Varicella-zoster virus (VZV) infection in the newborn

INTRODUCTION — 

Varicella-zoster virus (VZV) is the virus responsible for varicella (chickenpox) and herpes zoster ("shingles"). VZV is a member of the herpesvirus family, along with herpes simplex virus (HSV) types 1 and 2, cytomegalovirus, Epstein-Barr virus, and human herpesvirus (HHV) -6, -7, and -8.

In healthy children, varicella usually is a mild, self-limited illness. Rates of varicella infection in infants and children have declined considerably since the introduction of routine varicella vaccination. Rarely, varicella infection in a pregnant or postpartum individual causes infection in the fetus or newborn. Nosocomial acquisition of VZV also can occur in newborns.

Varicella-zoster infection in the newborn is reviewed here. Related topics include:

●(See "Varicella-zoster virus infection in pregnancy".)

●(See "Clinical features of varicella-zoster virus infection: Chickenpox".)

●(See "Epidemiology of varicella-zoster virus infection: Chickenpox".)

●(See "Treatment of varicella (chickenpox) infection".)

●(See "Vaccination for the prevention of chickenpox (primary varicella infection)".)

EPIDEMIOLOGY — 

The incidences of maternal, fetal, and neonatal varicella infections have declined dramatically since the introduction of routine varicella vaccination in the 1990s. In the contemporary era, neonatal varicella infection is a rare occurrence. In one study conducted in the varicella vaccine era (2006 to 2009), the annual incidence of congenital varicella infection was 0.19 per 100,000 live births, and the incidence of neonatal infection was 2 per 100,000 live births [1]. These incidence rates represented a >85 percent reduction compared with rates during the prevaccination era (1995 to 1997). The epidemiology of varicella infection in pregnancy is discussed in greater detail separately. (See "Varicella-zoster virus infection in pregnancy", section on 'Epidemiology'.)

CONGENITAL INFECTION — 

If maternal varicella infection occurs early in pregnancy (ie, between 8 to 20 weeks gestation), transmission to the fetus can occur, which rarely may result in congenital varicella syndrome (CVS). However, most cases of in utero transmission are asymptomatic. In studies of pregnancies affected by maternal varicella infection at <20 weeks gestation, the overall risk of CVS in the fetus was very low (approximately 0.5 to 2 percent) [2-5]. This is considerably less than with other viruses acquired during pregnancy (eg, cytomegalovirus). CVS occurring after 20 weeks gestation has been reported, but it is very rare [6]. There have been no reported cases of CVS occurring after 28 weeks gestation. (See "Varicella-zoster virus infection in pregnancy", section on 'Transmission'.)

●Clinical features – Affected infants may have a spectrum of findings or a single isolated finding. Characteristic findings of CVS include one or more of the following [6]:

•Cicatricial (scarring) skin lesions, which may be depressed and pigmented in a dermatomal distribution (picture 1) – Present in approximately 75 percent of cases

•Central nervous system (CNS) abnormalities (eg, cortical atrophy, seizures, microcephaly, hemiparesis, other motor abnormalities) – Present in approximately 60 percent of cases

•Ocular abnormalities (eg, cataracts, chorioretinitis, Horner syndrome, microphthalmos, nystagmus, optic atrophy, anisocoria) – Present in approximately 50 percent of cases

•Musculoskeletal abnormalities (eg, limb hypoplasia, muscle hypoplasia, club foot) – Present in approximately 40 to 50 percent of cases

•Intrauterine growth restriction – Present in approximately 20 to 30 percent of cases

•Gastrointestinal abnormalities – Present in approximately 10 to 15 percent of cases

•Genitourinary abnormalities – Present in approximately 10 to 15 percent of cases

Fetal death can occur if the fetus is severely affected.

●Diagnosis – The prenatal diagnosis of congenital varicella infection can be made by performing polymerase chain reaction (PCR) testing of fetal blood or amniotic fluid for VZV DNA in conjunction with ultrasonography for detection of fetal abnormalities. This is discussed separately. (See "Varicella-zoster virus infection in pregnancy", section on 'Prenatal diagnosis'.)

Postnatally, the diagnosis of CVS can be established based upon meeting all three of the following criteria [7]:

•History of varicella in the birth parent during the first or second trimester of pregnancy

•Presence of one or more finding of CVS in the newborn (eg, cicatricial skin lesions, CNS abnormalities, eye disease, musculoskeletal abnormalities)

•Evidence of intrauterine VZV infection in the newborn (eg, positive VZV DNA PCR, detection of VZV IgM, persistence of VZV IgG beyond seven months of age, or appearance of zoster during early infancy)

●Management – The management of maternal VZV infection during pregnancy is discussed in detail separately. (See "Varicella-zoster virus infection in pregnancy", section on 'Treatment of varicella infection'.)

Although acyclovir crosses the placenta, it is unknown if maternal treatment decreases the risk of CVS.

POSTNATAL INFECTION

Viral transmission

●Vertical transmission – Neonatal infection is most likely to occur if the birthing parent has onset of primary varicella infection within two weeks of delivery. The risk of severe neonatal infection is greatest when varicella infection occurs in the birthing parent from five days before to two days after delivery [4]. This is because there is insufficient time for the development of maternal IgG and passive transfer of antibody protection to the newborn. By contrast, postnatally acquired varicella occurring between 10 and 28 days after birth usually is mild [4]. Nevertheless, newborns are still at greater risk of having severe disease compared with older infants or children because of their relative immunologic immaturity [8].

●Horizontal transmission (nosocomial infection) – Nosocomial VZV infection also can occur, particularly in preterm neonates cared for in the neonatal intensive care unit (NICU). Preterm neonates are at increased risk for nosocomial acquisition of VZV compared with infants born at term because active transfer of maternal IgG antibodies occurs primarily during the third trimester of pregnancy [9]. (See "Prevention and control of varicella-zoster virus in health care facilities", section on 'Transmission of varicella zoster virus'.)

Clinical features — The clinical features of neonatal varicella can vary, ranging from a mild illness resembling chickenpox in older children to severe disseminated infection similar to manifestations seen in immunocompromised hosts. (See "Clinical features of varicella-zoster virus infection: Chickenpox", section on 'Clinical manifestations'.)

Vesicular rash — Fever may develop within the first days after birth, followed by a generalized vesicular eruption (picture 2). The rash starts as macules and rapidly progresses to papules and then to

characteristic vesicular lesions before crusting. It usually appears first on the head and then generalizes. The lesions characteristically are in various stages of development and healing. In mild cases of neonatal varicella, the lesions heal within 7 to 10 days.

Disseminated infection — Disseminated varicella infection can rarely occur. The risk is greatest among preterm or immunocompromised newborns. The onset of disseminated infection typically follows the vesicular eruption. The most common manifestations of disseminated infection include:

●Pneumonia

●Hepatitis

●Meningoencephalitis

●Disseminated intravascular coagulopathy (DIC) and thrombocytopenia

For infants born to a birthing parent with active varicella infection at delivery, prompt administration of VZV immune globulin may reduce the risk of disseminated disease, as discussed below. (See 'Postexposure prophylaxis' below.)

Diagnosis — The diagnosis of neonatal varicella is suspected based upon the characteristic appearance of generalized vesicular skin lesions in various stages of development and healing (picture 2) in an infant born to a parent who was exposed to VZV late in pregnancy or with clinical symptoms of varicella close to the time of delivery. The diagnosis is confirmed by detection of the virus using polymerase chain reaction (PCR).

●Preferred test (PCR) – PCR is the test of choice for diagnosis of neonatal varicella because it is highly sensitive and specific. PCR can detect VZV from vesicular swabs or scrapings, scabs from crusted lesions, blood samples, cerebral spinal fluid, and/or tissue from a biopsy specimen [4]. PCR can also distinguish between wild VZV and vaccine strains. (See "Diagnosis of varicella-zoster virus infection", section on 'Polymerase chain reaction'.)

●Other methods – Other diagnostic tests that play a limited role in the diagnosis of neonatal varicella include:

•Direct fluorescent antibody (DFA) – DFA on scrapings from active vesicular skin lesions can provide a rapid diagnosis. However, DFA should not be used in lieu of PCR testing, since PCR is more sensitive. (See "Diagnosis of varicella-zoster virus infection", section on 'Direct fluorescent antibody'.)

•Serologic tests – Serologic testing can be used to establish the diagnosis. However, this approach requires acute and convalescent titers, and therefore it is not helpful for rapidly establishing the diagnosis. In neonatal varicella infection, acute and convalescent sera demonstrate a rise in VZV IgG titers. In contrast, uninfected neonates who received passive transfer of maternal antibodies during pregnancy typically have low acute VZV titers and convalescent titers remain low. VZV IgM is insensitive in newborns and false positives can occur. (See "Diagnosis of varicella-zoster virus infection", section on 'Serologic testing'.)

•Viral culture – Viral culture is not helpful in making the diagnosis, since it has a much lower sensitivity compared with PCR and the virus takes several weeks to grow. (See "Diagnosis of varicella-zoster virus infection", section on 'Viral culture'.)

•Others – Other diagnostic tests, including fluorescent antimembrane antibody (FAMA), latex agglutination (LA), enzyme-linked immunosorbent assay (ELISA), and complement-enhanced neutralization, are available but are not recommended in neonates.

Differential diagnosis — The differential diagnosis of neonatal varicella includes other conditions that present with vesicular skin lesions in the newborn period (table 1). (See "Vesicular, pustular, and bullous lesions in the newborn and infant".)

In particular, herpes simplex virus (HSV) is an important consideration in the differential diagnosis. The appearance of the skin lesions can help to distinguish VZV from HSV. In neonates with VZV infection, there is often more generalized involvement, usually with lesions in different stages of development (picture 2). By contrast, the vesicular rash seen in neonatal HSV tends to occur in localized clusters (picture 3). Ultimately, PCR testing is required to definitively distinguish between the two conditions and the threshold for testing for HSV should be low. Testing for HSV is appropriate in most cases unless the newborn’s clinical picture is clearly consistent with VZV (ie, birthing parent had confirmed VZV infection, and the neonate has characteristic findings and is not severely ill). Testing for HSV in the newborn is discussed separately. (See "Neonatal herpes simplex virus (HSV) infection: Clinical features and diagnosis", section on 'Evaluation and diagnosis'.)

Management

Management of exposure — For newborns exposed to VZV from the birthing parent or contact with another infected individual, the need for postexposure prophylaxis and/or isolation depends upon the timing of exposure, the birthing parent's serologic status, and gestational age. Varicella vaccination, which is used for prevention in older children and adults, is not used for this purpose in newborns since it has not been adequately studied. (See "Post-exposure prophylaxis against varicella-zoster virus infection", section on 'Vaccine prophylaxis for eligible patients'.)

Postexposure prophylaxis — Postexposure prophylaxis with varicella-zoster immune globulin (Varizig) can prevent or reduce the severity of varicella in exposed neonates [10]. Varizig is a purified human immune globulin preparation made from plasma containing high levels of antivaricella antibodies. (See "Post-exposure prophylaxis against varicella-zoster virus infection", section on 'Passive immunoprophylaxis'.)

●Indications – For newborns who have had a significant exposure to varicella, we recommend Varizig if they meet any of the following criteria [4,11]:

•Symptomatic varicella infection in the birthing parent near time of delivery – If the birthing parent had onset of symptomatic varicella infection (chickenpox) within five days before or two days after delivery, the newborn should receive Varizig. Varizig is not indicated if the birthing parent had zoster.

•Preterm infants 28 to <34 weeks gestation if birthing parent lacks evidence of immunity to VZV – Hospitalized preterm infants born at 28 to <34 weeks gestation who have had a significant exposure to VZV and whose birthing parent does not have documented immunization, serologic immunity, or prior documented history of varicella infection should receive Varizig.

•Preterm infants <28 weeks of gestation regardless of birthing parent's immunity – Hospitalized preterm neonates born at <28 weeks gestation who have had a significant exposure to VZV should receive Varizig regardless of the birthing parent's history of varicella or vaccination.

Healthy term neonates who are postnatally exposed to VZV outside of the immediate perinatal period (including exposure from the birthing parent at >48 hours after delivery or exposure from other family members or health care personnel) generally do not require postexposure prophylaxis. This is because postnatally acquired varicella that occurs beyond the immediate perinatal period in a term infant generally is mild. However, some experts suggest administering Varizig in this setting (for exposures occurring up to seven days after birth) if the birthing parent does not have evidence of immunity to VZV [12,13].

Our suggested approach is consistent with guidelines of the American Academy of Pediatrics (AAP), Centers for Disease Control and Prevention (CDC), and the Advisory Committee on Immunization Practices (ACIP) [4,11]. Links to these and other guidelines are provided separately. (See 'Society guideline links' below.)

●Dosing and administration – Weight-based dosing for Varizig is as follows [4]:

•Infants weighing ≤2 kg: 62.5 units (0.5 vial) given intramuscularly (IM)

•Infants weighing >2 kg to 10 kg: 125 units (1 vial) given IMor  

Each vial of Varizig contains lyophilized powder, which must be reconstituted for IM injection.

