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
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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
| Parameter | Value |
|---|---|
| Causative agent | Varicella-zoster virus (VZV) — Human Herpesvirus 3 (HHV-3), Herpesviridae family |
| Transmission routes | Respiratory droplets (airborne), direct contact with vesicle fluid, vertical (transplacental) |
| Incubation period | 10-21 days (median 14-16 days) |
| Infectious period | 2 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 distribution | Centripetal: trunk predominant → spreads to face, scalp, limbs |
| Rash evolution | Macule → papule → vesicle → pustule → crust (24-48 hours per lesion) |
| Total lesion count | Typically 250-500 (range 10 to > 1500) |
| Complication rate | 2-6% in immunocompetent children; significantly higher in high-risk groups |
| Latency site | Dorsal root ganglia, cranial nerve ganglia |
| Reactivation disease | Herpes zoster (shingles) |
| Vaccine type | Live 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:
- Identification of high-risk patients requiring antiviral therapy or hospitalisation
- Recognition of complications — particularly secondary bacterial infection, pneumonitis, and neurological involvement
- Appropriate supportive care — including avoidance of NSAIDs
- Post-exposure management — VZIG for high-risk contacts, vaccination for eligible exposures
- 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:
| Component | Description |
|---|---|
| Genome | Linear double-stranded DNA (~125 kbp) |
| Nucleocapsid | Icosahedral symmetry, ~100 nm diameter |
| Tegument | Proteinaceous layer between capsid and envelope |
| Envelope | Lipid bilayer derived from host cell membrane |
| Glycoproteins | gB, gC, gE, gH, gI, gK, gL, gM, gN — essential for cell entry and cell-to-cell spread |
| Key glycoprotein | gE — most abundant; target of neutralising antibodies |
Unique Features of VZV:
- Highly cell-associated: Unlike HSV, VZV is extremely cell-associated; cell-free virus is unstable and difficult to culture
- Strict human tropism: No animal reservoir; humans are the only natural host
- Neurotropism: Establishes latency specifically in sensory neurons of dorsal root and cranial nerve ganglia
- 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
| Feature | VZV (HHV-3) | HSV-1 (HHV-1) | HSV-2 (HHV-2) |
|---|---|---|---|
| Primary disease | Chickenpox | Oral herpes, encephalitis | Genital herpes |
| Reactivation disease | Shingles | Cold sores, keratitis | Genital recurrence |
| Latency site | Dorsal root/cranial ganglia | Trigeminal ganglion | Sacral ganglia |
| Cell association | Highly cell-associated | Cell-free virus stable | Cell-free virus stable |
| Lesion distribution | Generalised (primary) | Localised (orolabial) | Localised (genital) |
| Transmission | Airborne + contact | Direct contact | Sexual contact |
| Vaccine | Available (live attenuated) | Not available | Not 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):
| Parameter | Data |
|---|---|
| Lifetime infection risk | > 95% by adulthood |
| Annual incidence | 3.5-4.0 million cases (UK); ~4 million (USA) |
| Peak age of infection | 4-10 years |
| Percentage infected by age 15 | 80-90% |
| Hospitalisation rate | 2-3 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:
| Outcome | Reduction |
|---|---|
| Varicella incidence | 85-90% decline |
| Varicella-related hospitalisations | 88-93% decline |
| Varicella-related deaths | 87-92% 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]
| Parameter | UK 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 age | 1-4 years (> 50% of cases); 90% occur in less than 14 years |
| Seasonality | Late winter to early spring peak (March-May) |
| Cyclical pattern | Epidemic peaks every 2-5 years |
Risk Factors for Severe Disease
| Risk Factor | Relative Risk/Odds Ratio | Key Complications |
|---|---|---|
| Age > 14 years | 15-25x mortality vs children | Pneumonitis, hepatitis |
| Age > 50 years | Further increased mortality | Multi-organ involvement |
| Pregnancy | 5x increased pneumonitis risk | Varicella pneumonitis (10-15% mortality) |
