Varicella-zoster virus (VZV) is a double-stranded DNA herpesvirus acquired predominately during childhood, and 90 percent of adults have serological evidence of immunity (Whitley, 2015). The incidence of adult varicella declined by 82 percent after the introduction of varicella vaccination, and this has resulted in a drop in maternal and fetal varicella rates (American College of Obstetricians and Gynecologists, 2017). In the United States between 2003 and 2010, the incidence of maternal varicella among 7.7 million pregnancy admissions was 1.21 per 10,000 (Zhang, 2015).
Primary infection-varicela or chickenpox-is transmitted by direct contact with an infected individual, although respiratory transmission has been reported. The incubation period is 10 to 21 days, and a nonimmune woman has a 60-to 95-percent risk of becoming infected after exposure (Whitley, 2015). Primary varicella presents with a 1-to 2-day flulike prodrome, which is followed by pruritic vesicular lesions that crust after 3 to 7 days. Infection tends to be more severe in adults (Marin, 2007). Afected patients are then contagious from 1 day before the onset of the rash until the lesions become crusted.
Mortality is predominately due to VZV pneumonia, which is thought to be more severe during adulthood and particularly in pregnancy. Although the incidence was once thought to be higher, only 2 to 5 percent of infected pregnant women develop pneumonitis (Marin, 2007; Zhang, 2015). Risk factors for VZV pneumonia include smoking and having more than 100 cutaneous lesions. Maternal mortality rates with pneumonia have decreased to 1 to 2 percent (Chandra, 1998).
Symptoms of VZV pneumonia usually appear 3 to 5 days into the course of illness. Fever, tachypnea, dry cough, dyspnea, and pleuritic pain are characteristic. Nodular iniltrates are similar to other viral pneumonias (Chap. 51, p. 994). Although resolution of pneumonitis parallels that of skin lesions, fever and compromised pulmonary function may persist for weeks.
If primary varicella is reactivated years later, it causes herpes zoster or shingles (Whirley, 2015). This presents as a unilateral dermatomal vesicular eruption associated with severe pain. Zoster does not appear to be more frequent or severe in pregnant women. Congenital varicella syndrome rarely develops in cases of maternal herpes zoster (hn, 2016; Enders, 1994). Zoster is contagious if blisters are broken, although less so than with primary varicella.
In women with varicella during the irst half of pregnancy, the fetus may develop congenital varicella syndrome. Some features include chorioretinitis, microphthalmia, cerebral cortical atrophy, growth restriction, hydronephrosis, limb hypoplasia, and cicatricial skin lesions as shown in Figure 64-3 (Ahn, 2016; Auriti, 2009). Enders and coworkers (1994) evaluated 13 3 pregnant women with varicella. When maternal infection developed before 13 weeks, only two of 472 pregnancies-O.4 and scarring in a fetus infected during the first trimester by vari cella. (Reproduced with permission from Paryani SG, Arvin AM: