Please note that all guidance is currently under review and some may be out of date. We recommend that you also refer to more contemporaneous evidence in the interim.
Introduction - definition
Chickenpox is an infectious childhood disease. It is rare in infants and newborns due to passive immunity received from the mother.
Chickenpox is caused by Varicella-zoster virus (VZV), an enveloped double-stranded DNA virus that belongs to the Herpesviridae family.1,2
In Australia the majority of women have either had primary chickenpox infection, or received the VZV vaccination, and therefore developed immunity against disease.3 It is therefore rare for young infants and newborns to contract disease, as they are protected by passive immunity received from the mother during the third trimester.2
People with chickenpox are infectious from 48 hours before the onset of the rash until all lesions have crusted. VZV is primarily transmitted via aerosols, and direct contact with skin lesions. The incubation period for chickenpox from time of exposure to appearance of rash varies from 10 to 21 days with an average of 14 days.4,5
The presentation of varicella zoster infection in the newborn depends upon the timing of maternal infection. Infection in early pregnancy (usually before 20 weeks gestation) can result in congenital varicella syndrome (described below), whereas maternal infection that occurs just prior to, or immediately following delivery, can result in neonatal chickenpox.
This can occur when the mother is infected during the last three weeks of pregnancy.6 The highest risk to the neonate for developing chickenpox is when maternal primary varicella infection has developed within the window of seven days before, to two days after, delivery, as passive immunity will not have been conferred to the newborn.4,7
A neonate born to a mother with chickenpox within this timeframe should be administered zoster immunoglobulin (ZIG). The untreated mortality for severe disease in an infant of this age is as high as 31%,4,8 however with the availability of ZIG and intensive care support, this has reduced to about 7%.7
A neonate whose mother developed chickenpox between 20 days to five days prior to delivery may still develop neonatal chickenpox,7 however the disease is generally mild to moderate.
Congenital varicella infection
Congenital varicella syndrome is a rare disorder. The risk of congenital varicella syndrome (CVS) following primary maternal varicella in pregnancy is highest when disease occurs before 20 weeks gestation, peaking at 1.4% in second trimester maternal infection.3,9
A mother who contracts chickenpox during pregnancy should be referred to a feto-maternal specialist for management and prenatal counselling. An amniocentesis is not routinely recommended if screening ultrasounds are normal. Although treatment with acyclovir is recommended to prevent severe maternal disease, there is no evidence that maternal treatment alters the risk of fetal infection.1 Regular ultrasound monitoring, beginning no sooner than five weeks after primary infection, should occur until delivery.
Affected newborns may have low birth weight and characteristic abnormalities of the skin (characteristic cicatricial lesions in a dermatomal distribution), brain, eyes (cataracts, chorioretinitis) and limbs.
After chickenpox infection, VZV remains dormant in neurons in the trigeminal and dorsal root ganglia.10,11 VZV can reactivate as shingles, also known as herpes zoster,3 usually causing painful vesicular lesions in a dermatomal distribution. These lesions are infectious via direct contact, and aerosol transmission does not usually occur.
A mother presenting with shingles during pregnancy will have immunity to VZV from previous infection, which will be transferred transplacentally to her fetus.7 Therefore infants of mothers with shingles are not at risk of serious varicella infection. A neonate whose mother develops shingles at any time during the pregnancy or after delivery does not require treatment or isolation precautions.
Clinical manifestations of neonatal chickenpox include a prodromal phase (usually febrile) followed by development of a widespread, intensely pruritic rash, which starts as macules which progress to papules and then become vesicular prior to crusting.
New crops of lesions appear over a few days, and lesions are often in different stages of development. Diagnosis should be confirmed by nucleic acid testing (NAT) (eg. Polymerase chain reaction (PCR)) from vesicular swabs.6
Intact lesions should be de-roofed, or scabs removed, prior to swabbing (use dry flocked swab) so that vesicular fluid is collected for PCR. Herpes simplex should always be considered in the differential diagnosis of a vesicular rash.
Congenital varicella syndrome
An infant affected by CVS will likely have clinical anomalies at birth. These can be skin lesions (76%), neurological deficits (60%), eye diseases (51%) and skeletal anomalies (49%).12 It is likely that affected infants will have had abnormalities recognized on antenatal ultrasound monitoring.