If Varizig is unavailable, intravenous immune globulin (IVIG) or prophylaxis with acyclovir can be considered [4].

●Timing – When postexposure prophylaxis is indicated, it should be given as soon as possible. The window of passive immunization with Varizig after varicella exposure is up to 10 days [14]. (See "Post-exposure prophylaxis against varicella-zoster virus infection", section on 'Passive immunoprophylaxis'.)

●Efficacy – There are no placebo-controlled clinical trials evaluating the efficacy of Varizig in neonates. Its efficacy is inferred from observational data demonstrating considerably lower transmission rates and milder disease course than would be expected based upon historical data. The supporting evidence is discussed in greater detail separately. (See "Post-exposure prophylaxis against varicella-zoster virus infection", section on 'Target groups'.)

Isolation — During the birth hospitalization, the need for isolation for the birthing parent and infant depends upon the timing of exposure and whether there are signs of active disease.

Hospitalized patients with primary varicella should be placed on standard, contact, and airborne precautions to prevent the spread of infection to others. A detailed discussion on infection control precautions for patients with primary varicella is found elsewhere. (See "Prevention and control of varicella-zoster virus in health care facilities", section on 'Isolation precautions for patients with varicella'.)

Patients who require isolation include:

●Active disease in the birthing parent or newborn – If the birthing parent has active VZV lesions, the birthing parent and the newborn should be isolated separately until the parent's vesicles have dried, even if the newborn received Varizig. (See 'Postexposure prophylaxis' above.)

Infants who develop signs of varicella while in the nursery or neonatal intensive care unit (NICU) are also isolated.

●Maternal exposure 6 to 21 days before hospitalization – If the birthing parent is seronegative and was exposed to VZV 6 to 21 days before hospital admission, the parent should be isolated from other patients because varicella may develop during the hospitalization. The infant, if born at term, should be isolated with the birthing parent. The parent and infant should be cared for only by staff with immunity to VZV. Both should be discharged as soon as possible.

This recommendation is based on the incubation period of varicella, which is usually 14 to 16 days but can be as long as 21 days after exposure [4]. The incubation may be prolonged for as long as 28 days after receipt of Varizig or IVIG, and it may be shortened in immunocompromised patients.

●Exposed infants in the NICU – Exposed infants in the NICU usually are cohorted and isolated from newly admitted patients until 21 days after the exposure (or 28 days if the neonate received Varizig).

Patients who generally do not require isolation include:

●Active disease in the birthing parent that resolved before delivery – A birthing parent who had active varicella within 21 days of delivery that resolved before hospitalization does not need to be isolated. However, the newborn should stay in the birthing parent's room and be isolated from other newborns. The newborn should have passively acquired maternal antibody and therefore does not need to receive passive immunoprophylaxis.

●Maternal exposure within six days of hospitalization – If a seronegative birthing parent was exposed within six days of admission and is discharged before 48 hours, isolation is not needed, because varicella would not be expected to develop during the hospital stay.

●Newborns who are exposed while in the nursery – If an infant in the newborn nursery is exposed to a visitor or hospital worker who is infectious, it is not necessary to isolate the newborn since in most cases, they would be discharged before they would be infectious. Isolation may be required for the rare exposed infant who remains hospitalized longer than eight days and whose birthing parent is seronegative. (See "Prevention and control of varicella-zoster virus in health care facilities".)

Treatment of confirmed VZV infection — For neonates with confirmed VZV infection, the need for antiviral therapy is determined by the severity of illness, gestational age, timing of exposure, and the serostatus of the neonate and birthing parent. If the neonate acquired the infection from a nonmaternal contact (eg, a healthcare worker), we suggest measuring the VZV IgG titer in either the neonate or the birthing parent to determine the serostatus (when measuring the infant's titer, testing should be performed before administering Varizig). Infants without detectable maternal VZV antibody are at increased risk of developing severe infection [12].

●Disseminated infection or high-risk newborn – For neonates with varicella infection that is severe or high-risk, we recommend intravenous (IV) acyclovir therapy. This includes the following patients:

•Newborns with disseminated varicella infection (eg, pneumonia, meningoencephalitis, hepatitis, DIC)

•Preterm neonates with varicella of any severity

•Neonates with immunodeficiency with varicella of any severity

•Newborns who acquired the infection from the birthing parent if the parent had onset of primary varicella infection (chickenpox) within five days before to two days after delivery

•Newborns who acquired the infection within first few days after birth from a nonmaternal source (eg, a healthcare worker) if the infant does not have detectable maternal VZV IgG

Acyclovir is given IV at a dose of 30 mg/kg per day in three divided doses for 7 to 10 days [4,15,16]. These neonates should also receive Varizig, if eligible. (See 'Postexposure prophylaxis' above.)

Antiviral treatment must be started as soon as possible after the onset of symptoms because most viral replication has stopped by 72 hours after appearance of the rash. Evidence supporting use of acyclovir in neonatal varicella is limited to case reports and case series [17,18]. Indirect evidence is provided from the experience in treating varicella in immunocompromised children and adults. (See "Treatment of varicella (chickenpox) infection", section on 'Immunocompromised hosts'.)

Like immunocompromised patients, neonates with disseminated varicella are at high risk of morbidity and mortality. (See 'Outcome' below.)

●Uncomplicated low-risk infection – For immunocompetent term infants exposed to varicella outside of the immediate perinatal period who develop mild signs of infection (ie, vesicular rash without other organ involvement) and without other risk factors for severe infection (listed above), varicella is generally a self-limited illness that resolves within 7 to 10 days. Supportive care alone is sufficient for mildly affected low-risk neonates, and antiviral therapy is not necessary unless the infant develops signs of worsening infection or dissemination.

Some experts suggest administering Varizig to healthy neonates with varicella infection within seven days after birth if the birthing parent does not have evidence of immunity to VZV [13]. Other experts suggest administering both Varizig and acyclovir in this scenario if the birthing parent had onset of primary varicella infection within seven days before to seven days after delivery [12].

Breastfeeding — Breastfeeding is encouraged in newborns exposed to or infected with VZV because antibody in breast milk may be protective [19]. Whether VZV is secreted in human milk is uncertain, although VZV DNA has been detected [20].

Outcome — In the postvaccine era, mortality due to neonatal varicella is exceedingly rare, with fewer than five fatal cases reported in infants <1 year in the United States from 2012 through 2021 [21].

Outcomes for neonates with confirmed varicella infection depend on the severity of infection, timing of exposure, status of the birthing parent's immunity to VZV, and the neonate's gestational age.

●Severe disseminated infection – The risk of severe disseminated infection is greatest among infants who acquired the infection from a birthing parent who developed primary varicella between five days before to two days after delivery [4]. Among neonates with severe disseminated infection, the risk of serious morbidity or mortality can be as high as 20 percent [22,23]. The risk is particularly high in preterm neonates.

●Nonsevere varicella - In most otherwise healthy term neonates who develop varicella, it is a self-limited illness that resolves within 7 to 10 days without long-term sequalae.

For all neonates with varicella infection, regardless of severity, there is a risk of developing reactivation of the virus (ie, zoster) later in infancy or early childhood.

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Varicella-zoster virus".)

SUMMARY AND RECOMMENDATIONS

●Congenital varicella syndrome (CVS) – CVS is a rare congenital infection that can develop as a consequence of maternal varicella infection during the first or second trimester of pregnancy. The most common clinical findings of CVS include:

•Cicatricial (scarring) skin lesions (picture 1)

•Central nervous system abnormalities (eg, cortical atrophy, seizures, microcephaly, hemiparesis)

•Ocular abnormalities (eg, cataracts, chorioretinitis, Horner syndrome, microphthalmos, nystagmus, optic atrophy, anisocoria)

•Musculoskeletal abnormalities (eg, limb hypoplasia, muscle hypoplasia, club foot)

•Intrauterine growth restriction

The prenatal diagnosis of CVS can be made by performing polymerase chain reaction (PCR) testing of fetal blood or amniotic fluid for VZV DNA in conjunction with ultrasonography for detection of fetal abnormalities. (See 'Congenital infection' above and "Varicella-zoster virus infection in pregnancy", section on 'Congenital varicella syndrome'.)

●Postnatal infection – Neonatal varicella results from perinatal or postnatal transmission of varicella-zoster virus (VZV). (See 'Postnatal infection' above.)

•Transmission – VZV infection in the newborn occurs due to either vertical transmission from the birthing parent or horizontal transmission from the environment or infected care providers. (See 'Viral transmission' above.)

