Vol.2, No.2, 143-152 (2010)
Copyright © 2010 Openly accessible at http://www.scirp.org/journal/
Review of varicella-zoster virus infections in pregnant
women and neonates
A. Sauerbrei
Institute of Virology and Antiviral Therapy, Friedrich-Schiller University of Jena, Jena, Germany;Adreas.Sauerbrei@med.uni-jena.de
Received 29 October 2009; revised 7 December 2009; accepted 9 December 2009.
Even though varicella is rare in pregnancy, the
disease can lead occasionally to disastrous
illnesses for both the mother and her neonate.
By contrast, normal zoster is not associated with
special problems during pregnancy and peri-
natal period. Pregnant women, who contract
varicella, are at risk of varicella pneumonia which
must be regarded as medical emergency. At any
stage during pregnancy, chickenpox may cause
intrauterine infection. The consequences for the
fetus depend on the time of maternal disease.
During the first two trimesters, maternal varicella
may result in congenital varicella syndrome
which may occur in nearly 2%. Typical symptoms
are skin lesions in dermatomal distribution,
neurological defects, eye diseases, and skeletal
anomalies. Maternal infection near term is
associated with a substantial risk of intrauterine
acquired neonatal chickenpox in the neonate. If
the mother develops varicella rash between day
4 (5) ante partum and day 2 post partum,
generalized neonatal varicella leading to death in
about 20% of the cases has to be expected. The
present paper reviews the clinical consequences
and the currently available concepts of prevention,
diagnosis, and therapy of varicella-zoster virus
infections during pregnancy.
Keywords: Varicella-Zoster Virus Infection;
Pregnancy; Neonate; Prevention; Diagnosis;
In most industrial countries, chickenpox is a rare disease
during pregnancy, as more than 90% of women of child-
bearing age have virus-specific immunoglobulin (Ig) G
class antibodies. The etiological agent, the varicella-
zoster virus (VZV), is spread by respiratory transmission
or direct contact with infectious lesions. Seronegative
persons are at high risk of primary infection manifest as
varicella. According to a seroepidemiological study in
Germany, the prevalence of VZV-specific IgG class an-
tibodies in women of reproductive age is 96-97% and
only 3-4% of women were found to be susceptible to
varicella [1]. The average incidence of varicella in preg-
nant women has been calculated as 0.7-3 per 1,000
pregnancies [2-4]. Information on a positive history of
varicella correlates well with serological findings.
However, VZV IgG can be detected in 85% of persons
with negative history of varicella [5]. Although the
clinical course of chickenpox is usually mild, varicella in
pregnant women may occasionally lead to serious ma-
ternal and fetal diseases (Table 1).
Pregnant women who contract varicella are at risk of
severe pneumonia associated with life-threatening
ventilatory compromise and death. The disease seems to
occur more often in the third trimester [6]. At any stage
during pregnancy, chickenpox may cause intrauterine
infection. Maternal varicella leading to viremia may
transmit the virus to the fetus by either transplacental
spread or by ascending infection from lesions in the birth
canal. The fetal consequences depend on the time of
maternal disease. They range from asymptomatic
infection to fetal loss especially in case of severe maternal
disease. Neonatal varicella can be expected if a mother
contracts chickenpox during the last 3 weeks of pregnancy.
After maternal varicella between 4-5 days before and 2
days after delivery, generalized neonatal varicella, leading
to death in up to 20% of the cases, may occur since these
neonates have not acquired protecting antibodies [7].
1.1. Varicella Pneumonia
Although chickenpox is much less common in adults
than in children, the infection is associated with greater
morbidity, namely pneumonia, hepatitis and encephalitis.
Varicella pneumonia during pregnancy must be regarded
as a medical emergency. On the basis of retrospective
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Table 1. Varicella-zoster virus infections and their potential consequences during pregnancy.
Maternal disease Timing during pregnancy Consequences for mother, fetus, term neonate
At any stage Intrauterine death, neonatal or infantile zoster
5-24th weeks Congenital varicella syndrome (risk: 2%, mortality: 30%)
At any stage, especially in the third trimester Maternal pneumonia (risk: 10-20%, mortality: 10-45%)
Near term: 5 days before delivery Neonatal varicella at ages 10 (-12) days (risk: 20-50%, mor-
tality: 0%)
Near term: 4-5 days before to 2 days after delivery
Neonatal varicella 0-4 days after birth (risk: 20-50%; mor-
tality: 0-3%); neonatal varicella 5-10 (-12) days after birth
(risk: 20-50%; mortality: 20-25%)
Normal zoster At any stage No risk for severe maternal, fetal or neonatal infections
hospital-based studies, an incidence of 10-20% among
adults with chickenpox has been reported [6,8]. The
clinical course is unpredictable and may rapidly progress
to hypoxia and life-threatening respiratory failure. Ret-
rospective studies suggest that varicella pneumonia may
be more severe, although not more frequent, in pregnant
compared to non-pregnant women [9]. Risk factors for
the development of pneumonia are smoking and the oc-
currence of at least 100 skin lesions [10]. The disease
usually develops within 3-5 days of the rash and is asso-
ciated with cough, dyspnea, fever, and tachypnea. Addi-
tionally, cyanosis, pleuritic pain in the chest and hemop-
tysis can occur and secondary bacterial infections are
frequent. The chest x-ray findings include a diffuse or
miliary/nodular infiltrative pattern often in the peribron-
chial distribution involving both lungs [11]. Without
antiviral treatment, the mortality of the disease may be
as high as 45%. However, more recent studies suggest
that the mortality has decreased to 10-11% for both
non-pregnant and pregnant patients most likely due to
the effects of antiviral therapy and better respiratory
management [12]. Nevertheless, the risk of fatal course
appears to be considerably higher in pregnant than in
non-pregnant immunocompetent adults.
1.2 Congenital Varicella Syndrome
Primary VZV infection during first two trimesters of
pregnancy may result in intrauterine infection in up to a
quarter of the cases [13]. However, the reported rate of
spontaneous abortion following acute varicella did not
exceed the rate of abortion in pregnant women without
chickenpox. Congenital anomalies described as cong-
enital varicella syndrome (CVS) can be expected in
about 12% of infected fetuses [14]. Prospective studies
in Europe and North America revealed that the incidence
of congenital anomalies after maternal varicella infection
in the first 20 weeks of pregnancy is about 1-2% [15,16].
The first case of CVS was reported by Laforet and
Lynch in 1947 [17]. Since then, more than 130 neonates
born with signs of CVS have been described in the
English and German literature [13]. Since most of them
have been reported during the last 15-20 years, it can be
concluded that many cases of this syndrome were
formerly not seen in connection with chickenpox during
pregnancy. CVS has generally to be expected after
maternal chickenpox between the 5th and 24th gestational
weeks. Nearly 80% of all cases have been observed
between the 9th and 20th weeks of gestation. Before the
5th and after the 24th gestational weeks, the probability of
CVS is extremely low. The characteristic clinical symptoms
consist of skin lesions in dermatomal distribution,
neurological defects, eye diseases, and limb hypoplasia
(Table 2). Less frequent abnormalities include muscle
hypoplasia, affections of the internal organs as well as
gastrointestinal, genitourinary, and cardiovascular mani-
festations [18]. Nearly 30% of neonates born with signs
of CVS died during the first months of life. A follow-up
report in the literature demonstrated that in spite of
initially poor prognosis a good long-term outcome can
occur in patients with CVS [19]. On the basis of the
segmental distribution of some of the signs, there was
postulated that the CVS is not the immediate consequence
of intrauterine varicella, but caused by intrauterine
zoster-like VZV reactivations with accompanying encepha-
litis [20]. Immunologic studies suggest that the fetus is
not able to mount a VZV-specific cell-mediated immune
response [21].