| Trimester 1-2 | Risk of CVS | Congenital varicella syndrome (0.5-2%) |
| Peripartum (5 days pre to 2 days post delivery) | Severe neonatal disease | Neonatal varicella (30% mortality untreated) |
| Neonates (less than 28 days) | Very high mortality | Disseminated disease, pneumonitis |
| Primary immunodeficiency | Markedly increased | Progressive varicella, visceral dissemination |
| Secondary immunodeficiency | 10-30% mortality (untreated) | Fulminant hepatitis, DIC |
| Malignancy (esp. leukaemia) | 7-10% mortality (untreated) | Disseminated disease, haemorrhagic varicella |
| Solid organ transplant | Significantly increased | Prolonged disease, visceral involvement |
| HIV/AIDS (CD4 less than 200) | Increased severity | Chronic varicella, VZV retinitis |
| High-dose corticosteroids | Increased (> 2 mg/kg/day or > 20 mg/day for > 14 days) | Severe disseminated disease |
| Chronic lung disease | Increased pneumonitis risk | Respiratory failure |
| Chronic skin disease (eczema) | More extensive cutaneous disease | Secondary infection, scarring |
Transmission Dynamics
Routes of Transmission:
- Airborne (respiratory droplets and aerosols): Primary route — virus shed from respiratory tract and aerosolised from vesicle fluid
- Direct contact: Contact with vesicle fluid; less efficient than airborne
- Vertical transmission: Transplacental (congenital varicella syndrome); perinatal (neonatal varicella)
Attack Rates by Setting:
| Setting | Attack Rate (Susceptible Contacts) |
|---|---|
| Household | > 90% |
| Classroom/daycare | 10-35% |
| Hospital (shared room) | 70-90% |
| Casual contact | Low (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:
| Feature | Description |
|---|---|
| Location | Intraepidermal (within stratum spinosum) |
| Type | Unilocular (single cavity) |
| Contents | Serous fluid with high viral titre, inflammatory cells, epithelial cells |
| Base | Erythematous due to dermal inflammation |
| Evolution | Clouding (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:
| Component | Role in VZV Control |
|---|---|
| Type I interferons (IFN-α/β) | Limit viral replication; activate antiviral state |
| NK cells | Early cytotoxic response to infected cells |
| Complement | Antibody-dependent neutralisation |
| Pattern recognition | TLR detection of viral nucleic acids |
Adaptive Immunity:
| Component | Timing | Function |
|---|---|---|
| VZV-specific IgM | Day 3-5 post-rash | Acute phase; wanes within months |
| VZV-specific IgG | Day 5-7 post-rash | Long-term protection; prevents reinfection |
| CD4+ T cells | Week 1-2 | Helper function; cytokine production |
| CD8+ T cells | Week 1-2 | Cytotoxic killing of infected cells; CRITICAL for clearance |
| Memory T cells | Weeks to months | Long-term cellular immunity; prevents reactivation |
Critical Role of Cell-Mediated Immunity (CMI):
CMI, particularly VZV-specific CD8+ T cell responses, is essential for:
- Clearance of primary infection
- Limitation of disease severity
- Prevention of reactivation (herpes zoster)
- 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:
| Feature | Description |
|---|---|
| Vesicle location | Intraepidermal (stratum spinosum) |
| Keratinocyte changes | Ballooning degeneration, acantholysis |
| Multinucleated giant cells | Syncytial formation (pathognomonic for herpesvirus) |
| Nuclear inclusions | Cowdry type A bodies (eosinophilic intranuclear) |
| Dermal changes | Perivascular lymphocytic infiltrate, oedema |
| Vessel involvement | Endothelial infection, vasculitis (severe cases) |
Tzanck Smear:
A rapid bedside diagnostic test involving:
- Unroofing a fresh vesicle
- Scraping the vesicle base
- Smearing on a glass slide
- Staining (Giemsa, Wright, or Diff-Quik)
- 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]
| Symptom | Frequency | Notes |
|---|---|---|
| Fever | 70-90% | Low-grade (37.5-38.5°C) in children; higher in adults |
| Malaise | 60-80% | General unwellness, fatigue |
| Headache | 30-50% | More common in adolescents/adults |
| Anorexia | 40-60% | Loss of appetite common in young children |
| Myalgia | 20-40% | Muscle aches; more prominent in adults |