•Clinical features – The clinical features of neonatal varicella can vary, ranging from a mild illness resembling chickenpox in older children to severe disseminated infection. The rash starts as macules and rapidly progresses to papules and then to characteristic vesicular lesions before crusting (picture 2). It usually appears first on the head and then generalizes. The lesions characteristically are in various stages of development and healing. (See 'Vesicular rash' above.)

Disseminated varicella infection can rarely occur. The risk is greatest among preterm or immunocompromised newborns. The onset of disseminated infection typically follows the vesicular eruption. The most common manifestations of disseminated infection include pneumonia, hepatitis, meningoencephalitis, and disseminated intravascular coagulopathy. (See 'Disseminated infection' above.)

•Diagnosis – The diagnosis of neonatal varicella is suspected based upon the characteristic appearance of generalized vesicular skin lesions in various stages of development and healing (picture 2) in an infant born to a parent who was exposed to VZV late in pregnancy or with clinical symptoms of varicella close to the time of delivery. The diagnosis is confirmed by detection of the virus with PCR. (See 'Diagnosis' above.)

•Differential diagnosis – The differential diagnosis of neonatal varicella includes other conditions that present with vesicular skin lesions in the newborn period (table 1). In particular, herpes simplex virus (HSV) is an important consideration in the differential diagnosis. Testing for HSV is appropriate in most cases unless the newborn's clinical picture is clearly consistent with VZV (ie, birthing parent had confirmed VZV infection, and the neonate has characteristic findings and is not severely ill). (See 'Differential diagnosis' above and "Vesicular, pustular, and bullous lesions in the newborn and infant" and "Neonatal herpes simplex virus (HSV) infection: Clinical features and diagnosis", section on 'Evaluation and diagnosis'.)

●Postexposure prophylaxis – For neonates with significant exposure to VZV plus one of the following circumstances, we suggest postexposure prophylaxis with varicella-zoster immune globulin (Varizig) (Grade 2C) (see 'Postexposure prophylaxis' above and "Post-exposure prophylaxis against varicella-zoster virus infection", section on 'Target groups'):

•Newborns whose birthing parent had onset of symptomatic varicella infection (chickenpox) within five days before or two days after delivery. Varizig is not indicated if the birthing parent had zoster.

•Hospitalized preterm infants born at 28 to <34 weeks gestation who have had a significant exposure to VZV and whose birthing parent does not have documented immunization, serologic immunity, or prior documented history of varicella infection.

•Any hospitalized preterm neonate born at <28 weeks gestation who had a significant exposure to VZV regardless of the birthing parent's history of varicella or vaccination.

●Isolation – During the birth hospitalization, the need for isolation for the birthing parent and infant depends upon the timing of exposure and whether there are signs of active disease. (See 'Isolation' above and "Prevention and control of varicella-zoster virus in health care facilities", section on 'Isolation precautions for patients with varicella'.)

●Treatment of confirmed infection

•Disseminated or high-risk infection – For newborns with severe or disseminated varicella infection (eg, pneumonia, encephalitis, hepatitis, DIC) and those with less severe manifestations who are at risk for dissemination (ie, preterm neonates, infants with immunodeficiency), we recommend treatment with acyclovir (Grade 1B). Acyclovir is given intravenously at a dose of 30 mg/kg per day in three divided doses for 7 to 10 days. (See 'Treatment of confirmed VZV infection' above.)

•Uncomplicated low-risk infection – For immunocompetent term infants exposed to varicella outside of the immediate perinatal period who develop mild signs of infection (ie, vesicular rash without other organ involvement), varicella is generally a self-limited illness that resolves within 7 to 10 days. Supportive care alone is sufficient for mildly affected neonates, and antiviral therapy is not necessary unless the infant develops signs of worsening infection or dissemination. However, some experts suggest administering Varizig to healthy neonates with varicella infection within two weeks after birth if the birthing parent does not have evidence of immunity to VZV. Other experts suggest administering both Varizig and acyclovir in this scenario if the birthing parent had onset of primary varicella infection within seven days before to seven days after delivery. (See 'Treatment of confirmed VZV infection' above and 'Postexposure prophylaxis' above.)

●Outcome – Outcomes for neonates with varicella infection depend on the severity of infection, timing of exposure, status of the birthing parent's immunity to VZV, and the neonate's gestational age. In the postvaccine era, mortality due to neonatal varicella is exceedingly rare. (See 'Outcome' above.)