Case report [22]: After a mother had chickenpox with
characteristic skin rash between the 13th and 15th
gestational weeks, a stillborn girl with typical clinical
signs of CVS was delivered by caesarean section at the
34th week of gestation. Postmortal findings included
hypoplasia of the left upper and the right lower limb,
dermatomally distributed skin lesions in the region of the
left anterior thorax, axilla and shoulder as well as on the
right lower extremity (Figure 1). The autopsy and
histological investigations revealed microphthalmia of
the left eye associated with opticus atrophia and chorio-
retinitis pigmentosa. Additional findings were coarcatio
aortae of preductal type, Meckel’s diverticulum, miliary
calcified necroses in the lungs, liver and adrenal glands as
well as one-sided cell reduction of the motor anterior
column of the cervical and lumbar spinal cord. The
eumature placenta showed a focal villous fibrosis,
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Table 2. Main symptoms of neonates with congenital varicella syndrome cited in the literature.
Neonates (n=125)
Symptoms n %
Skin lesions (cicatrical scars, skin loss) 90 72
Neurological defects or diseases (cortical atrophy, spinal cord atrophy, limb paresis, seizures, microcephaly,
Horner’s syndrome, encephalitis, dysphagia) 78 62
Eye diseases (microphthalmia, enophthalmia, chorioretinitis, cataract, nystagmus, anisocoria, optic atrophy) 66 53
Limb hypoplasia and other skeletal anomalies 55 44
Intrauterine retardation 28 22
Gastrointestinal abnormalities 25 20
Muscle hypoplasia 24 19
Genitourinary abnormalities 15 12
Affections of internal organs 15 12
Developmental delay 14 11
Defects of the cardiovascular system 9 7
Defects of other organs 9 7
Figure 1. Female stillborn with cicatricial skin lesions involv-
ing the left side of chest, axilla, and shoulder as well as hy-
poplasia of the left upper limb after maternal varicella between
the 13th and 15th gestational weeks.
intervillous thrombosis and chronic infarcts. VZV DNA
could be detected by polymerase chain reaction (PCR) in
the lungs, spleen, adrenal glands, bulbus oculi, and
placenta. In addition, VZV DNA/antigens were localized
in some organs by means of in situ hybridization/
monoclonal antibodies.
1.3. Zoster During Pregnancy
On the basis of current knowledge, zoster during preg-
nancy is not associated with birth defects [15,23]. Al-
though there are some reports of neonates with congeni-
tal malformations being born to mothers with history of
zoster during early pregnancy, no case showed labora-
tory evidence of intrauterine infection with VZV. In ad-
dition, maternal zoster during the perinatal period does
not cause problems for neonates [24] as they possess
specific maternal IgG class antibodies and there is usu-
ally no longer viremic spread of VZV unless the woman
is immunocompromised.
2.1. Neonatal Varicella
During the perinatal period, maternal varicella can infect
the infant by: 1) transplacental viremia, 2) ascending
infection during birth, or 3) respiratory droplet/direct
contact with infectious lesions after birth. Varicella of
the neonate can be expected if a mother contracts chick-
enpox during the last 3 weeks of pregnancy. Chickenpox
occurring in the first 12 days of life is described as in-
trauterine acquired neonatal varicella. Clinical observa-
tions suggest that the incubation period of intrauterine
transmitted varicella from the beginning of maternal
varicella rash to the onset of rash in the neonate is about
12 days, but it can be reduced to few days [4]. On the
basis of these data, neonatal chickenpox occurring after
the 12th day of the neonatal period is most likely not
transmitted by intrauterine infection, but it is acquired by
postnatal VZV infection. Maternal chickenpox few days
before or after delivery may cause life-threatening neo-
natal chickenpox. The disease was first recognized by
Hubbard in 1878 [25]. To date, hundreds of cases have
been reported [7].
The severity of intrauterine acquired neonatal chick-
enpox is closely related to the time of onset of maternal
infection as transplacentally transmitted antibodies may
reduce the severity of symptoms in the neonate. Fetuses
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exposed to VZV between 20 and 6 days before delivery
may develop neonatal chickenpox however with nonfatal
course. These neonates got maternal antibodies and have
therefore a lower risk of complications. Generalized
neonatal varicella associated with fatal course has to be
expected if mothers develop varicella rash between 4-5
days before and 2 days after delivery [7] since these
neonates did not acquire protecting maternal antibodies.
