Chicken pox
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I now have comprehensive information from multiple authoritative textbooks. Here is the full answer:
Chickenpox (Varicella)
What Is It?
Chickenpox is an acute, highly contagious disease caused by the varicella-zoster virus (VZV), a member of the alpha herpesvirus family. It has a DNA core enclosed in a nucleocapsid surrounded by a glycoprotein-studded envelope. The same virus causes herpes zoster (shingles) when it reactivates from latency in sensory ganglia, sometimes decades after the initial infection.
- Goldman-Cecil Medicine, p. 3611
- Park's Textbook of Preventive & Social Medicine, p. 163
Epidemiology
- Before vaccination, >95% of children in temperate climates were infected, usually before age 5.
- Globally, varicella causes ~4.2 million severe complications and ~4,200 deaths per year.
- More common in winter and spring; tropical countries tend to have later age of acquisition.
- The varicella vaccine reduced incidence by ~90% in the US within 13 years of its 1995 licensure.
- Secondary attack rate in susceptible household contacts: approximately 85% (range 61-100%).
Transmission
- Spreads by respiratory droplets, aerosols, and direct contact with vesicular fluid.
- Contagious from 1-2 days before rash onset until all lesions have crusted.
- The virus is heat labile and survives only hours in the environment - fomites play a minimal role.
- Herpes zoster is only about 20% as contagious as chickenpox; exposure to zoster in a susceptible person causes varicella, not zoster.
Incubation Period
14-16 days (range: 10-21 days).
Clinical Features
Pre-eruptive Stage (Prodrome)
- Sudden onset of mild to moderate fever, back pain, shivering, malaise.
- Lasts ~24 hours in children; up to 2-3 days in adults (who have more severe prodrome).
Eruptive Stage (Rash)
The rash is the hallmark of chickenpox with the following distinctive features:
| Feature | Detail |
|---|---|
| Distribution | Centripetal - starts on trunk (where it is most dense), spreads to face, then limbs; mucosal surfaces often involved; palms and soles usually spared |
| Evolution | Rapid progression: macule → papule → vesicle → scab (all stages may be present simultaneously - "dew drops on a rose petal") |
| Crops | New crops appear over 3-5 days - multiple stages visible at once |
| Lesion character | Thin-walled vesicles on a reddish base, superficial and fragile |
| Duration | Crusting complete in 7-10 days |
In healthy children, the illness is usually self-limiting. Disease is more severe in adults, neonates, pregnant women, and immunocompromised individuals.
Complications
| Complication | Notes |
|---|---|
| Bacterial superinfection | Most common complication (skin - Staph/Strep) |
| Varicella pneumonia | Most serious complication in adults; estimated to occur in a significant proportion of adult cases |
| Encephalitis/cerebellar ataxia | CNS involvement; cerebellar ataxia more common in children |
| Thrombocytopenia | Can occur |
| DIC | Rare, rapidly fatal; more common in immunocompromised |
| Reye syndrome | Associated with aspirin use in children - avoid ASA |
| Congenital varicella syndrome | In 0.4-2% of infants born to mothers infected during first 20 weeks gestation |
| Neonatal varicella | Severe if mother develops rash 5 days before to 2 days after delivery |
Immunocompromised patients (malignancies, organ transplants, HIV, high-dose steroids) are at the highest risk for severe disseminated disease.
Diagnosis
Diagnosis is usually clinical based on the characteristic rash and exposure history. Lab confirmation is rarely needed but can be done by:
- PCR (most sensitive) - from vesicular fluid, crusts, saliva, or CSF
- Viral culture - isolation from vesicular fluid in first 3 days
- Direct immunofluorescence - rapid but less sensitive than PCR
- Serology (IgM) - considerably less sensitive than PCR, not the method of choice
- IgG antibody - used to assess immunity/susceptibility
Treatment
Healthy Children
Routine antiviral treatment is not recommended for otherwise healthy children because complications are infrequent. Supportive care: antipyretics (avoid aspirin - risk of Reye syndrome), antihistamines/calamine for pruritus, maintain good skin hygiene to prevent secondary infection.
Groups That Should Receive Antivirals
Acyclovir (and alternatives) is recommended for:
- Adolescents and adults
- Newborns whose mothers had varicella near the time of delivery
- Children with chronic pulmonary or skin disease
- Mildly immunocompromised persons
- Patients with complications of varicella
- Pregnant women with serious complications
Oral acyclovir dose: 800 mg 5 times/day for 7 days (adults); start within 24 hours of rash onset for best effect.
Alternatives: Valacyclovir 1000 mg 3x/day or famciclovir 500 mg 3x/day (more convenient dosing).
IV acyclovir: reserved for immunocompromised patients and severe disease.
Mechanism: VZV encodes a thymidine kinase that phosphorylates acyclovir, which then inhibits viral DNA polymerase.
Note: Acyclovir does not prevent post-herpetic neuralgia.
Prevention
1. Varicella Vaccine
- Live attenuated (Oka strain) - given subcutaneously
- Schedule: 2 doses recommended for all persons; first dose at 12-18 months, second dose at 4-6 years. For persons ≥13 years without immunity: 2 doses at least 4 weeks apart.
- Efficacy: 92% against any disease; >95% against severe disease.
- Contraindicated in: immunocompromised persons, pregnant women, persons with anaphylactic allergy to vaccine components.
- Post-exposure vaccination within 3 days can reduce symptomatic infection by ~two-thirds.
2. Varicella-Zoster Immunoglobulin (VZIG / VariZIG)
Given within 72-96 hours of exposure (FDA-approved up to 10 days) to high-risk susceptible individuals:
- Immunosuppressed persons
- Susceptible pregnant women
- Newborns whose mothers had chickenpox within 5 days before or 48 hours after delivery
- Premature infants
- HIV-infected individuals without immunity
Dose: 12.5 units/kg IM (max 625 units); repeat in 3 weeks if high-risk patient remains exposed.
Latency and Reactivation
After primary infection, VZV establishes latency in sensory ganglia (cranial nerve ganglia, dorsal root ganglia). With waning cell-mediated immunity (age, immunosuppression), the virus can reactivate as herpes zoster (shingles) - a painful unilateral dermatomal vesicular eruption. About 10-30% of persons who had varicella will develop zoster in their lifetime; risk rises sharply after age 50.
Sources: Goldman-Cecil Medicine (p. 3610-3613) | Park's Textbook of Preventive & Social Medicine (p. 163-165) | Fitzpatrick's Dermatology | Andrews' Diseases of the Skin | Rosen's Emergency Medicine
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