INFECTIOUS DISEASES,  INFECTIOUS DISEASES PAEDS,  PAEDIATRICS

Varicella/Chickenpox

Chickenpox vs. Shingles

1. Etiology & Virology

  • Caused by primary infection with human α-herpesvirus type 3 (Varicella-Zoster Virus, VZV).
  • Following primary viraemia and cutaneous replication, VZV establishes lifelong latency in dorsal-root and cranial nerve ganglia.
  • Reactivation (Herpes Zoster) occurs when cell-mediated immunity wanes.

2. Epidemiology

  • Incubation period: 10–21 days (mean ≈ 14 days).
  • Lifetime risk of reactivation (shingles) ≈ 30 %; increases with age (≈ 50 % by 85 years).

3. Transmission & Infectious Period

  • Transmission: aerosolised respiratory droplets or direct contact with vesicular fluid.
  • Infectious:
    • from 8–21 days post-exposure (extends to 8–28 days if VZIG given) and
    • from 2 days before rash onset until all vesicles are crusted.

4. Pathophysiology of Primary Varicella

StageEventsClinical Correlate
InoculationVirus enters via nasopharyngeal/conjunctival mucosa10–21 day incubation
may have mild prodrome (fever, malaise)
Primary viraemiaHaematogenous spread to RESOften asymptomatic
Secondary replicationAmplification in liver, spleen, RES (days 4–6)Rising fever
Secondary viraemiaSeeding of capillary endothelium & epidermis → polymorphic vesicles“Dew-drop on a rose petal” vesicles in crops at different stages
Immune containmentHumoral + cell-mediated responses → lesion crusting (by day 10)Crusted lesions = non-infectious; virus transported to ganglia

5. Clinical Features

  • Prodrome (variable):
    • fever
    • malaise
    • headache.
  • Rash:
    • pruritic, polymorphic vesicles on erythematous base
    • lesions in successive “crops” on scalp, face, trunk, extremities, oral mucosa.
  • Severity screening:
    • assess for high fever
    • respiratory distress
    • neurological signs
    • dehydration
    • extensive rash (> 20 lesions)
    • risk factors
      • age > 12 years unvaccinated
      • pregnancy
      • eczema
      • chronic lung disease
      • immunosuppression

6. Complications

  • Skin & soft tissue:
    • secondary bacterial infection (GAS, S. aureus)
    • necrotising fasciitis.
  • Respiratory:
    • viral pneumonitis
    • secondary bacterial pneumonia.
  • Neurological:
    • acute cerebellar ataxia
    • encephalitis
    • aseptic meningitis
    • Guillain–Barré syndrome.
  • Haematologic:
    • thrombocytopenia
    • purpura fulminans.
  • Hepatic/metabolic:
    • hepatitis
    • Reye syndrome (with aspirin).
  • Other:
    • arthritis
    • osteomyelitis
    • glomerulonephritis
    • uveitis.
  • Pregnancy:
    • congenital varicella syndrome (≤ 20 weeks gestation)
    • severe neonatal disease (maternal rash 5 days before to 2 days after delivery).
  • Immunocompromised:
    • disseminated visceral disease (high mortality without IV aciclovir).

7. Diagnosis

  • Clinical: typical rash ± known exposure.
  • Virology (if atypical or severe):
    • PCR of vesicle fluid; serology (IgM) for retrospective confirmation.

8. Management

8.1 Supportive Care (Immunocompetent, < 12 years, uncomplicated)

  • Paracetamol for fever.
  • Oral antihistamines or wet wraps for pruritus.
  • Avoid NSAIDs and aspirin (risk of invasive GAS and Reye syndrome).
  • Pruritus relief
    • wet wrap dressings
    • calamine/luliconazole lotion
    • sedating antihistamine at night

8.2 Antiviral Therapy

  • Oral aciclovir
    • 20 mg/kg/dose (max 800 mg) QID for 5 days if started ≤ 24 h from rash onset in high-risk but well patients (≥ 12 years unvaccinated; severe eczema; chronic lung disease; on steroids/salicylates).
  • IV aciclovir
    • 10 mg/kg Q8 h (with renal monitoring) for severe disease, immunocompromise, neonates (< 7 days), or CNS involvement.

8.3 Secondary Bacterial Infection

  • Empirical anti-staphylococcal therapy (e.g. flucloxacillin ± clindamycin) guided by local antimicrobial guidelines.

9. Infection Control

  • Airborne + contact precautions:
    • N95/P2 mask
    • gown
    • gloves
    • eye protection.
  • Single-room isolation
  • clinic appointments – schedule at day’s end
  • virucidal cleaning and adequate air exchange.
  • Exclude non-immune staff/patients for 21 days after last exposure (28 days if VZIG received).

10. Vaccination & Post-Exposure Prophylaxis

  • Routine schedule (AIR):
    • 1 dose MMRV at 18 months (funded)
    • 2nd dose ≥ 4 weeks later (ATAGI recommends a 2nd dose ≥ 4 weeks later (but not funded))
  • Catch-up:
    • < 14 years: 2 total doses if not vaccinated.
    • ≥ 14 years/adults: 2 doses ≥ 4 weeks apart.
  • Post-exposure:
    • live vaccine within 3–5 days (up to 7 days) for non-immune ≥ 12 months.
  • Zoster immunoglobulin (ZIG):
    • within 96 h (≤ 10 days if supply delayed) for high-risk susceptibles (pregnant women, neonates of peripartum cases, immunocompromised).

11. Public Health & Reporting

  • Varicella is notifiable in all Australian jurisdictions
  • notify local Public Health Unit promptly.
  • Exclude cases from school/childcare until all lesions crusted.
  • Offer completion of 2-dose schedule to household contacts.


Reactivation – Herpes Zoster


1. Epidemiology & Risk Factors

  • Lifetime risk ≈ 30 % (≈ 1 in 3); rises to ~50 % by 85 years.
  • Major risk factors:
    • Age-related immunosenescence (usually > 50 years)
    • Immunosuppression (malignancy, HIV, transplant, corticosteroids, biologics)
    • Psychological/physical stress
    • Local trauma to a dermatome

2. Pathophysiology

  • Declining VZV-specific cell-mediated immunity permits latent virus in sensory ganglia to resume lytic replication.
  • Virus travels anterograde along sensory axons, causing a dermatomal vesicular eruption.
  • In severe immunodeficiency, visceral dissemination can occur.

3. Clinical Features

  • Prodrome (1–5 days): pain, tingling, itching, or burning in the affected dermatome; may have low-grade fever.
  • Rash: unilateral, grouped vesicles on erythematous base localized to one or adjacent dermatomes (thoracic and trigeminal most common).
  • Pain: often severe, can precede rash by days.

4. Complications

ComplicationKey FeaturesAt-Risk Groups
Post-herpetic neuralgia (PHN)Persistent neuropathic pain > 90 days after rash onset; can last months to yearsOlder age, severe acute pain, rash extent
Ophthalmic zosterInvolvement of V1 distribution; keratitis, uveitis, optic neuritis, acute retinal necrosisImmunocompromise, older adults
Ramsay Hunt syndromeGeniculate ganglion involvement; vesicles in ear canal, facial palsy, hearing lossAny age with VZV reactivation in geniculate
NeurologicalMeningo-encephalitis, myelitis, cranial or peripheral motor neuropathiesImmunocompromised, older adults
VZV vasculopathyStroke, transient ischemic attacksHIV, haematological malignancy
Disseminated zoster> 20 lesions outside primary dermatome; visceral involvement (pneumonitis, hepatitis)Severe immunosuppression
Secondary bacterial infectionSuperinfection of lesions (GAS, S. aureus)Atopic dermatitis, NSAID use, immunosuppression

5. Diagnosis

  • Clinical: characteristic dermatomal distribution, acute pain.
  • Laboratory (if atypical/severe): PCR of vesicular fluid or crusts; VZV IgM serology.

6. Management

6.1 Antiviral Therapy

  • Initiate within 72 hours of rash onset to reduce acute pain, lesion duration, and PHN risk.
  • First-line agents (oral):
    • Valaciclovir 1 g TDS for 7 days
    • Famciclovir 500 mg TDS for 7 days
    • Aciclovir 800 mg five times daily for 7–10 days
  • IV aciclovir 10 mg/kg Q8 h for disseminated zoster, severe ophthalmic involvement, neurological complications, or in immunocompromised patients.

6.2 Analgesia & Symptom Control

  • Acute pain:
    • Simple analgesics (paracetamol, NSAIDs unless contraindicated)
    • Opioids for severe pain
  • Neuropathic pain:
    • Gabapentin or pregabalin
    • Tricyclic antidepressants (e.g., amitriptyline)
    • Topical lidocaine patches or capsaicin cream

6.3 Adjunctive Therapies

  • Corticosteroids: limited evidence; may be considered in immunocompetent patients to reduce acute pain and improve quality of life, but do not prevent PHN.
  • Ophthalmic involvement: urgent ophthalmology referral; combine antiviral with topical steroids/antibiotics per specialist guidance.

7. Prevention

  • Herpes Zoster Vaccination (recommended by ATAGI):
    • Zostavax (live attenuated) for 50–59 years (once only)
    • Shingrix (recombinant subunit) for ≥ 50 years, two doses 2–6 months apart (preferred for immunocompetent adults)
  • Post-exposure prophylaxis:
    • Varicella vaccination if no prior immunity and exposure to disseminated zoster

Clinical Tip: Early recognition and prompt antiviral therapy are key to reducing acute morbidity and the risk/severity of post-herpetic neuralgia. Ensure high-risk patients (elderly, immunosuppressed) are vaccinated according to current recommendations.


Vaccine “Breakthrough” Infections

No vaccine is 100 % effective. A small proportion of fully vaccinated individuals can still develop disease if exposed—so-called “breakthrough” infections.

1. Varicella (Chickenpox)

  • One-dose effectiveness:
    • ~ 80–85 % against any varicella
    • ~ 95–98 % against severe disease (> 500 lesions)
  • Breakthrough varicella: Occurs in ≈ 15–20 % after a single dose.
    • Clinical pattern: Usually mild (most have < 50 lesions, low or no fever).
    • Contagiousness: Still transmissible to others.
  • Two-dose schedule: Significantly reduces breakthrough risk; recommended at ≥ 4 weeks after first dose for children < 14 years
    • While ATAGI advises two doses for optimal protection, the government currently funds one dose at 18 months based on cost-effectiveness and programmatic considerations
      • MMRV – Priorix Tetra – $80
      • MMR – Priorix – $30

Implication: A vaccinated child can still develop chickenpox if exposed, but the illness is typically milder and less likely to require hospitalisation.

2. Measles

  • One-dose effectiveness: ≈ 96 % in Australia
  • Two-dose effectiveness: ≈ 99 % in Australia; one Cochrane review reports 95 % for a single dose and near-complete protection after two doses
  • Breakthrough measles: Very rare after two doses; most “cases” in vaccinated individuals occur with only one dose or waning immunity in adults.

Implication: Two doses confer near-complete protection; measles in a fully two-dose vaccinated person is extremely uncommon.

3. Mumps

  • One-dose effectiveness: 60–90 % (varies by strain; Jeryl Lynn strain ≈ 69–81 %)
  • Two-dose effectiveness: Up to ~ 95–100 % in immunogenicity studies; real-world effectiveness ≈ 86 % (range 32–95 %)
  • Breakthrough mumps: More common than measles or rubella; outbreaks in highly vaccinated populations have occurred, particularly among young adults.

Implication: Even with two doses, a small percentage remain susceptible; mumps can still spread in close-contact settings, though disease tends to be milder in vaccinated individuals.

4. Rubella

  • One-dose effectiveness: ≈ 94.5–97 % against clinical rubella
  • Two-dose schedule: Ensures herd immunity and prevents congenital rubella; breakthrough rubella is very rare.
  • Breakthrough rubella: Uncommon in well-vaccinated populations; most vaccinated non-immune individuals are identified via serology before pregnancy.

Implication: Single-dose rubella vaccination protects the vast majority; two doses are recommended for women of childbearing age to maximise protection.

Key Take-Home Points

  1. Breakthrough disease is usually milder than in unvaccinated individuals.
  2. Two-dose schedules (for varicella and MMR) significantly enhance protection and are routinely recommended.
  3. Ongoing surveillance and high coverage (≥ 95 %) are critical to minimise circulation and protect vulnerable groups (e.g., infants too young to be vaccinated, immunocompromised people, and pregnant women).

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