Additionally, the cell-mediated immune response of the
neonate is likely insufficient to retard the hematogene-
ous dissemination of VZV after transplacental spread
[26]. Thus, a fatal outcome has been reported in nearly
20% of these cases (Table 3). Furthermore, there is a
close relationship between the prognosis of intrauterine
acquired neonatal varicella and the onset of disease in
the neonate. A fatal outcome is more likely if the neona-
tal disease occurs between 5 and 10 days after delivery.
To our knowledge, 23% of the neonates reported in the
literature died from a disseminated and fulminant neo-
natal infection [7]. In comparison, neonatal varicella
within the first 4 days after birth has usually been found
to be mild (Table 3).
Case report [27]: Two days before delivery, the
mother of a female neonate had chickenpox with char-
acteristic skin rash. The girl was transferred from the
nursery to the isolation ward and received 1.5 ml varicella-
zoster immune globulin (VZIG) Zostergam. After one
week, she was discharged home since she was healthy.
On the tenth day, the girl was hospitalized again because
of unclear skin lesions appearing on the face. One day
later, she developed generalized varicella skin rash. The
neonate died from respiratory distress on the 16th day.
Autopsy revealed typical varicella rash on the skin
(Figure 2) and the mucous membrane of the mouth,
confluent hemorrhagic-necrotizing pneumonia, necrotiz-
ing hepatitis as well as focal necroses of the intestinal
mucous membranes, spleen, adrenal glands and brain.
Virological investigations confirmed the diagnosis of
varicella by detecting VZV DNA in liver tissue using
PCR and in situ hybridization. By electron microscopy,
intranuclear herpesvirus-like particles could be seen in
specimens from skin lesions as well as in necrotic le-
sions of liver and lungs.
Postnatal VZV infections during the neonatal period
have a low morbidity rate [28] as most neonates are pro-
tected by maternally derived antibodies. However, pre-
mature neonates younger than 28 weeks gestation must
be considered to have an increased risk for severe
varicella during the first 6 weeks after birth [29,30]. It
has been suggested they have got no protecting maternal
antibodies because of the reduced gestation period.
2.2. Zoster in Neonates and Young Infants
Nearly 20% of infants with intrauterine acquired VZV
primary infection develop neonatal or infantile zoster,
usually with uncomplicated course [18]. The disease is
thought to represent reactivation of the virus after pri-
mary infection in uteri. The relatively short viral latency
period may be explained by the immature cell-mediated
immune response in young infants.
3.1. Congenital Varicella Syndrome
Most cases of CVS have been reported on the basis of the
described main clinical symptoms without laboratory
evidence of intrauterine infection. However, the causal
relationship between maternal varicella infection and
congenital abnormalities can be most convincingly veri-
fied by detection of viral DNA or viral antigens in the
neonates [22]. Therefore, molecular biological methods
should be regularly included in the diagnosis of
CVS. In particular, cases presented with rare malforma-
tions or after sub-clinical maternal VZV infection need
confirmation by virological methods, otherwise the
causal relationship between maternal infection and con-
genital abnormalities remains doubtful [31]. Unlike in
cases of intrauterine rubella or cytomegalovirus infection,
Figure 2. Female neonate with lethal neonatal varicella.
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Table 3. Prognosis of neonatal varicella without antiviral treatment in 136 term neonates cited in the literature.
Number of cases of neonatal varicella
Mother/Neonate Total number Day of onset of varicellaNon-fatal Fatal
57 5 days before delivery 57 (100%) 0
79 4 days before to 2 days
after delivery 65 (82%) 14 (18%)
35 0-4 days after birth 34 (97%) 1 (3%)
Neonate* 47 5-10 days after birth 36 (77%) 11 (23%)
* Data of 54 neonates have not been described.
VZV has not been isolated in cell cultures from any
neonate with CVS. Usually, the detection of virus-specific
antibodies in neonates has been reported to confirm a
suspected prenatal infection with VZV. Serologic diag-
nosis is mostly based on the persistence of VZV-specific
IgG class antibodies beyond 7 months of life when ma-
ternal antibodies should normally have disappeared
[32,33]. The presence of virus-specific IgM has only
been described in about 25% of the cases with CVS [23].
