VZV-a double-stranded DNA virus in the family Herpesviridae-has a pathogenic cycle similar to that of HSV. Primary infection is transmitted by the respiratory route. The virus replicates and causes viremia, which is reflected by the diffuse and scattered skin lesions in varicella; it then establishes latency in the dorsal root ganglia and can reactivate through unknown mechanisms at a later time.
Epidemiology and Clinical Manifestations 
VZV causes two distinct entities: primary infection (varicella or chickenpox) and reactivation infection (herpes zoster or shingles). Humans are the only known reservoir for VZV.
Chickenpox
Pts present with fever, malaise, and rash characterized by maculopapules, vesicles, and scabs in various stages of evolution. The skin lesions are small, with an erythematous base of 5-10 mm, and appear in successive crops over 2-4 days. Severity varies from person to person, but older pts tend to have more severe disease.
- In immunocompetent hosts, the disease is benign and lasts 3-5 days. In contrast, immunocompromised pts have numerous slower-healing lesions (often with a hemorrhagic base) and are more likely to develop visceral complications that, if not treated, are fatal in 15% of cases.
- The incubation period ranges from 10 to 21 days but is usually 14-17 days. Pts are infectious for 48 h before onset of rash and remain infectious until all vesicles have crusted.
- The virus is highly contagious, with an attack rate of 90% among susceptible persons. Historically, children 5-9 years old accounted for half of all cases; vaccination has dramatically changed the epidemiology of infection and has caused a significant decrease in the annualized incidence of chickenpox.
- Complications of varicella include bacterial superinfection of the skin, CNS involvement, pneumonia, myocarditis, and hepatic involvement.
- Bacterial superinfection is usually caused by Streptococcus pyogenes or Staphylococcus aureus.
- CNS involvement, usually manifesting as acute cerebellar ataxia and meningeal irritation ∼21 days after the onset of rash, runs a benign course. Aseptic meningitis, encephalitis, transverse myelitis, Guillain-Barré syndrome, or Reye's syndrome (which mandates the avoidance of aspirin administration to children) can occur. There is no specific therapy other than supportive care.
- VZV pneumonia is the most serious complication and develops more frequently among adults (occurring in up to 20% of cases) than among children. The onset comes 3-5 days into illness, with tachypnea, cough, dyspnea, fever, cyanosis, pleuritic chest pain, and hemoptysis. CXR shows nodular infiltrates and interstitial pneumonitis. Resolution of pneumonitis parallels improvement of the skin rash.
Herpes Zoster (Shingles)
Herpes zoster represents a reactivation of VZV from dorsal root ganglia and usually manifests as a unilateral vesicular eruption within a dermatome, often associated with severe pain.
- Dermatomal pain may precede lesions by 48-72 h, and dermatomes T3 to L3 are most frequently involved.
- The usual duration of disease is 7-10 days, but it may take as long as 2-4 weeks for the skin to return to normal.
- With ≥1.2 million cases each year in the United States, the incidence is highest among pts ≥50 years of age.
- Pts with herpes zoster can transmit infection to seronegative individuals, with consequent chickenpox.
- Complications include zoster ophthalmicus (which can lead to blindness), Ramsay Hunt syndrome (characterized by pain and vesicles in the external auditory canal, loss of taste in the anterior two-thirds of the tongue, and ipsilateral facial palsy), and postherpetic neuralgia (pain persisting for months after resolution of cutaneous disease).
- Immunocompromised pts-particularly those with Hodgkin's disease and non-Hodgkin's lymphoma-are at greatest risk for severe zoster and progressive disease. Cutaneous dissemination occurs in 40% of these pts and increases the risk for other complications (pneumonitis, meningoencephalitis, hepatitis).
Definitive diagnosis requires isolation of VZV in culture, detection of VZV by molecular means (PCR, immunofluorescent staining of cells from the lesion base), or serology (seroconversion or a ≥4-fold rise in antibody titer between convalescent- and acute-phase serum specimens).
| TREATMENT | ||
Varicella-Zoster Virus Infections
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Three methods are used for the prevention of VZV infections.
- Active immunization: For all children and seronegative adults, two doses of a live attenuated varicella vaccine are recommended. Irrespective of serologic status, pts >50 years old should receive a vaccine with 18 times the viral content of varicella vaccine; zoster vaccine reduces the incidence of zoster and postherpetic neuralgia.
- Passive immunization:Varicella-zoster immune globulin (VZIg) can be given to VZV-susceptible hosts within 96 h (ideally 72 h) of a significant exposure if the risk of complications from varicella is high (e.g., immunocompromised pts, susceptible pregnant women, premature infants, neonates whose mothers had chickenpox onset within 5 days before or 2 days after delivery).
- Antiviral treatment: Seven days after intense exposure, antiviral prophylaxis can be given to high-risk pts who are ineligible for vaccine or for whom the 96-h window after direct contact has passed. This intervention may lessen illness severity.