It is not always possible to isolate varicella from an affected neonate; this may be due to the timing of the infection, with no persistent replicating virus present at the time of birth.13 Diagnostic testing may include nucleic acid testing for VZV DNA on tissue (e.g. skin lesions, CSF, blood), and varicella serology (although all these tests have low sensitivity).2
- For an infant whose mother developed symptoms of chickenpox between seven days prior to until two days following delivery, ZIG should be administered as soon as possible after birth and the infant and mother observed in hospital, in airborne and contact precautions, for at least three days.6 If the infant develops chickenpox then they should also be treated with IV acyclovir.9
- An infant whose mother had chickenpox within the first or second trimester is likely to have already been reviewed and monitored by a feto-maternal specialist. If antenatal ultrasounds have been unremarkable, and the baby is well at the time of delivery, with no features of concern on examination (including an ophthalmological review), then no further investigations are required for the infant.12
- Clinical Guidance can been sought from the Management of Perinatal Infections guideline published by the Australasian Society for Infectious Diseases on Varicella zoster infection9 and the Australian Immunisation Handbook14
Follow up and documentation
- A neonate born to a mother who contracted primary varicella during pregnancy should have a full examination after birth. If primary maternal infection had occurred during the first or second trimester of pregnancy, clinical examination is normal and all antenatal monitoring has been unremarkable, then no further follow up is required for the infant.
- For neonates born to a mother who has developed primary varicella infection within the three weeks prior to delivery, full examination should occur and management undertaken according to the ASID Management of Perinatal Infections guideline. Families should be educated to look for the development of a rash and to present early for medical review should they occur.
- Subclinical neonatal disease can occur in infants born to mothers with chickenpox in the 3rd trimester. These infants may subsequently present with shingles during infancy or early childhood.1
- Discuss with an Infectious Diseases consultant if you have any doubt regarding management or treatment.
1. Whitley R. Medical Microbiology: Chp 68 Herpesviruses. 4th edition ed. Galveston (TX): University of Texas Medical Branch at Galveston; 1996.
2. De Paschale M, Clerici P. Microbiology laboratory and the management of mother-child varicella-zoster virus infection. World J Virol. 2016;5(3):97-124.
3. Dwyer DE, Cunningham AL. 10: Herpes simplex and varicella-zoster virus infections. Med J Aust. 2002;177(5):267-73.
4. Chickenpox (Varicella): For Healthcare Professionals Centers for Disease Control and Prevention [updated December 31, 2018; cited 2019 July 19]. Available from: https://www.cdc.gov/chickenpox/index.html.
5. WHO. Immunization, Vaccines and Biologicals: Varicella World Health Organisation: World Health Organisation; 2015 [updated April 4, 2015; cited 2019 July 19]. Available from: https://www.who.int/immunization/diseases/varicella/en/.
6. Sauerbrei A, Wutzler P. Neonatal varicella. J Perinatol. 2001;21(8):545-9.
7. Blumental S, Lepage P. Management of varicella in neonates and infants. BMJ Paediatr Open. 2019;3(1):e000433.
8. Kett JC. Perinatal Varicella. Pediatrics in Review. 2013;34(1):49.
9. Palasanthiran P, Starr M, Jones C, Giles M, editors. Management of Perinatal Infections Sydney: Australasian Society for Infectious Diseases (ASID); 2014 [81-8]. Available from: https://www.asid.net.au/documents/item/368
10. Eshleman E, Shahzad A, Cohrs RJ. Varicella zoster virus latency. Future Virol. 2011;6(3):341-55.
11. Kennedy PG, Grinfeld E, Gow JW. Latent varicella-zoster virus is located predominantly in neurons in human trigeminal ganglia. Proc Natl Acad Sci U S A. 1998;95(8):4658-62.
12. Sauerbrei A, Wutzler P. The congenital varicella syndrome. J Perinatol. 2000;20(8 Pt 1):548-54.
13. Wilson C, Nizet V, Maldonado Y, Remington J, Klein J. Remington and Klein's Infectious Diseases of the Fetus and Newborn Infant. Chapter 23: Varicella, Measles and Mumps. 8th ed. Philadelphia: Elsevier; 2016.
14. Australian Immunisation Handbook: Varicella (chickenpox). Australian Goverment, Department of Health; [updated 23 April 2019; cited 2019 July 23]. Available from: https://immunisationhandbook.health.gov.au/vaccine-preventable-diseases/varicella-chickenpox.
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First published: October 2015
Last web update: November 2019
Review by: November 2022
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Page last updated: 17 Feb 2021