| Abdominal pain | 10-20% | 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":
| Feature | Description |
|---|---|
| Appearance | Clear, superficial, thin-walled vesicle |
| Size | 2-4 mm diameter (range 1-5 mm) |
| Shape | Round or ovoid; becomes umbilicated |
| Base | Erythematous ("rose petal" — surrounding red halo) |
| Contents | Clear serous fluid (initially); becomes cloudy/pustular |
| Wall | Fragile; easily ruptured |
| Tzanck | Positive for multinucleated giant cells |
Rash Distribution:
| Pattern | Description |
|---|---|
| Overall | Centripetal — concentrated centrally with peripheral spread |
| Most dense | Trunk (chest, back, abdomen) |
| Moderate | Face, scalp |
| Least dense | Extremities (arms, legs) |
| Sparing | Palms and soles typically spared (unlike hand, foot and mouth disease) |
| Mucosal involvement | Oral cavity (palate, buccal mucosa), conjunctiva, genitalia |
Characteristic Features:
| Feature | Significance |
|---|---|
| Crops | New lesions appear in waves over 3-5 days |
| Pleomorphism ("Starry Sky") | Lesions at ALL stages visible simultaneously |
| Pruritus | Intense itching is characteristic; main symptom in many children |
| Number | Typically 250-500 lesions (range 10 to > 1500) |
| Duration of new lesions | 3-5 days (healthy); prolonged in immunocompromised |
| Time to crusting | 4-7 days from vesicle formation |
| Crusts fall off | 1-3 weeks after formation |
Disease Severity Grading
| Severity | Lesion Count | Clinical Features |
|---|---|---|
| Mild | less than 50 | Minimal systemic symptoms; brief illness |
| Moderate | 50-250 | Typical presentation; fever, pruritus, full course |
| Severe | > 250-500 | Higher fever; more systemic symptoms |
| Very severe | > 500-1000+ | Confluent lesions; haemorrhagic; immunocompromised |
Mucosal Involvement
| Site | Manifestation | Clinical Significance |
|---|---|---|
| Oral cavity | Vesicles → shallow ulcers on palate, buccal mucosa, gingiva, tongue | Pain; decreased oral intake; dehydration risk |
| Oropharynx | Pharyngeal ulceration | Odynophagia |
| Conjunctiva | Conjunctival vesicles, conjunctivitis | Usually self-limiting; rarely corneal involvement |
| Genitalia | Vulvar/scrotal vesicles → ulcers | Painful; secondary infection risk |
| Larynx | Laryngeal lesions (rare) | Stridor; airway compromise (very rare) |
Special Populations
Neonatal Varicella:
The timing of maternal infection relative to delivery determines neonatal risk:
| Maternal Infection Timing | Neonatal Presentation | Mortality (Untreated) |
|---|---|---|
| > 7 days before delivery | Mild disease (passive maternal antibodies transferred) | Low |
| 5 days before to 2 days after delivery | Severe disseminated varicella (no passive antibodies) | 20-30% |
| Congenital (in utero, weeks 1-20) | Congenital varicella syndrome | Variable |
Congenital Varicella Syndrome (CVS):
Occurs with maternal infection in first 20 weeks (highest risk 13-20 weeks):
| Feature | Description |
|---|---|
| Cutaneous | Cicatricial (zigzag) skin scarring in dermatomal distribution |
| Limb | Limb hypoplasia, limb shortening |
| Neurological | Microcephaly, cortical atrophy, mental retardation |
| Ophthalmological | Chorioretinitis, cataracts, microphthalmos, Horner syndrome |
| Other | Low birth weight, IUGR |
| Risk | 0.5% (weeks 1-12); 2% (weeks 13-20); rare after 20 weeks |
Immunocompromised Patients:
| Feature | Presentation |
|---|---|
| Lesion count | Often > 1500; continuous crops for > 7 days |
| Lesion type | Haemorrhagic (purpuric), necrotic, umbilicated, confluent |
| Duration | Prolonged (weeks without treatment) |
| Visceral involvement | Pneumonitis, hepatitis, encephalitis, DIC common |
| New lesion development | Beyond day 7-10 indicates progressive disease |
| Mortality | 7-10% (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:
| Finding | Significance |
|---|---|
| Alertness | Drowsiness may indicate encephalitis |
| Toxic appearance | Suggests secondary bacterial infection |
| Respiratory distress | Suggests pneumonitis |
| Hydration status | Oral intake often reduced |
Skin Examination:
| Assessment | Method | Findings |
|---|---|---|
| Lesion description | Systematic description | "Dewdrops on rose petals" — vesicles on erythematous base |
| Lesion stages | Identify all stages present | Macules, papules, vesicles, pustules, crusts (simultaneously) |
| Distribution | Map body involvement | Centripetal: trunk > face/scalp > limbs |
| Density estimation | Count sample area, extrapolate | Mild (less than 50), Moderate (50-250), Severe (> 250) |
| Mucosal examination | Inspect mouth, conjunctivae | Oral vesicles/ulcers, conjunctivitis |
| Signs of superinfection | Look for bacterial infection | Spreading erythema, honey crusting, warmth, tenderness |
| Staging of lesions | Assess if all crusted | All crusted = no longer infectious |
| Scarring | Document any already present | Scratching, secondary infection increase risk |
Secondary Bacterial Infection Signs:
| Finding | Concern |
|---|---|
| Enlarging erythema around lesions | Cellulitis |
| Honey-coloured crusting | Impetigo (S. aureus, GAS) |
| Warmth, fluctuance | Abscess formation |
| Pain disproportionate to appearance | Necrotising fasciitis |
| Crepitus | Gas-forming organism; necrotising infection |
| Rapid spread | Invasive GAS |
| Systemic toxicity | Bacteraemia, sepsis |
Systems Examination (If Complications Suspected)
Respiratory Examination:
| Finding | Suggests |
|---|---|
| Tachypnoea | Pneumonitis, respiratory distress |
| Hypoxia | Significant pneumonitis |
| Cough (dry) | Early pneumonitis |
| Crackles (bilateral) | Varicella pneumonitis |
| Reduced air entry | Consolidation, effusion |
Neurological Examination:
| Finding | Suggests |
|---|---|
| Ataxia (truncal) | Cerebellar ataxia (most common CNS complication) |
| Nystagmus | Cerebellar involvement |
| Dysarthria | Cerebellar involvement |
| Altered GCS | Encephalitis |
| Seizures | Encephalitis |
| Neck stiffness | Meningitis, meningoencephalitis |
| Focal neurological signs | Focal encephalitis, stroke (VZV vasculopathy) |
Abdominal Examination:
| Finding | Suggests |
|---|---|
| Hepatomegaly | Hepatitis (common subclinically) |
| Tender hepatomegaly | Significant hepatic involvement |
| Splenomegaly | Haematological involvement |
| Abdominal tenderness | Visceral 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):
| Investigation | Specimen | Method | Notes |
|---|---|---|---|
| VZV PCR | Vesicle fluid/swab | PCR | Gold standard; highly sensitive and specific |
| VZV DFA | Vesicle scraping | Direct fluorescent antibody | Rapid (hours); less sensitive than PCR |
| Tzanck smear | Vesicle scraping | Cytology | Rapid bedside; multinucleated giant cells; non-specific (also positive in HSV) |
| Viral culture | Vesicle fluid | Cell culture | Slow (7-14 days); low sensitivity; rarely used |
| VZV IgM/IgG serology | Blood | ELISA/EIA | IgM = acute; IgG = past infection/immunity |
Preferred test: VZV PCR from vesicle fluid (sensitivity > 95%, specificity > 99%)
2. Assessing Immunity (Pre-Exposure):
| Test | Use |
|---|---|
| VZV IgG | Confirms immunity (past infection or vaccination) |
| Interpretation | Positive = immune; Negative = susceptible |
3. Investigations for Complications:
| Complication | Investigations |
|---|---|
| Bacterial superinfection | FBC, CRP, blood culture, wound swab M/C/S |
| Varicella pneumonitis | CXR, SpO2, ABG, VZV PCR (BAL if intubated) |
| Encephalitis/cerebellar ataxia | LP (CSF analysis, VZV PCR), MRI brain, EEG |
| Hepatitis | LFTs (ALT, AST often mildly elevated subclinically) |
| Haemorrhagic varicella | FBC (thrombocytopenia), coagulation screen, film |
| Reye syndrome | LFTs, ammonia, glucose, coagulation, lactate |
4. Expected Findings:
| Investigation | Uncomplicated | Complicated |
|---|---|---|
| FBC | Normal or mild lymphocytosis | Leukocytosis (bacterial); leukopenia (severe); thrombocytopenia |
| CRP | Normal or mildly elevated | Markedly elevated (bacterial superinfection) |
| LFTs | Often mildly elevated AST/ALT | Significant elevation (hepatitis) |
| CXR | Normal | Bilateral nodular/reticulonodular infiltrates (pneumonitis) |
| CSF | N/A | Lymphocytic pleocytosis, normal glucose, VZV PCR positive (encephalitis) |
Chest X-Ray Findings in Varicella Pneumonitis:
| Finding | Description |
|---|---|
| Pattern | Bilateral, diffuse, nodular or reticulonodular infiltrates |
| Distribution | Perihilar and basal predominance |
| Evolution | May develop rapidly; can progress to ARDS |
| Resolution | Typically resolves over weeks with treatment |
| Calcification | Small 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:
| Scenario | Management |
|---|---|
| Mild impetigo | Topical fusidic acid or mupirocin |
| Extensive impetigo/cellulitis | Oral flucloxacillin (or co-amoxiclav if GAS suspected) |
| Severe infection/systemic toxicity | IV antibiotics (flucloxacillin + clindamycin for toxin suppression) |
| Necrotising fasciitis | Urgent surgical debridement + IV broad-spectrum antibiotics |
Varicella Pneumonitis:
| Action | Details |
|---|---|
| Admit | High-dependency or ICU setting |
| Antiviral | IV aciclovir 10 mg/kg TDS |
| Oxygen | Supplemental O2 to maintain SpO2 > 94% |
| Respiratory support | NIV or mechanical ventilation if required |
| Steroids | Role controversial; sometimes used in severe cases |
| Monitoring | Close respiratory monitoring; ABGs |
Encephalitis/Cerebellar Ataxia:
| Feature | Encephalitis | Cerebellar Ataxia |
|---|---|---|
| Timing | Days 3-8 post-rash | Days 2-6 post-rash |
| Presentation | Altered consciousness, seizures | Ataxia, nystagmus, dysarthria |
| CSF | Lymphocytic pleocytosis | Often normal |
| Imaging | MRI may show changes | Usually normal |
| Treatment | IV aciclovir + supportive | Supportive (± aciclovir) |
| Prognosis | Variable; 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):
| Indication | Timing | Notes |
|---|---|---|
| Immunocompromised (susceptible) | Within 10 days of exposure | Highest priority |
| Pregnant (susceptible) | Within 10 days of exposure | Reduces maternal severity |
| Neonate — maternal varicella -7 to +7 days of delivery | ASAP after birth | High-risk period |
| Neonate — VZV-exposed less than 7 days if mother non-immune | Within 10 days | Depends on maternal status |
| Infants of mothers with varicella at delivery | ASAP | Regardless 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:
| Indication | Timing | Efficacy |
|---|---|---|
| Healthy susceptible contacts (≥12 months) | Within 3-5 days of exposure | 70-100% prevention; reduces severity if infection occurs |
| Not indicated | Immunocompromised, pregnant, infants less than 12 months |
Pregnancy Management
| Scenario | Management |
|---|---|
| Susceptible pregnant woman exposed | Check 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 delivery | Paediatric 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:
- Masking of early signs of bacterial superinfection (anti-inflammatory effect)
- Impaired neutrophil function and chemotaxis
- Enhanced bacterial virulence (streptococcal toxin production)
- 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
| Complication | Incidence | Organism | Features | Management |
|---|---|---|---|---|
| Secondary bacterial skin infection | 5-10% | S. aureus, GAS | Impetiginised lesions, cellulitis | Topical/oral antibiotics |
| Invasive GAS disease | Rare but serious | Group A Streptococcus | Rapid spread, toxicity | IV antibiotics; surgical debridement |
| Necrotising fasciitis | less than 0.1% | GAS, mixed flora | Pain > appearance, crepitus, rapid progression | Emergency surgery + IV antibiotics |
| Staphylococcal scalded skin syndrome | Rare | S. aureus (toxin) | Desquamation | IV flucloxacillin |
| Scarring | Common | N/A | Pitted scars (scratching, secondary infection) | Prevention by minimising scratching |
Respiratory Complications
| Complication | Incidence | Risk Groups | Features | Management |
|---|---|---|---|---|
| Varicella pneumonitis | 1:400 adults; rare in children | Adults, pregnant, smokers, immunocompromised | Cough, dyspnoea, hypoxia, bilateral infiltrates | IV aciclovir, supportive, ± ventilation |
| Secondary bacterial pneumonia | Uncommon | Any | Fever, productive cough, focal consolidation | Antibiotics targeting respiratory pathogens |
| Respiratory failure/ARDS | Rare | Severe pneumonitis | Progressive hypoxia | ICU; mechanical ventilation |
