Summary / Overview
- Highly contagious primary VZV infection affecting children worldwide.
- Secondary attack rate in households > 85–90%.
- More severe in adolescents, adults, pregnant women, and immunocompromised persons.
- High-dose steroid therapy significantly increases risk of severe varicella.
- Cell-mediated immunodeficiency is the strongest predictor of life-threatening disease.
- Pregnancy—especially late gestation—predisposes to severe maternal pneumonia and neonatal varicella.
- Cell-mediated immune defects are far more critical than humoral defects.
Etiology
- Caused by Varicella-Zoster Virus (VZV), a human herpesvirus (HHV-3).
- Primary infection produces varicella; reactivation causes herpes zoster.
- Humans are the only known reservoir.
- There is no animal host or environmental persistence due to the virus’s fragile lipid envelope.
- Transmission occurs through:
- • Airborne droplets from respiratory secretions
- • Aerosolization from vesicular skin lesions
- • Direct contact with vesicle fluid
- VZV is highly infectious — household secondary attack rates exceed 85%.
Pathogenesis
- Initial replication occurs in the nasopharynx and regional lymph nodes.
- Primary viremia leads to infection of the reticuloendothelial system.
- Secondary viremia produces the classic diffuse vesicular rash.
- VZV demonstrates strong tropism to skin, T cells, and sensory ganglia.
Symptoms
- Prodrome: fever, malaise, headache, anorexia (more common in adults).
- Pruritic rash beginning on trunk → face → extremities (“centripetal distribution”).
- Crops of lesions appearing over 2–4 days.
- Tiredness and mild upper-respiratory symptoms in prodrome.
Signs
- “Dew drop on a rose petal” vesicles—clear vesicle on erythematous base.
- Lesions in multiple stages simultaneously: papules, vesicles, pustules, crusts.
- Centripetal rash: most dense on trunk, fewer on extremities.
- Oral, conjunctival, and genital mucosal lesions may occur.
Clinical Features
- Successive crops of lesions over 3–5 days.
- Pruritic vesicular exanthem with synchronous systemic symptoms.
- More severe disease in adults than children.
- Vesicles evolve to crusts within 24–48 hours.
Investigations
- Diagnosis usually clinical; lab testing only for atypical or severe cases.
- PCR from vesicle fluid is the gold standard.
- Serology (IgM/IgG) useful in pregnancy or immunocompromised assessment.
- CBC may show mild leukopenia; LFTs usually normal.
Differential Diagnosis
- Herpes zoster (shingles) — unilateral dermatomal vesicles, not generalized.
- Hand-foot-mouth disease — oral ulcers + vesicles on palms/soles (Coxsackie virus).
- Impetigo — honey-colored crusts; bacterial (Staph/Strep).
- Disseminated herpes simplex — punched-out lesions, severe in immunocompromised.
- Drug rash (Stevens–Johnson/TEN) — painful purpuric lesions, mucosal involvement.
Complications
- Bacterial superinfection of skin — most common (Staph/Strep).
- Varicella pneumonia — severe in adults, pregnant women, smokers.
- Cerebellitis / ataxia — common neurological complication.
- Encephalitis — rare but life-threatening.
- Hepatitis, pancreatitis — in immunocompromised patients.
- High-dose steroid therapy (1–2 mg/kg/day prednisolone for ≥2 weeks) markedly increases severity risk.
- Even short courses of high-dose steroids during incubation can produce severe or fatal varicella.
- Cellular immunodeficiency (HIV, cancer chemotherapy, congenital/acquired T-cell defects) strongly predisposes to severe disease.
- Pregnant women have higher risk of pneumonia and disseminated varicella.
- Maternal varicella with viremia can cause neonatal varicella via transplacental transmission.
Treatment
- Acyclovir is indicated for adults, adolescents, and high-risk groups.
- Best given within 24 hours of rash onset.
- Supportive care: antihistamines, antipyretics (avoid aspirin).
- Hospitalize severe cases, immunocompromised, pregnant women with complications.
Prevention
- Varicella vaccine (live attenuated) — highly effective.
- Two-dose schedule is recommended for full protection.
- Post-exposure prophylaxis with vaccine within 3–5 days.
- Varicella-zoster immune globulin (VZIG) for high-risk non-immune contacts.
Serotypes / Subtypes
- Varicella-zoster virus (VZV) has no serotypes — only one serotype.
- VZV has multiple genetic clades (genotypes), not clinically distinct.
- All clades cause identical clinical disease and are cross-protective.
Pathology
- Intraepidermal vesicles with ballooning degeneration of keratinocytes.
- Multinucleated giant cells with intranuclear inclusions (Cowdry type A).
- Early lesions show neutrophils; late lesions show mononuclear infiltrates.
Radiology / Imaging
- Chest X-ray: diffuse interstitial infiltrates in varicella pneumonia.
- CT chest: ground-glass opacities, nodular infiltrates.
- Neuroimaging usually normal unless encephalitis or vasculopathy.
Notes / Teaching points
- “Dew drop on rose petal” is the classical description of vesicles.
- Presence of lesions in multiple stages at once differentiates varicella from smallpox.
- Contagious from 1–2 days before rash until crusting.
- Adults have more severe disease than children.
Successive crops of lesions over 3–5 days.
Pruritic vesicular exanthem with synchronous systemic symptoms.
More severe disease in adults than children.
Vesicles evolve to crusts within 24–48 hours.
Fever subsides when crusting begins.
Rash heals without scarring unless complicated by secondary bacterial infection.
Bacterial superinfection of skin — most common (Staph/Strep).
Varicella pneumonia — severe in adults, pregnant women, smokers.
Cerebellitis / ataxia — common neurological complication.
Encephalitis — rare but life-threatening.
Hepatitis, pancreatitis — in immunocompromised patients.
Secondary bacterial infection may progress to cellulitis, necrotizing fasciitis.
Pneumonia presents with dyspnea, cough, hypoxia, diffuse infiltrates.
Neurological: acute cerebellar ataxia (most common), meningoencephalitis, stroke (VZV vasculopathy).
Hematologic: thrombocytopenia, hemorrhagic varicella, DIC.
Pregnancy: congenital varicella syndrome if infection at 8–20 weeks.
Neonatal varicella if maternal infection 5 days before to 2 days after delivery.
High-dose steroid therapy (1–2 mg/kg/day prednisolone for ≥2 weeks) markedly increases severity risk.
Even short courses of high-dose steroids during incubation can produce severe or fatal varicella.
Cellular immunodeficiency (HIV, cancer chemotherapy, congenital/acquired T-cell defects) strongly predisposes to severe disease.
Pregnant women have higher risk of pneumonia and disseminated varicella.
Maternal varicella with viremia can cause neonatal varicella via transplacental transmission.
Infants born 5 days before to 2 days after maternal rash onset are at highest risk of severe neonatal varicella.
Neonates <28 weeks gestation are particularly vulnerable due to absent transplacental IgG transfer.
Herpes zoster (shingles) — unilateral dermatomal vesicles, not generalized.
Hand-foot-mouth disease — oral ulcers + vesicles on palms/soles (Coxsackie virus).
Impetigo — honey-colored crusts; bacterial (Staph/Strep).
Disseminated herpes simplex — punched-out lesions, severe in immunocompromised.
Drug rash (Stevens–Johnson/TEN) — painful purpuric lesions, mucosal involvement.
Eczema herpeticum — vesicles over eczematous skin; HSV infection.
Rickettsial infections — maculopapular rash, systemic toxicity.
Insect bites — papular urticaria, not true vesicles.
Smallpox (eradicated) — lesions in same stage, deep and firm.
Caused by Varicella-Zoster Virus (VZV), a human herpesvirus (HHV-3).
Primary infection produces varicella; reactivation causes herpes zoster.
Varicella is caused by the Varicella-Zoster Virus, a double-stranded DNA virus belonging to the Herpesviridae family. It has a lipid envelope and replicates initially in the respiratory mucosa before disseminating via viremia.
Humans are the only known reservoir.
There is no animal host or environmental persistence due to the virus’s fragile lipid envelope.
Transmission occurs through:
• Airborne droplets from respiratory secretions
• Aerosolization from vesicular skin lesions
• Direct contact with vesicle fluid
VZV is highly infectious — household secondary attack rates exceed 85%.
Individuals are contagious from 1–2 days before rash onset until all lesions crust.
Reactivation of latent virus in sensory ganglia leads to herpes zoster (shingles), but this is not part of the etiology of primary varicella — only a consequence of initial infection and latency.
Diagnosis usually clinical; lab testing only for atypical or severe cases.
PCR from vesicle fluid is the gold standard.
Serology (IgM/IgG) useful in pregnancy or immunocompromised assessment.
CBC may show mild leukopenia; LFTs usually normal.
PCR of vesicle fluid or throat swab is highly sensitive and specific.
Serology helps differentiate primary infection from past immunity.
“Dew drop on rose petal” is the classical description of vesicles.
Presence of lesions in multiple stages at once differentiates varicella from smallpox.
Contagious from 1–2 days before rash until crusting.
Adults have more severe disease than children.
Primary VZV infection = Varicella.
Reactivation decades later = Herpes zoster (shingles).
Vaccine escape (breakthrough varicella) is usually mild and <50 lesions.
Fetal varicella syndrome includes limb hypoplasia, microcephaly, and eye defects.
References
PDF
NHL- Genotypes
Dr Ssnksrsn • 2025-11-17 09:50:09
Initial replication occurs in the nasopharynx and regional lymph nodes.
Primary viremia leads to infection of the reticuloendothelial system.
Secondary viremia produces the classic diffuse vesicular rash.
VZV demonstrates strong tropism to skin, T cells, and sensory ganglia.
Transmission occurs by inhalation of aerosolized virus or direct contact with vesicular fluid.
After local replication, virus spreads via lymphatics → primary viremia → seeding in spleen, liver, and mononuclear cells.
Secondary viremia (around day 10–12) disseminates virus to the skin → successive crops of vesicles.
The virus reaches sensory ganglia where it establishes lifelong latency.
Intraepidermal vesicles with ballooning degeneration of keratinocytes.
Multinucleated giant cells with intranuclear inclusions (Cowdry type A).
Early lesions show neutrophils; late lesions show mononuclear infiltrates.
Skin biopsy shows acantholysis, necrosis of keratinocytes, and vesicle formation within epidermis.
Dermal inflammation mild.
Electron microscopy: herpesvirus particles in nuclei and cytoplasm.
Varicella vaccine (live attenuated) — highly effective.
Two-dose schedule is recommended for full protection.
Post-exposure prophylaxis with vaccine within 3–5 days.
Varicella-zoster immune globulin (VZIG) for high-risk non-immune contacts.
1st dose: age 12–15 months
2nd dose: age 4–6 years
Immunity is long-lasting; breakthrough infections are mild.
VZIG indicated for pregnant women, immunocompromised, newborns exposed at delivery.
Infected individuals remain contagious until all lesions are crusted.
Chest X-ray: diffuse interstitial infiltrates in varicella pneumonia.
CT chest: ground-glass opacities, nodular infiltrates.
Neuroimaging usually normal unless encephalitis or vasculopathy.
Varicella pneumonia more common in adults; early imaging may show patchy or diffuse infiltrates.
MRI brain may show lesions in cerebellum or temporal lobes in encephalitis.
Varicella-zoster virus (VZV) has no serotypes — only one serotype.
VZV has multiple genetic clades (genotypes), not clinically distinct.
All clades cause identical clinical disease and are cross-protective.
Recognized VZV clades (per whole-genome sequencing):
– Clade 1
– Clade 2
– Clade 3
– Clade 4
– Clade 5
– Clade VI (proposed)
– Clade VII (proposed)
Clade distribution:
• Clade 1 & 3 – Europe, Americas
• Clade 2 – East Asia
• Clade 4 – Indian subcontinent
• Clade 5 – Africa
Vaccine strains:
• Oka strain (Japan) – belongs to Clade 2.
• All vaccine strains produce immunity against all wild VZV clades.
No genotype is linked to increased virulence, severity, or complications.
“Dew drop on a rose petal” vesicles—clear vesicle on erythematous base.
Lesions in multiple stages simultaneously: papules, vesicles, pustules, crusts.
Centripetal rash: most dense on trunk, fewer on extremities.
Oral, conjunctival, and genital mucosal lesions may occur.
Cervical and post-auricular lymphadenopathy is common.
Mucosal erosions may cause pain.
Highly contagious primary VZV infection affecting children worldwide.
Secondary attack rate in households > 85–90%.
More severe in adolescents, adults, pregnant women, and immunocompromised persons.
Varicella (chickenpox) is an acute, highly contagious viral infection caused by the Varicella-Zoster Virus (VZV), a human herpesvirus (HHV-3). It predominantly affects children aged 2–10 years, though unvaccinated adolescents and adults experience more severe disease.
Transmission occurs via airborne droplets, aerosolization from skin lesions, and direct contact. The incubation period is 10–21 days (average 14–16). Patients are infectious from 1–2 days before rash onset until all lesions crust over.
Epidemiologically, varicella shows seasonal peaks in late winter and early spring. Before universal vaccination programs (where available), annual incidence exceeded 90% by adolescence. Herd immunity and vaccination have significantly reduced morbidity in many countries; however, the disease remains common in low- and middle-income regions.
Clinically, the hallmark is a generalized pruritic vesicular rash appearing in successive crops (“pleomorphic rash”), often accompanied by fever, malaise, and anorexia. Breakthrough varicella (in partially immune individuals) is typically milder.
Although usually self-limiting, varicella can cause complications such as secondary bacterial infections, pneumonia, hepatitis, cerebellar ataxia, and rarely encephalitis. Maternal infection in pregnancy carries risks for congenital varicella syndrome or severe neonatal varicella.
Following primary infection, VZV establishes latency in sensory dorsal root ganglia and may reactivate years later to cause Herpes Zoster (shingles), especially in older adults or immunosuppressed hosts.
Long-lasting immunity follows natural infection; reinfection is uncommon. Vaccination provides strong protection and reduces disease severity and complications.
Risk Factor
High-dose steroid therapy significantly increases risk of severe varicella.
Cell-mediated immunodeficiency is the strongest predictor of life-threatening disease.
Pregnancy—especially late gestation—predisposes to severe maternal pneumonia and neonatal varicella.
Severe varicella in adolescents and adults is associated with the following:
• **Systemic corticosteroid therapy**
- Doses equivalent to **1–2 mg/kg/day prednisolone for ≥2 weeks** markedly increase risk.
- Even **short high-dose courses** during the incubation period can precipitate severe or fatal disease.[5]
• **Immunocompromised states**
- Hematologic malignancies
- Antineoplastic chemotherapy
- HIV infection
- Congenital or acquired cellular immunodeficiency
Cell-mediated immune defects are far more critical than humoral defects.
• **Pregnancy**
- Increased risk of **severe varicella pneumonia** in pregnant individuals.
- Maternal viremia enables **transplacental transmission** to the fetus.
- **Neonatal varicella** is most severe if maternal rash occurs **5 days before to 2 days after delivery**, due to inadequate maternal antibody transfer.[6]
• **Neonates**
- Infants in the **first month of life**, especially if the mother is seronegative.
- Preterm infants < **28 weeks gestation**, as transplacental IgG transfer occurs mainly after this period.
References
PDF
StatPearls
2025-11-17 07:00:41
Prodrome: fever, malaise, headache, anorexia (more common in adults).
Pruritic rash beginning on trunk → face → extremities (“centripetal distribution”).
Crops of lesions appearing over 2–4 days.
Tiredness and mild upper-respiratory symptoms in prodrome.
Fever ranges from 38–39.5°C.
Children often have minimal prodrome; adults have stronger systemic symptoms.
Itching can be intense.
New lesions appear in waves, often 200–500 lesions.
Acyclovir is indicated for adults, adolescents, and high-risk groups.
Best given within 24 hours of rash onset.
Supportive care: antihistamines, antipyretics (avoid aspirin).
Hospitalize severe cases, immunocompromised, pregnant women with complications.
Children (healthy): supportive care only.
Adults/adolescents: oral acyclovir 800 mg 5× daily × 5 days.
Immunocompromised: IV acyclovir 10 mg/kg q8h.
Avoid NSAIDs like ibuprofen (associated with severe skin infections).
Maintain hydration; trim nails to prevent scratching.
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