The reason for that is primarily the low sensitivity of
commercially distributed enzyme immuneo-assays, which
are most frequently used to detect VZV-specific IgM. To
establish a relationship between maternal VZV infection
and congenital anomalies of neonates, the criteria listed
in Table 4 should be used as guideline.
The differential diagnosis of CVS includes congenital
infections caused by rubella virus, cytomegalovirus, her-
pes simplex virus (HSV), coxsackie virus or Toxo-
plasma gondii [23,34,35] and the specific genetic disor-
der called MIDAS (Microphthalmus, Dermal Aplasia,
Sclerokornea) syndrome [36], whose cardinal symptoms
represent congenital skin defects in dermatomal distribu-
tion associated with microphthalmia.
3.2. Neonatal Varicella and Varicella
The diagnosis of neonatal varicella is usually based on
the typical clinical picture. The characteristic point in
(1) Appearance of maternal varicella during pregnancy
(2) Neonate or fetus with
congenital skin lesions in dermatomal distribution and/or
neurological defects,
eye diseases,
limb hypoplasia
(3) Proof of intrauterine VZV infection by
detection of viral DNA using polymerase chain reaction and/or
presence of specific IgM/persistence of IgG beyond 7 months of age,
appearance of zoster during early infancy
time of infection and the maternal history of chickenpox
during the last weeks of pregnancy have to be consid-
ered to diagnose the intrauterine acquired disease. Clini-
cal findings have been usually confirmed by serological
Table 4. Criteria used for diagnosis of congenital varicella
syndrome.methods, but they are not useful for early di-
agnosis. For laboratory diagnosis of VZV infection, PCR
technique should be used as method of choice. Suitable
patient materials are skin swabs or biopsies, liquor
specimens and tissue samples. HSV and enterovirus in-
fections should be considered in differential diagnosis
[37,38]. On suspicion of varicella pneumonia, a labora-
tory diagnosis is necessary for reason of differential di-
agnosis. As method of choice, the PCR should be used to
detect viral DNA in broncho-alveolar lavage.
4.1. Preventive Measures
An effective prophylaxis of chickenpox in pregnant
women and neonates is only possible by active immuni-
zation of seronegative women before pregnancy. A live
attenuated varicella vaccine has been shown to be safe
and effective in preventing chickenpox in adults [39].
Varicella vaccine, as all live-attenuated vaccines, is con-
traindicated in pregnant women and pregnancy has to be
avoided for at least 4 weeks following vaccination. The
Pregnancy Registry managed by the Merck Research
Laboratories (USA) in collaboration with the Centers for
Disease Control and Prevention (USA), records women,
who exposed to varicella vaccine during pregnancy or
within 3 months before conception. Preliminary results
showed no hints to any birth defects related to vaccine
exposure [40,41]. In few cases, vaccines can develop
breakthrough varicella that occurs 42 days after vaccina-
tion and represents wild virus infection [42]. Most dis-
eases are very mild, the infectivity is relatively low and
there is a low or no risk for complications [43]. Thus, the
risk for CVS from breakthrough varicella can be regarded
as considerably lower than that for CVS in unvaccinated
women with varicella. However, prophylactic and thera-
peutic measures in women with breakthrough varicella
should be considered as in unvaccinated women who
develop varicella since data about the risk for CVS after
breakthrough varicella are not available to date.
Non-immune pregnant women should be advised to
avoid exposure to chickenpox and zoster. If pregnant
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women with a negative or indeterminate history of
varicella have been exposed significantly to VZV by
household contact, face-to-face contact for at least 5
minutes or indoors contact for more than 15 minutes,
virus-specific IgG class antibodies should be measured
immediately. If the woman is seronegative or there is an
indeterminate or unknown status of immunity, she should
be regarded as susceptible. Antibodies detected within
7-10 days of contact must have been acquired before
exposure. For pregnant women, who were adequately
vaccinated with 2 vaccine doses, routine serologic test-
ing cannot be recommended since 99% of persons be-
come seropositive after the second dose of varicella vac-
cination [44]. Furthermore, most currently used enzyme
immunoassays are too insensitive to detect vaccine-induced
VZV-specific IgG class antibodies [45] and sensitive
procedures such as the fluorescent antibody to mem-
brane antigen assay or tests for the determination of the
cell-mediated immune response are too laborious and/or
time consuming for daily routine. Recently, a new gen-
eration of VZV glycoprotein-based enzyme immunoas-
says has been shown to have higher sensitivity for the
determination of VZV IgG [46].