Neurological Complications
| Complication | Incidence | Timing | Features | Outcome |
|---|---|---|---|---|
| Cerebellar ataxia | 1:4,000 | Days 2-6 post-rash | Truncal ataxia, nystagmus, dysarthria | Usually self-limiting (2-4 weeks); full recovery |
| Encephalitis | 1:4,000 | Days 3-8 post-rash | Altered consciousness, seizures, focal signs | Variable; 5-10% mortality; 10-20% sequelae |
| Meningitis | Rare | Variable | Headache, neck stiffness, photophobia | Usually good prognosis |
| Transverse myelitis | Very rare | Weeks post-infection | Ascending weakness, sensory level | Variable outcome |
| Guillain-Barré syndrome | Very rare | 2-4 weeks post-infection | Ascending weakness, areflexia | Variable; may require ventilation |
| Stroke (VZV vasculopathy) | Rare | Weeks to months post-infection | Focal neurological signs | Antivirals; variable outcome |
| Reye syndrome | Now rare | If aspirin given | Encephalopathy, hepatic failure | High mortality; avoid aspirin |
Haematological Complications
| Complication | Incidence | Features | Management |
|---|---|---|---|
| Thrombocytopenia | Uncommon | Petechiae, bleeding, low platelets | Usually self-limiting; rarely transfusion |
| Purpura fulminans | Very rare | DIC, skin necrosis | ICU; supportive; treat DIC |
| Haemorrhagic varicella | Rare (immunocompromised) | Purpuric lesions, mucosal bleeding | IV aciclovir; supportive; platelet/FFP |
Other Complications
| Complication | Incidence | Notes |
|---|---|---|
| Hepatitis | Common (subclinical) | Transient transaminase elevation; clinical hepatitis rare |
| Arthritis | Rare | Self-limiting; reactive |
| Myocarditis | Very rare | Chest pain, arrhythmias |
| Glomerulonephritis | Very rare | Haematuria, oedema |
| Pancreatitis | Very rare | Abdominal pain, elevated amylase |
| Orchitis | Rare | Testicular swelling, pain |
Pregnancy-Related Complications
| Timing | Fetal/Neonatal Risk | Incidence |
|---|---|---|
| Weeks 0-12 | Congenital varicella syndrome (CVS) | 0.5% |
| Weeks 13-20 | Congenital varicella syndrome (CVS) | 2% |
| Weeks 20-36 | Herpes zoster in infancy (not CVS) | Low |
| 5 days pre to 2 days post delivery | Severe neonatal varicella | 17-30% mortality (untreated) |
Late Complications
| Complication | Timeframe | Notes |
|---|---|---|
| Herpes zoster (shingles) | Years to decades post-infection | VZV reactivation from latent ganglia |
| Post-herpetic neuralgia | Following zoster | Not following primary varicella |
| VZV retinitis | Immunocompromised | Late reactivation manifestation |
10. Prognosis and Outcomes
Immunocompetent Children
| Outcome | Expected |
|---|---|
| Duration of illness | 5-10 days |
| Time to all lesions crusted | 5-7 days (marks end of infectious period) |
| Full recovery | > 99% |
| Complication rate | 2-6% |
| Hospitalisation rate | 2-3 per 1,000 cases |
| Mortality | ~1 per 60,000-100,000 cases |
| Scarring | Common if scratching or secondary infection occurs |
| Lifelong immunity | Yes (reinfection extremely rare) |
| Future shingles risk | 10-30% lifetime risk |
High-Risk Populations
| Population | Key Outcomes |
|---|---|
| Adults | 15-25x 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 ataxia | Excellent; complete recovery in 2-4 weeks in most |
| Encephalitis | 5-10% mortality; 10-20% neurological sequelae |
Factors Associated with Poor Outcomes
| Factor | Impact |
|---|---|
| Immunocompromise | Strongest predictor of severe disease and mortality |
| Age (adults, neonates) | Increased complication rates |
| Pregnancy | Pneumonitis risk; fetal risks |
| Delayed antiviral therapy | Poorer outcomes if > 24-48 hours post-rash onset |
| High lesion count | Correlates with severity |
| NSAID use | Increased bacterial superinfection risk |
| Underlying lung disease | Increased pneumonitis risk |
11. Prevention
Varicella Vaccination
Vaccine Characteristics:
| Feature | Details |
|---|---|
| Type | Live attenuated (Oka strain) |
| Storage | Frozen (-15°C) or refrigerated (2-8°C for shorter periods) |
| Administration | Subcutaneous injection |
| Doses | 2 doses recommended for full protection |
| Schedule (where routine) | Dose 1: 12-15 months; Dose 2: 4-6 years |
