


9. Complications

Overview

Complications occur in approximately 2-6% of immunocompetent children with chickenpox, but rates are significantly higher in high-risk populations. [2,3,17]

Cutaneous and Soft Tissue Complications

ComplicationIncidenceOrganismFeaturesManagement
Secondary bacterial skin infection5-10%S. aureus, GASImpetiginised lesions, cellulitisTopical/oral antibiotics
Invasive GAS diseaseRare but seriousGroup A StreptococcusRapid spread, toxicityIV antibiotics; surgical debridement
Necrotising fasciitisless than 0.1%GAS, mixed floraPain > appearance, crepitus, rapid progressionEmergency surgery + IV antibiotics
Staphylococcal scalded skin syndromeRareS. aureus (toxin)DesquamationIV flucloxacillin
ScarringCommonN/APitted scars (scratching, secondary infection)Prevention by minimising scratching

Respiratory Complications

ComplicationIncidenceRisk GroupsFeaturesManagement
Varicella pneumonitis1:400 adults; rare in childrenAdults, pregnant, smokers, immunocompromisedCough, dyspnoea, hypoxia, bilateral infiltratesIV aciclovir, supportive, ± ventilation
Secondary bacterial pneumoniaUncommonAnyFever, productive cough, focal consolidationAntibiotics targeting respiratory pathogens
Respiratory failure/ARDSRareSevere pneumonitisProgressive hypoxiaICU; mechanical ventilation

Neurological Complications

ComplicationIncidenceTimingFeaturesOutcome
Cerebellar ataxia1:4,000Days 2-6 post-rashTruncal ataxia, nystagmus, dysarthriaUsually self-limiting (2-4 weeks); full recovery
Encephalitis1:4,000Days 3-8 post-rashAltered consciousness, seizures, focal signsVariable; 5-10% mortality; 10-20% sequelae
MeningitisRareVariableHeadache, neck stiffness, photophobiaUsually good prognosis
Transverse myelitisVery rareWeeks post-infectionAscending weakness, sensory levelVariable outcome
Guillain-Barré syndromeVery rare2-4 weeks post-infectionAscending weakness, areflexiaVariable; may require ventilation
Stroke (VZV vasculopathy)RareWeeks to months post-infectionFocal neurological signsAntivirals; variable outcome
Reye syndromeNow rareIf aspirin givenEncephalopathy, hepatic failureHigh mortality; avoid aspirin

Haematological Complications

ComplicationIncidenceFeaturesManagement
ThrombocytopeniaUncommonPetechiae, bleeding, low plateletsUsually self-limiting; rarely transfusion
Purpura fulminansVery rareDIC, skin necrosisICU; supportive; treat DIC
Haemorrhagic varicellaRare (immunocompromised)Purpuric lesions, mucosal bleedingIV aciclovir; supportive; platelet/FFP

Other Complications

ComplicationIncidenceNotes
HepatitisCommon (subclinical)Transient transaminase elevation; clinical hepatitis rare
ArthritisRareSelf-limiting; reactive
MyocarditisVery rareChest pain, arrhythmias
GlomerulonephritisVery rareHaematuria, oedema
PancreatitisVery rareAbdominal pain, elevated amylase
OrchitisRareTesticular swelling, pain
TimingFetal/Neonatal RiskIncidence
Weeks 0-12Congenital varicella syndrome (CVS)0.5%
Weeks 13-20Congenital varicella syndrome (CVS)2%
Weeks 20-36Herpes zoster in infancy (not CVS)Low
5 days pre to 2 days post deliverySevere neonatal varicella17-30% mortality (untreated)

Late Complications

ComplicationTimeframeNotes
Herpes zoster (shingles)Years to decades post-infectionVZV reactivation from latent ganglia
Post-herpetic neuralgiaFollowing zosterNot following primary varicella
VZV retinitisImmunocompromisedLate reactivation manifestation

10. Prognosis and Outcomes

Immunocompetent Children

OutcomeExpected
Duration of illness5-10 days
Time to all lesions crusted5-7 days (marks end of infectious period)
Full recovery> 99%
Complication rate2-6%
Hospitalisation rate2-3 per 1,000 cases
Mortality~1 per 60,000-100,000 cases
ScarringCommon if scratching or secondary infection occurs
Lifelong immunityYes (reinfection extremely rare)
Future shingles risk10-30% lifetime risk

