Varicella (commonly known as chickenpox) is caused by varicella-zoster virus. It usually occurs in childhood and is characterized by a generalized pruritic vesicular rash and fever.¹

Symptoms that develop prior to the onset of rash include malaise, pruritus, anorexia, and listlessness.^1,2

Skin manifestations in varying stages of evolution consist of maculopapules, vesicles, pustules, and scabs.^1,2

At first, the lesions contain clear fluid, pustulating and scabbing over a short period of time. Rash initially appears on the trunk and face, quickly spreading to other areas of the body. Successive crops of lesions generally continue over a period of 2 to 4 days. Crusts completely fall off within 1 to 2 weeks after infection begins and can leave a slightly depressed area in the skin.^1,2

The most common mode of transmission of varicella-zoster virus is believed to be person to person from infected respiratory tract secretions containing the varicella-zoster virus that come into contact with the mucosa of the upper respiratory tract or the conjunctiva of the eye.¹ The virus is believed to replicate at the site entry in the nasopharynx and in regional lymph nodes. Varicella is usually contagious from 1 to 2 days before onset of rash until lesions have formed crusts.¹

Pathogenesis of varicella

 1. INFECTION
DAY 0 

Varicella-zoster virus infects the mucosa of the upper respiratory tract or the conjunctiva of the eye. The virus is thought to replicate in the nasopharynx and regional lymph nodes of the head and neck.^1,3,4

2. PRIMARY VIREMIA
DAY 4–6 

Infected T-cells enter the blood stream causing a primary viremia characterized by malaise, fever, and aching back/extremities. Infected T-cells then move to the viscera and sensory ganglia. On the sensory ganglia, a second round of viral replication takes place.^1,2,3,4

 3. SECONDARY VIREMIA
~DAY 14 (can range from 10–21 days) 

Varicella-zoster virus spreads to the skin by way of a secondary viremia, leading to a generalized, pruritic vesicular rash.^1,2,3,4

A varicella diagnosis can be typically based on:

Populations at increased risk of severe varicella illness and/or complications^1,9:

• Healthy adults
• Immunocompromised individuals
• Children with lymphoma, leukemia, or HIV
• Pregnant women
• Developing fetuses
• Susceptible infants and neonates

There is a risk of congenital varicella syndrome if the mother contracts varicella in the first 20 weeks of pregnancy. Infant abnormalities include low birth weight, skin scarring, hypoplasia of an extremity, localized muscular atrophy, chorioretinitis, encephalitis, brain atrophy, and death.^1,6

If the mother contracts varicella during the perinatal phase, varicella can infect the infant by transplacental viremia (intrauterine exposure), ascending infection during birth, or direct contact with infectious lesions after birth.¹⁰

Varicella during the first 12 days of life is attributed to intrauterine exposure, whereas infection after 12 days of birth is attributed to postnatal infection, given a rough 12-day incubation period in the neonate.¹⁰

Maternal disease between 20 to 6 days before delivery, or neonatal onset from 5 to 10 days post delivery has resulted in somewhat mild outcomes as infants have had a chance to acquire maternal antibodies to avoid long-term complications. However, maternal disease between 5 days before to 2 days after delivery, or neonatal onset from 5 to 10 days after delivery has resulted in fatal outcomes in 20%-23% of the cases reported.¹⁰

Premature neonates aged <28 weeks gestation at birth have a high risk of severe varicella during the first 6 weeks after birth as there appears to be no protective maternal antibodies because of reduced gestational period.¹⁰

From 1995 to 2010 in the US surveillance sites of West Philadelphia, PA and Antelope Valley, CA, there was a¹²:

~98% decline in the number of varicella cases at both surveillance sites since 1995

>85% decline in the number of varicella-related hospitalizations in 2006-2010, compared with 1995-1998