| Efficacy | 80-85% against any varicella; 95-99% against severe disease |
| Duration of protection | Long-term; likely lifelong for most |
Vaccine-Eligible Groups (UK — Targeted Programme):
| Group | Indication |
|---|---|
| Healthcare workers | Non-immune HCWs with patient contact |
| Household contacts of immunocompromised | To protect vulnerable family members |
| Laboratory staff | Working with VZV |
| Non-immune women | Pre-conception (not if pregnant) |
Contraindications:
| Contraindication | Reason |
|---|---|
| Pregnancy | Theoretical risk of fetal varicella (avoid pregnancy for 1 month post-vaccination) |
| Immunocompromise | Risk of vaccine-strain disease (live vaccine) |
| Recent immunoglobulin | May reduce vaccine efficacy |
| Severe allergic reaction to previous dose | Anaphylaxis risk |
| Severe allergy to gelatin or neomycin | Vaccine 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
| Issue | Details |
|---|---|
| Herd immunity | High 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 evidence | Mixed; some studies show increased zoster, others do not |
| Mitigation | Zoster vaccination in older adults |
12. Evidence and Guidelines
Key Guidelines
| Guideline | Organisation | Year | Key Recommendations |
|---|---|---|---|
| Chickenpox CKS | NICE | 2023 | Primary care diagnosis, management, referral criteria |
| PHE Guidance on VZV | UKHSA (formerly PHE) | 2019 | Post-exposure prophylaxis, VZIG indications |
| Green Book Chapter 34 | UKHSA | 2022 | Varicella vaccination, immunisation schedules |
| AAP Red Book | American Academy of Pediatrics | 2021 | Comprehensive paediatric infectious disease guidance |
| RCPCH Guidelines | Royal College of Paediatrics | Various | Paediatric-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
| Intervention | Evidence Level | Evidence Source |
|---|---|---|
| Varicella vaccination | 1a | Multiple RCTs, systematic reviews |
| Oral aciclovir in high-risk immunocompetent | 1b | RCTs |
| IV aciclovir in immunocompromised | 2a | Cohort studies, consensus |
| VZIG for post-exposure prophylaxis | 2a | Cohort studies |
| Avoidance of NSAIDs | 2a | Case-control studies |
| Supportive care (paracetamol, antihistamines) | 5 | Expert 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
| Topic | Key Points |
|---|---|
| Causative organism | Varicella-zoster virus (VZV), Human Herpesvirus 3, Herpesviridae family |
| Transmission | Airborne (respiratory droplets) + direct contact with vesicle fluid; highly contagious |
| Incubation | 10-21 days (typically 14-16 days) |
| Infectious period | 2 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 evolution | Macule → Papule → Vesicle → Pustule → Crust (24-48 hours per lesion) |
| Distribution | Centripetal (trunk predominant → face → limbs); crops at different stages simultaneously |
| Avoid NSAIDs | Associated with increased risk of necrotising fasciitis (use paracetamol only) |
| Aciclovir indications | Adults, immunocompromised, pregnant, neonates, severe disease; within 24 hours of rash |
| IV aciclovir dose | 10 mg/kg TDS (children and adults) |
| VZIG indications | High-risk contacts (immunocompromised, pregnant, neonates) within 10 days of exposure |
| Latency | Dorsal root ganglia → reactivates as herpes zoster (shingles) |
| Cerebellar ataxia | Most common CNS complication; usually self-limiting |
| Congenital varicella syndrome | Risk if maternal infection less than 20 weeks; limb hypoplasia, cicatricial scars, eye/CNS abnormalities |
| Neonatal varicella | Severe 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:
- Anti-inflammatory effects may mask early signs of bacterial superinfection
- NSAIDs may impair neutrophil function and chemotaxis
- There may be effects on bacterial virulence or toxin production
- 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:
- Maternal risk: Varicella pneumonitis is more severe in pregnancy with significant mortality without treatment
- 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:
-
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
-
Varicella pneumonitis — presenting with cough, dyspnoea, hypoxia, and bilateral infiltrates on chest X-ray