High-Risk Populations

PopulationKey Outcomes
Adults15-25x higher mortality than children; 1:400 pneumonitis risk
Pregnant (varicella pneumonitis)10-15% mortality without treatment; ~1% with treatment
Neonatal varicella (untreated)20-30% mortality
Neonatal varicella (with VZIG/aciclovir)less than 5% mortality
Immunocompromised (untreated)10-30% mortality
Immunocompromised (with IV aciclovir)less than 3% mortality
Cerebellar ataxiaExcellent; complete recovery in 2-4 weeks in most
Encephalitis5-10% mortality; 10-20% neurological sequelae

Factors Associated with Poor Outcomes

FactorImpact
ImmunocompromiseStrongest predictor of severe disease and mortality
Age (adults, neonates)Increased complication rates
PregnancyPneumonitis risk; fetal risks
Delayed antiviral therapyPoorer outcomes if > 24-48 hours post-rash onset
High lesion countCorrelates with severity
NSAID useIncreased bacterial superinfection risk
Underlying lung diseaseIncreased pneumonitis risk

11. Prevention

Varicella Vaccination

Vaccine Characteristics:

FeatureDetails
TypeLive attenuated (Oka strain)
StorageFrozen (-15°C) or refrigerated (2-8°C for shorter periods)
AdministrationSubcutaneous injection
Doses2 doses recommended for full protection
Schedule (where routine)Dose 1: 12-15 months; Dose 2: 4-6 years
Efficacy80-85% against any varicella; 95-99% against severe disease
Duration of protectionLong-term; likely lifelong for most

Vaccine-Eligible Groups (UK — Targeted Programme):

GroupIndication
Healthcare workersNon-immune HCWs with patient contact
Household contacts of immunocompromisedTo protect vulnerable family members
Laboratory staffWorking with VZV
Non-immune womenPre-conception (not if pregnant)

Contraindications:

ContraindicationReason
PregnancyTheoretical risk of fetal varicella (avoid pregnancy for 1 month post-vaccination)
ImmunocompromiseRisk of vaccine-strain disease (live vaccine)
Recent immunoglobulinMay reduce vaccine efficacy
Severe allergic reaction to previous doseAnaphylaxis risk
Severe allergy to gelatin or neomycinVaccine components

Breakthrough Varicella:

Varicella in a vaccinated person:

  • Usually milder (less than 50 lesions, often maculopapular rather than vesicular)
  • Lower fever, shorter duration
  • Lower complication rate
  • Still contagious
  • May occur in 10-20% of vaccinated individuals

Herd Immunity and Zoster Concerns

IssueDetails
Herd immunityHigh vaccination coverage reduces circulation and protects unvaccinated
Zoster concern (theoretical)Reduced wild-type VZV circulation may reduce natural "boosting" of latent immunity in adults, potentially increasing zoster incidence
Current evidenceMixed; some studies show increased zoster, others do not
MitigationZoster vaccination in older adults

12. Evidence and Guidelines

Key Guidelines

GuidelineOrganisationYearKey Recommendations
Chickenpox CKSNICE2023Primary care diagnosis, management, referral criteria
PHE Guidance on VZVUKHSA (formerly PHE)2019Post-exposure prophylaxis, VZIG indications
Green Book Chapter 34UKHSA2022Varicella vaccination, immunisation schedules
AAP Red BookAmerican Academy of Pediatrics2021Comprehensive paediatric infectious disease guidance
RCPCH GuidelinesRoyal College of PaediatricsVariousPaediatric-specific management

Landmark Studies

1. Varicella Vaccine Efficacy (Kuter et al. 1991) [5]

  • Design: RCT of Oka/Merck varicella vaccine in healthy children
  • Finding: 95% efficacy in preventing varicella
  • Impact: Foundation for routine childhood vaccination programmes
  • PMID: 1651974

2. NSAIDs and Necrotising Fasciitis (Lesko et al. 2001) [7]

  • Design: Population-based case-control study
  • Finding: OR 4.9 for invasive GAS disease with ibuprofen use in varicella
  • Impact: Basis for avoiding NSAIDs in chickenpox
  • PMID: 11331692

3. Aciclovir in Varicella (Dunkle et al. 1991) [9]

  • Design: Double-blind RCT of oral aciclovir in healthy children
  • Finding: Reduced duration of fever, lesion count, and time to crusting
  • Impact: Established role of antivirals in high-risk groups
  • PMID: 1738170

