Fetal viral infections

26.03.2019
1
Congenital Viral Infections
TEVFİK YOLDEMİR MD. BSc. MA. PhD.
tyoldemir
profdrdryoldemir
Viruses which are perinatally acquired and
which can cause fetal/neonatal damage.
TERATOGENIC VIR
cytomegalic inclusion disease (CID), occurs at a ra
approximately 1 in 5000 to 1 in 20000 births.
Perinatal transmission of CMV has been demonstrat
cases where the pregnant woman develops either a prima
recurrent CMV infection. Transmission rates of CMV
primary infection range from 15% to 50%,6
whereas n
tal infection occurs in approximately 0.5–1.0% of cases w
there is a recurrent infection in the mother. In general, th
lowing principles apply to fetal infection with CMV: (1) s
damage, such as that seen in fully developed CID, r
almost exclusively from primary maternal infection, an
clinically evident manifestations in the newborn are
common following primary infection in the mother.
Clinical manifestations
In general, maternal infection with CMV is asymptom
Symptomatic patients develop fever, pharyngitis,
phadenopathy, and other generalized symptoms of
illness. Primary CMV infection has been described
Table 17.1 Viruses which are perinatally acquired and which can cause fetal/neonatal damage.
Virus Perinatal/neonatal effects
Known teratogenic viruses See text for perinatal effects
Cytomegalovirus
Rubella virus
Varicella zoster virus
Herpes simplex virus (HSV1, HSV2)
Parvovirus B19
Venezuelan equine encephalitis virus
Viruses that have been shown to cause fetal damage after transmission
Coxsackieviruses (group B) Myocarditis, meningoencephalitis, pleurodynia
Dengue virus Fever, leucopenia, thrombocytopenia
Echovirus (14 and 19) Apneic spells, hepatitis, thrombocytopenia
Hepatitis B virus Hepatitis
Hepatitis C virus Hepatitis
Human immunodeficiency virus Growth restriction, leukopenia, failure to thrive, hypogammaglobulinemia, AIDS-related infec
Human papillomavirus Laryngeal papilloma
Influenza virus Endocardial fibroelastosis (?)
Mumps virus Pneumonitis, endocardial fibroelastosis (?)
Parvovirus B19 Nonimmune fetal hydrops, anemia
Poliovirus Paralysis
Rubeola (measles) virus Premature delivery, measles, otitis media
Vaccinia virus Spontaneous miscarriage, fetal death
Variola virus Spontaneous miscarriage, fetal death
Western equine encephalitis virus Meningitis
Viruses that have not been shown to cause fetal damage after transmission or when data on fetal transmission are inconclusive
Coxsackieviruses (group A)
Epstein–Barr virus
Hepatitis A virus
Non-A, non-B, non-C hepatitis viruses
Rabies virus
Smallpox virus
Table 17.2 Frequency of teratogenic viral infections in pregnant
women and their children.
Virus Mother Child
(per 10000) (per 10000)
Cytomegalovirus 300–500 50–150
Rubella virus
Epidemic 200–400 20–40
Nonepidemic 10–20 1–2
Currently in the USA < 1 < 0.1
Herpes simplex virus 50–150 0.5–5.0
Parvovirus B19 25 5–10
Varicella zoster virus 1–2 < 0.01–1.0
Venezuelan equine encephalitis With epidemics With epidemics
approximately 40000 infants are born annually with either
clinical or laboratory evidence of CMV infection. Worldwide,
it is estimated that 1% of all newborns are infected with CMV.
