Varicella or chickenpox presents as fever, vesicular rash, itching and tiredness. It is caused by the varicella-zoster virus (VZV), also known as human herpesvirus 3 (HHV-3). It undergoes latency after primary infection and later reactivates as herpes zoster (HZ, shingles). Seroconversion in tropical countries occurs at a later age than in temperate countries making varicella common in adolescents and adults. The spectrum of varicella varies from mild in some people, to significant morbidity and some mortality in previously healthy persons. The live attenuated varicella vaccine (Oka strain) was developed by Takahashi in 1974, and it was registered in Japan in 1986. Since then monovalent varicella vaccines have been made available throughout the world for the prevention of infection in healthy children, adolescents and adults. Combination vaccines for the prevention of measles, mumps, rubella, and varicella became available in 2005.

VZV is transmitted by the airborne route or direct contact with vesicular fluid. It is highly contagious with secondary attack rates in susceptible household contacts ranging from 61-100%. VZV can also be transmitted to susceptible persons from patients with HZ.  Studies suggest that the risk of viral transmission is considerably less from HZ than from varicella.

In an immunocompetent person, malaise and fever occur 1 or 2 days before the onset of rash. Patients with varicella typically have a generalised vesicular rash concentrated on the head and trunk. The rash appears in crops; each crop usually progresses within 24 hours from macules to papules, vesicles, pustules and finally crusts. New lesions occur in crops over the next few days, with various stages of healing. The lesions are pruritic and may cause scars.  Adults with varicella have significantly higher morbidity than varicella in children.

VZV has the capacity to persist in the body after primary infection as latent infection in sensory nerve ganglia. VZV specific cell mediated immunity (CMI) plays import role in limiting reactivation of latent VZV. Decline in CMI leads to reactivation of VZV and herpes zoster.

The two-dose varicella vaccination programme has lowered the varicella incidence, outbreaks and hospitalisations, and has squashed concerns that routine childhood vaccination could lead to increase in HZ.

Varicella may be more severe in pregnant women (especially in the last trimester). Foetal morbidity is increased in maternal varicella. Varicella during pregnancy may damage the foetal central nervous system (CNS), resulting in permanent scarring of the skin, aplasia of extremities, chorioretinitis, microphthalmia, optic atrophy, cataract, Horner’s syndrome, blindness, mental retardation, foetal demise, and a high incidence of zoster and death in infancy. This constellation of problems in infants whose mothers had varicella in pregnancy is clinically diagnostic of the congenital varicella syndrome.

Maternal varicella that develops within 5 days before or 2 days after delivery, is potentially most serious for the newborn. Maternal antibodies to VZV may not have been formed or crossed the placenta and VZV may infect the baby before or after delivery. Immaturity of the infant’s cellular immunity, put the infant at risk for severe varicella. The infected infant may develop haemorrhagic skin lesions and primary varicella pneumonia. Severe varicella can usually be avoided with prophylactic administration of passive immunisation and acyclovir (ACV) therapy. Vaccination of women before pregnancy is the preferable strategy.