-
Neurological complications — encephalitis or severe cerebellar ataxia (though cerebellar ataxia is often self-limiting, IV aciclovir is often given)
-
Neonatal varicella — particularly if maternal infection occurred 5 days before to 2 days after delivery
-
Severe or haemorrhagic varicella — disseminated disease, purpuric lesions
-
Pregnant women with severe disease — particularly varicella pneumonitis
-
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
| Error | Correct Approach |
|---|---|
| Prescribing ibuprofen for fever | Use paracetamol only — NSAIDs increase necrotising fasciitis risk |
| Giving oral aciclovir to all children | Antivirals only for high-risk groups — not healthy children with uncomplicated disease |
| Stating chickenpox is infectious only when rash visible | Infectious from 2 days BEFORE rash appears |
| Forgetting VZIG for high-risk contacts | VZIG within 10 days for susceptible immunocompromised, pregnant, and neonatal contacts |
| Confusing CVS timing | CVS risk is less than 20 weeks gestation; after 20 weeks = shingles in infancy, not congenital syndrome |
| Stating chickenpox is always mild | Severe in immunocompromised, pregnant, neonates, and adults — recognise high-risk groups |
| Missing latency concept | VZV remains dormant in dorsal root ganglia and can reactivate as shingles years later |
| Ordering investigations for uncomplicated cases | Diagnosis is clinical; no tests needed for typical presentations in healthy children |
15. References
Guidelines
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NICE Clinical Knowledge Summaries. Chickenpox. 2023. Available at: https://cks.nice.org.uk/topics/chickenpox/
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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
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Arvin AM. Varicella-zoster virus. Clin Microbiol Rev. 1996;9(3):361-381. doi:10.1128/CMR.9.3.361 PMID: 8809466
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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
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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
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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
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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
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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
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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
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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
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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
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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
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Heininger U, Seward JF. Varicella. Lancet. 2006;368(9544):1365-1376. doi:10.1016/S0140-6736(06)69561-5 PMID: 17046469
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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
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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
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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
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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
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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
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Preblud SR. Varicella: complications and costs. Pediatrics. 1986;78(4 Pt 2):728-735. PMID: 3093960
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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
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists for complex or high-risk cases.
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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.
- Herpes Zoster (Shingles)
- Post-herpetic Neuralgia