In case of negative, indeterminate or unknown sero-
logic status, the application of VZIG within 72 (-96) hours
has been recommended [47,48] (Figure 3) intramuscu-
larly at a concentration of 125 U/10 kg of body weight, up
to a maximum of 625 U [29] or 0.5 ml/kg of body weight
[30]. A dosage of 1 ml/kg of body weight can be adminis-
tered intravenously as alternative [30]. Even though the
passive immunization does not prevent varicella, it may
reduce most likely the risk of severe varicella as well as
fetal infection. However, there is no evidence that this
prevents fetal viremia or CVS. Thus, the primary reason
for VZIG is to prevent severe maternal chickenpox and its
complications, such as pneumonia. If there is a definitive
past history of chickenpox, it is reasonable to assume that
the woman is immune to varicella. Vaccinated pregnant
women who were tested VZV IgG-negative should be
managed as a seronegative pregnant woman without
varicella vaccination. However, in most cases, seronega-
tive vaccinees have most likely acquired VZV-specific
cell-mediated immunity.
In the United States, VZV vaccine was licensed in
1995 and decreased the incidence of varicella by 85-90%
in the decade following licensure as result of a vaccine
coverage rate of about 80% [49]. Even though varicella
incidence decreased most significantly in children aged
1-4 years, the incidence also declined nearly 75% among
adults despite of low vaccination rates [50]. These data
suggest that the universal childhood immunization,
introduced also in Germany as the only country in Euro-
pe during 2004, has the potential to reduce the occurren-
ce of varicella in pregnant women through herd immun-
ity. However, recent publications demonstrate that varic-
ella during pregnancy is still a problem in many countries
which do not offer a routine universal childhood varicella
immunization program [51,52]. In Italy, epidemiological
data suggest that the risk of acquiring varicella during
pregnancy is increasing [53]. Therefore, information prog-
rams are recommended to disseminate and to promote
screenng and immunization against varicella in susceptible
women of childbearing age [54].
4.2. Diagnostic and Therapeutic Measures
Mothers with varicella during the first or second trimester
should be carefully monitored since intrauterine infection
may lead to CVS. Fetal ultrasound and magnetic resonance
imaging at 16 to 22 weeks gestational age or 5 weeks after
infection can identify signs of CVS (Figure 3) [55,56].
Laboratory investigations for VZV DNA in placental villi,
fetal blood or amniotic fluid and for VZV IgM in fetal
blood are only indicated if suspicious fetal abnormalities
can be detected [55]. However, several studies have
shown that the presence of VZV DNA alone does not
necessarily correlate with fetal disease [57]. Thus, the
question of how severely the fetus is affected cannot be
answered definitely. This and the low risk of CVS should
be considered in counseling women with varicella in early
pregnancy. Termination of pregnancy is only indicated if
there are definitive signs of serious fetal abnormalities.
An antiviral treatment has immediately to be intro-
duced at first signs of varicella pneumonia or other dis-
seminated infections. As the only therapeutic agent, aci-
clovir is indicated in pregnant women. Aciclovir has to
be administered orally at a dosage of 5 x 800 mg or in-
travenously at a concentration of 3 x 10-15 mg/kg for
7-10 days. Zoster during pregnancy should only be
treated with aciclovir in severe courses of the disease
[58]. To date, there are no controlled studies concerning
antiviral chemotherapy in preventing CVS [59].
5.1. Preventive Measures
Mothers and neonates suffering from or being at risk of
varicella have to be isolated on maternity wards. To re-
duce the mortality from neonatal chickenpox, the date of
delivery may be postponed for several days to allow
maternal antibodies to pass the placental barrier (Figure 3).