4. VZIG Efficacy in Immunocompromised (Zaia et al. 1983) [12]

  • Design: Prospective study of VZIG in leukaemic children
  • Finding: Reduced severity and mortality of varicella
  • Impact: Established post-exposure prophylaxis protocols
  • PMID: 6297988

5. Varicella Pneumonia in Adults (Haake et al. 1990) [18]

  • Design: Retrospective cohort analysis
  • Finding: Documented 1:400 incidence of pneumonitis in adult varicella
  • Impact: Highlighted severity of adult disease
  • PMID: 2393200

Evidence Levels Summary

InterventionEvidence LevelEvidence Source
Varicella vaccination1aMultiple RCTs, systematic reviews
Oral aciclovir in high-risk immunocompetent1bRCTs
IV aciclovir in immunocompromised2aCohort studies, consensus
VZIG for post-exposure prophylaxis2aCohort studies
Avoidance of NSAIDs2aCase-control studies
Supportive care (paracetamol, antihistamines)5Expert consensus, standard practice

13. Patient and Family Information

What is Chickenpox?

Chickenpox is a very common and highly contagious infection caused by a virus called varicella-zoster virus. It causes an itchy rash of blisters that appear all over the body, along with fever and feeling unwell. Most children in the UK get chickenpox before age 10.

What are the Symptoms?

Early symptoms (before the rash):

  • Feeling tired and unwell
  • Mild fever
  • Poor appetite
  • Headache

The rash:

  • Starts as small red spots that quickly become fluid-filled blisters
  • Blisters appear in "crops" — new ones keep appearing for 3-5 days
  • You'll see spots at different stages at the same time (some new, some crusting over)
  • Very itchy
  • Usually starts on the chest, back, and tummy, then spreads to face and limbs
  • Spots in the mouth are common and can be sore
  • Blisters dry up and form scabs over 5-7 days

How Does it Spread?

Chickenpox spreads very easily through:

  • Coughs and sneezes — tiny droplets in the air
  • Direct contact — touching the blisters

Important: Your child is infectious from about 2 days BEFORE the rash appears until all the blisters have crusted over (usually 5-7 days after the rash starts).

How to Treat Chickenpox at Home

To reduce fever and discomfort:

  • Give paracetamol (Calpol, Panadol) as directed for age
  • Do NOT give ibuprofen (Nurofen, Calprofen) — this may increase the risk of skin infections

To help with itching:

  • Antihistamines like chlorphenamine (Piriton) can help reduce itching and help sleep
  • Calamine lotion or cooling gels applied to the spots
  • Cool baths (tepid, not cold) may soothe the skin
  • Oatmeal baths (colloidal oatmeal preparations or porridge oats in a sock)
  • Keep nails short and clean to reduce scratching damage
  • Consider mittens at night for young children

General care:

  • Dress in loose, cool cotton clothes
  • Keep well hydrated — encourage plenty of fluids
  • Offer soft, cool foods if mouth ulcers are present
  • Let your child rest

Keeping Others Safe

  • Keep your child away from school, nursery, and playgroups until all blisters have crusted over
  • Avoid contact with:
    • Pregnant women who haven't had chickenpox
    • Newborn babies
    • Anyone with a weak immune system (e.g., receiving chemotherapy)
  • Inform the school or nursery so they can alert other parents

When to Seek Medical Advice

Contact your GP or call NHS 111 if your child has:

  • A very high temperature that doesn't come down with paracetamol
  • Signs of skin infection — redness spreading around spots, spots becoming very painful, hot, or oozing pus
  • Not drinking enough and showing signs of dehydration
  • Rash is very severe or spots are bleeding
  • You are worried about your child

Seek URGENT medical attention (A&E or 999) if your child has:

  • Difficulty breathing or fast breathing
  • Confusion, drowsiness, or difficulty waking up
  • Becomes wobbly or unsteady on their feet (ataxia)
  • Stiff neck or sensitivity to light
  • Seizures/fits
  • The rash is turning purple or looks like bruises

Also seek advice if:

  • Your child is under 4 weeks old
  • Your child is under 1 year old (especially if mother never had chickenpox)
  • Your child has a condition affecting their immune system or takes medicines that weaken their immune system

Can Chickenpox be Prevented?