However, there is only little experience with successful
delay of labor when neonatal varicella must be expected
[60,61]. The administration of aciclovir at a dosage of 5
x 800 mg orally or 3 x 10-15 mg/kg intravenously for 7
days has been recommended for pregnant women within
24 hours of the varicella rash when the disease occurs
within 4-5 days before delivery. VZIG is indicated for
neonates whose mothers have signs and symptoms of
varicella between 5 days before and 2 days after delivery
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Measures in varicella occurring at every time of pregnancy
After exposure to VZV, detection of VZV IgG in women with negative or indeterminate history of varicella
Figure 3. Measures in case of varicella during pregnancy depending on the point of time of infection; MRI: magnetic resonance im-
aging, VZIG: varicella-zoster immune globulin, VZV: varicella-zoster virus.
Table 5. Administration of varicella-zoster immune globulin (VZIG) and aciclovir in neonates to prevent neonatal varicella.
VZIG after intrauterine exposure to VZV
Neonates whose mothers develop varicella within
5 days before and 2 days after delivery
Intravenously: 1 ml/kg [30] or intramus-
cularly: 125 U [29] or 0.5 mg/kg [30]
Immediately after birth or
onset of maternal rash
VZIG after postnatal exposure
Premature neonates with negative varicella his-
tory of the mother
Intravenously: 1 ml/kg [30] or intramus-
cularly: 125 U [29] or 0.5 mg/kg [30]
Within 96 hours after expo-
Premature neonates <28 weeks gestation or
<1,000 g birth weight independent of maternal
varicella history
Intravenously: 1 ml/kg [30] or intramus-
cularly: 125 U [29] or 0.5 mg/kg [30]
Within 96 hours after expo-
Antiviral treatment of neonatal varicella
Suspected neonatal varicella Aciclovir intravenously: 3 x 10-15
mg/kg Length of therapy: 5-7 days
(Table 5). Passive immunization is probably not neces-
sary for neonates whose mothers have sings of varicella
>5 days before or >2 days after delivery [14,62] because
those neonates are not at risk of severe neonatal varicella.
Hospitalized premature neonates, younger than 28 weeks
gestation, who are exposed to VZV, have to receive
VZIG, regardless of the maternal history of chickenpox
as these neonates may not have acquired maternal anti-
bodies (Table 5) [29]. Following treatment, these neo-
nates should be under surveillance in the hospital for 2
weeks, i.e. to the end of incubation period [14,30]. When
a neonate who has received VZIG is discharged home, it
Administration of VZIG in women with negative, indeterminate or unknown VZV immunity status
Administration of aciclovir at first signs of varicella pneumonia or other disseminated VZV infections
Measures in varicella at 1st and 2nd trimesters
Monitoring pregnancy
Prenatal diagnosis:
Ultrasound, MRI (16.-22. weeks of gestation)
Detection of VZV DNA in fetal blood,
amniotic fluid or placental villi
Detection of VZV IgM in fetal blood
Termination of pregnancy if there are
significant signs of fetal abnormalities
Measures in varicella during perinatal period
Mother: Delaying the birth, aciclovir
2 weeks under surveillance in the
On suspicion of neonatal varicella:
Isolation of mother and newborn
Varicella in the first 2 trimesters
Congenital varicella syndrome
Varicella at any stage of Varicella 5 days ante partum
to 2 days post partum
Neonatal varicella
pregnancy, especially
in the 3rd trimester
Maternal varicella pneumonia
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Openly accessible at
should be made clear to the parents that prompt hospital
review should be undertaken if the neonate becomes
unwell or develops rash. It has been generally accepted
that passive immunization of the neonate can modify the
clinical course of neonatal varicella but it does not pre-
vent the disease and, although decreased, the risk of
death is not completely eliminated [63,64].
5.2. Therapeutic Measures
An antiviral treatment of neonates with CVS has only
been described in few cases [65-67]. Clinical observ-
ations suggest that aciclovir therapy may be helpful
especially to stop the progression of eye diseases or to
prevent neurological diseases after VZV reactivations.
Suspected cases of neonatal chickenpox should be treated
promptly with aciclovir (Figure 3, Table 5). Prophylactic
intravenous administration of aciclovir can prevent
neonatal varicella or can reduce the severity of the disease
markedly [68]. Well-controlled studies on the use of
aciclovir in neonates have not been reported to date [59].
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