  • There is a vaccine for chickenpox, but it's not part of the routine NHS childhood programme in the UK
  • If someone in your household is immunocompromised or pregnant and has been exposed, they may be offered an injection (VZIG) to help prevent or reduce severity

After Chickenpox

  • Your child will be immune for life and won't get chickenpox again
  • The virus stays dormant in the body and can reactivate years later as shingles (usually in older adults)
  • Scars from spots can occur, especially if they were scratched or got infected — they usually fade over time

14. Examination Focus

High-Yield Exam Topics

TopicKey Points
Causative organismVaricella-zoster virus (VZV), Human Herpesvirus 3, Herpesviridae family
TransmissionAirborne (respiratory droplets) + direct contact with vesicle fluid; highly contagious
Incubation10-21 days (typically 14-16 days)
Infectious period2 days BEFORE rash until ALL lesions crusted (~5-7 days post-rash onset)
Classic rash description"Dewdrop on a rose petal" — clear vesicle on erythematous base
Rash evolutionMacule → Papule → Vesicle → Pustule → Crust (24-48 hours per lesion)
DistributionCentripetal (trunk predominant → face → limbs); crops at different stages simultaneously
Avoid NSAIDsAssociated with increased risk of necrotising fasciitis (use paracetamol only)
Aciclovir indicationsAdults, immunocompromised, pregnant, neonates, severe disease; within 24 hours of rash
IV aciclovir dose10 mg/kg TDS (children and adults)
VZIG indicationsHigh-risk contacts (immunocompromised, pregnant, neonates) within 10 days of exposure
LatencyDorsal root ganglia → reactivates as herpes zoster (shingles)
Cerebellar ataxiaMost common CNS complication; usually self-limiting
Congenital varicella syndromeRisk if maternal infection less than 20 weeks; limb hypoplasia, cicatricial scars, eye/CNS abnormalities
Neonatal varicellaSevere if maternal infection 5 days before to 2 days after delivery; 30% mortality without treatment

OSCE/Clinical Exam Approach

Rash Description Station:

"This is a vesicular rash with lesions at multiple stages of development. I can see macules, papules, vesicles, and crusted lesions present simultaneously, giving a 'starry sky' appearance. The distribution is centripetal, with the trunk more densely affected than the limbs. The vesicles appear as clear, superficial blisters on an erythematous base — the classic 'dewdrop on a rose petal' appearance. This is consistent with a clinical diagnosis of chickenpox."

History Station Checklist:

  • Timing of rash onset and evolution
  • Associated symptoms (fever, malaise, pruritus)
  • Exposure history (contact with chickenpox or shingles)
  • Immunisation status
  • Past medical history (immunocompromise)
  • Medications (steroids, immunosuppressants)
  • Complications (respiratory, neurological, skin infection)
  • Home management so far (NSAIDs?)
  • Contacts who may be high-risk (pregnant, newborn, immunocompromised)

Viva Voce Questions and Model Answers

Q1: A 5-year-old presents with an itchy vesicular rash for 2 days. How do you manage this?

Model Answer: "This presentation is consistent with chickenpox in a healthy child. I would confirm this clinically based on the characteristic rash — crops of vesicles at different stages in a centripetal distribution. No investigations are needed for uncomplicated cases.

For a healthy child, management is supportive:

  • Paracetamol for fever and discomfort — importantly, I would advise AGAINST NSAIDs due to the association with necrotising fasciitis
  • Antihistamines such as chlorphenamine for pruritus
  • Calamine lotion topically
  • Keep nails short and consider mittens to prevent scratching
  • Maintain good hydration

I would advise the parents that the child is infectious until all lesions have crusted over, usually 5-7 days, and should stay away from school and avoid contact with pregnant women, newborns, and immunocompromised individuals.

No antivirals are indicated for uncomplicated chickenpox in a healthy child. I would provide safety-netting advice to return if there are signs of secondary bacterial infection, respiratory symptoms, or neurological symptoms such as ataxia or altered consciousness."

Q2: Why should NSAIDs be avoided in chickenpox?

Model Answer: "NSAIDs, particularly ibuprofen, should be avoided in chickenpox because of an association with an increased risk of invasive Group A Streptococcal infection and necrotising fasciitis.

This association was demonstrated in case-control studies, including the study by Lesko and colleagues, which showed an odds ratio of approximately 5 for invasive GAS disease in children who received ibuprofen compared with those who did not.

Several mechanisms have been proposed:

  1. Anti-inflammatory effects may mask early signs of bacterial superinfection
  2. NSAIDs may impair neutrophil function and chemotaxis
  3. There may be effects on bacterial virulence or toxin production
  4. There is also potential selection bias, as sicker children are more likely to receive NSAIDs

Based on this evidence, guidelines from NICE and UKHSA recommend paracetamol only for symptomatic relief in chickenpox."

Q3: A pregnant woman at 14 weeks gestation is exposed to chickenpox. What is your management?

Model Answer: "This is a significant situation requiring urgent action. My first step is to determine her immunity status.

I would take a history of previous chickenpox or shingles, and check for vaccination history. I would then request urgent VZV IgG serology.

If she is IgG positive, she is immune and no action is needed — I would reassure her.

If she is IgG negative and the exposure is significant — defined as face-to-face contact for 5 minutes or more, same room for 15 minutes or more, or household contact — she is at risk.

For a susceptible pregnant woman with significant exposure, I would arrange for VZIG as soon as possible, ideally within 10 days of exposure. This can modify or prevent infection. The vaccine is contraindicated in pregnancy.

I would counsel her about the risks:

  1. Maternal risk: Varicella pneumonitis is more severe in pregnancy with significant mortality without treatment
  2. Fetal risk: At 14 weeks, she is in the highest risk period for congenital varicella syndrome, with approximately 2% risk if she develops varicella

I would advise her to report immediately if she develops a rash or systemic symptoms. If she develops chickenpox, she should receive aciclovir (which is considered safe in pregnancy) within 24 hours of rash onset, and close monitoring for pneumonitis. I would also arrange a fetal medicine referral for detailed ultrasound monitoring for signs of congenital varicella syndrome."

Q4: What are the indications for IV aciclovir in chickenpox?

Model Answer: "IV aciclovir is indicated in chickenpox for patients with severe disease or at high risk of complications:

  1. Immunocompromised patients — any cause, including:

    • Primary immunodeficiencies
    • Haematological malignancy
    • Solid organ or bone marrow transplant recipients
    • HIV with low CD4 count
    • High-dose corticosteroids (> 2 mg/kg/day or > 20 mg/day for > 14 days)
    • Chemotherapy or immunosuppressive therapy
  2. Varicella pneumonitis — presenting with cough, dyspnoea, hypoxia, and bilateral infiltrates on chest X-ray

  3. Neurological complications — encephalitis or severe cerebellar ataxia (though cerebellar ataxia is often self-limiting, IV aciclovir is often given)

  4. Neonatal varicella — particularly if maternal infection occurred 5 days before to 2 days after delivery

  5. Severe or haemorrhagic varicella — disseminated disease, purpuric lesions

  6. Pregnant women with severe disease — particularly varicella pneumonitis

  7. Any patient unable to tolerate oral therapy

The dose is 10 mg/kg IV three times daily (every 8 hours), with dose adjustment for renal impairment. Treatment continues until no new lesions appear for at least 48 hours, typically 7-14 days. Patients need adequate hydration and renal function monitoring given the nephrotoxic potential of aciclovir."

Common Exam Errors

ErrorCorrect Approach
Prescribing ibuprofen for feverUse paracetamol only — NSAIDs increase necrotising fasciitis risk
Giving oral aciclovir to all childrenAntivirals only for high-risk groups — not healthy children with uncomplicated disease
Stating chickenpox is infectious only when rash visibleInfectious from 2 days BEFORE rash appears
Forgetting VZIG for high-risk contactsVZIG within 10 days for susceptible immunocompromised, pregnant, and neonatal contacts
Confusing CVS timingCVS risk is less than 20 weeks gestation; after 20 weeks = shingles in infancy, not congenital syndrome
Stating chickenpox is always mildSevere in immunocompromised, pregnant, neonates, and adults — recognise high-risk groups
Missing latency conceptVZV remains dormant in dorsal root ganglia and can reactivate as shingles years later
Ordering investigations for uncomplicated casesDiagnosis is clinical; no tests needed for typical presentations in healthy children

15. References

Guidelines

  1. NICE Clinical Knowledge Summaries. Chickenpox. 2023. Available at: https://cks.nice.org.uk/topics/chickenpox/

  2. UK Health Security Agency (UKHSA). Guidance on varicella-zoster post-exposure prophylaxis. 2019. Available at: https://www.gov.uk/government/publications/varicella-the-green-book-chapter-34

Key Studies and Reviews

  1. Arvin AM. Varicella-zoster virus. Clin Microbiol Rev. 1996;9(3):361-381. doi:10.1128/CMR.9.3.361 PMID: 8809466

  2. Gershon AA, Gershon MD. Pathogenesis and current approaches to control of varicella-zoster virus infections. Clin Microbiol Rev. 2013;26(4):728-743. doi:10.1128/CMR.00052-13 PMID: 24092852

  3. Kuter BJ, Weibel RE, Guess HA, et al. Oka/Merck varicella vaccine in healthy children: final report of a 2-year efficacy study and 7-year follow-up studies. Vaccine. 1991;9(9):643-647. doi:10.1016/0264-410X(91)90189-D PMID: 1659702

  4. Marin M, Güris D, Chaves SS, et al. Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2007;56(RR-4):1-40. PMID: 17585291

  5. Lesko SM, O'Brien KL, Schwartz B, et al. Invasive group A streptococcal infection and nonsteroidal antiinflammatory drug use among children with primary varicella. Pediatrics. 2001;107(5):1108-1115. doi:10.1542/peds.107.5.1108 PMID: 11331692

  6. Mikaeloff Y, Kezouh A, Suissa S. Nonsteroidal anti-inflammatory drug use and the risk of severe skin and soft tissue complications in patients with varicella or zoster disease. Br J Clin Pharmacol. 2008;65(2):203-209. doi:10.1111/j.1365-2125.2007.02997.x PMID: 17714817

  7. Dunkle LM, Arvin AM, Whitley RJ, et al. A controlled trial of acyclovir for chickenpox in normal children. N Engl J Med. 1991;325(22):1539-1544. doi:10.1056/NEJM199111283252203 PMID: 1658649

  8. Lamont RF, Sobel JD, Carrington D, et al. Varicella-zoster virus (chickenpox) infection in pregnancy. BJOG. 2011;118(10):1155-1162. doi:10.1111/j.1471-0528.2011.02983.x PMID: 21585641

  9. Enders G, Miller E, Cradock-Watson J, et al. Consequences of varicella and herpes zoster in pregnancy: prospective study of 1739 cases. Lancet. 1994;343(8912):1548-1551. doi:10.1016/S0140-6736(94)92943-2 PMID: 7802770

  10. Zaia JA, Levin MJ, Preblud SR, et al. Evaluation of varicella-zoster immune globulin: protection of immunosuppressed children after household exposure to varicella. J Infect Dis. 1983;147(4):737-743. doi:10.1093/infdis/147.4.737 PMID: 6302172

  11. Heininger U, Seward JF. Varicella. Lancet. 2006;368(9544):1365-1376. doi:10.1016/S0140-6736(06)69561-5 PMID: 17046469

  12. Hope-Simpson RE. The nature of herpes zoster: a long-term study and a new hypothesis. Proc R Soc Med. 1965;58(1):9-20. PMID: 14267505

  13. Zerboni L, Sen N, Oliver SL, Arvin AM. Molecular mechanisms of varicella zoster virus pathogenesis. Nat Rev Microbiol. 2014;12(3):197-210. doi:10.1038/nrmicro3215 PMID: 24509782

  14. Ross AH. Modification of chicken pox in family contacts by administration of gamma globulin. N Engl J Med. 1962;267:369-376. doi:10.1056/NEJM196208232670801 PMID: 14494142

  15. Seward JF, Watson BM, Peterson CL, et al. Varicella disease after introduction of varicella vaccine in the United States, 1995-2000. JAMA. 2002;287(5):606-611. doi:10.1001/jama.287.5.606 PMID: 11829699

  16. Haake DA, Zakowski PC, Haake DL, Bryson YJ. Early treatment with acyclovir for varicella pneumonia in otherwise healthy adults: retrospective controlled study and review. Rev Infect Dis. 1990;12(5):788-798. doi:10.1093/clinids/12.5.788 PMID: 2237119

  17. Preblud SR. Varicella: complications and costs. Pediatrics. 1986;78(4 Pt 2):728-735. PMID: 3093960

  18. Gnann JW Jr. Varicella-zoster virus: atypical presentations and unusual complications. J Infect Dis. 2002;186 Suppl 1:S91-S98. doi:10.1086/342963 PMID: 12353193


Last Reviewed: 2025-01-09 | MedVellum Editorial Team


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Learning map

Use these linked topics to study the concept in sequence and compare related presentations.

Prerequisites

Start here if you need the foundation before this topic.

  • Viral Immunology
  • Paediatric Infectious Disease Principles

Differentials

Competing diagnoses and look-alikes to compare.

  • Hand, Foot and Mouth Disease
  • Impetigo
  • Herpes Simplex Infection
  • Monkeypox

Consequences

Complications and downstream problems to keep in mind.