Severe damage from congenital infection, such as the classic
TCO17 9/13/06 4:58 PM Page 249
Clinical obstetrics : the fetus & mother 3rd edition 2007 p.249
cytomegalic inclusion disease (C
approximately 1 in 5000 to 1 in 2
Perinatal transmission of CMV
cases where the pregnant woman d
recurrent CMV infection. Transm
primary infection range from 15%
tal infection occurs in approximate
there is a recurrent infection in the
lowing principles apply to fetal inf
damage, such as that seen in fu
almost exclusively from primary
clinically evident manifestations
common following primary infect
In general, maternal infection w
Symptomatic patients develop
phadenopathy, and other gener
illness. Primary CMV infection
Cytomegalovirus
Rubella virus
Parvovirus B19
Human immunodeficiency virus Growth restriction, leukopenia, failure to thrive, hypogammaglobuli
Viruses that have not been shown to cause fetal damage after transmission or when data on fetal transmission ar
Hepatitis A virus
Rabies virus
Smallpox virus
Virus Mother Child
(per 10000) (per 10000)
Rubella virus
Epidemic 200–400 20–40
Viruses that cause fetal damage
TERATOGENIC VIRUSES
cytomegalic inclusion disease (CID), occurs at a rate of
Perinatal transmission of CMV has been demonstrated in
cases where the pregnant woman develops either a primary or
recurrent CMV infection. Transmission rates of CMV after
whereas neona-
tal infection occurs in approximately 0.5–1.0% of cases where
there is a recurrent infection in the mother. In general, the fol-
lowing principles apply to fetal infection with CMV: (1) severe
damage, such as that seen in fully developed CID, results
almost exclusively from primary maternal infection, and (2)
clinically evident manifestations in the newborn are more
In general, maternal infection with CMV is asymptomatic.
Symptomatic patients develop fever, pharyngitis, lym-
phadenopathy, and other generalized symptoms of viral
illness. Primary CMV infection has been described as a
249
Cytomegalovirus
Rubella virus
Parvovirus B19
Human immunodeficiency virus Growth restriction, leukopenia, failure to thrive, hypogammaglobulinemia, AIDS-related infections
Hepatitis A virus
Rabies virus
Smallpox virus
Virus Mother Child
(per 10000) (per 10000)
Rubella virus
Epidemic 200–400 20–40
TCO17 9/13/06 4:58 PM Page 249
Viruses that do not cause fetal damage
TERATOGENIC VIRUSES
cytomegalic inclusion disease (CID), occurs at a rate of
Perinatal transmission of CMV has been demonstrated in
cases where the pregnant woman develops either a primary or
recurrent CMV infection. Transmission rates of CMV after
whereas neona-
tal infection occurs in approximately 0.5–1.0% of cases where
there is a recurrent infection in the mother. In general, the fol-
lowing principles apply to fetal infection with CMV: (1) severe
damage, such as that seen in fully developed CID, results
almost exclusively from primary maternal infection, and (2)
clinically evident manifestations in the newborn are more
In general, maternal infection with CMV is asymptomatic.
Symptomatic patients develop fever, pharyngitis, lym-
phadenopathy, and other generalized symptoms of viral
illness. Primary CMV infection has been described as a
249
Cytomegalovirus
Rubella virus
Parvovirus B19
Human immunodeficiency virus Growth restriction, leukopenia, failure to thrive, hypogammaglobulinemia, AIDS-related infections
Hepatitis A virus
Rabies virus
Smallpox virus
Virus Mother Child
(per 10000) (per 10000)
Rubella virus
Epidemic 200–400 20–40
TCO17 9/13/06 4:58 PM Page 249
Consequences of viral infections during pregnancy
VIRAL INFECTIONS IN PREGNANCY OTHER THAN HIV
433
to microbes such as double-stranded RNA, peptidoglycans
and lipopolysacharides [10]. Adaptive immunity requires
contact with the microbe; hence it is very specific but takes at
least 3–4 days to reach minimally effective levels; however,
it is followed by immunologic memory, which offers partial
if not total protection against subsequent infections by the
same organism. Activation of the adaptive immunity requires
the prior activation of innate immunity and “antigen presen-
tation” by antigen-presenting cells (APC) to T-lymphocytes.
Antigens are presented by molecular histocompatibility com-
plex (MHC) membrane proteins; MHC-I are present in all
somatic cells (except neurons and red blood cells (RBC)) and
MHC-II only on APC, like macrophages. Human leukocyte
antigens (HLA) are the MHC in humans.
Simplistically, following infection viruses undergo rapid
replication using the host cell apparatus for protein synthesis
Table 17.1 Consequences of viral infections during pregnancy
Viruses by predominant
clinical consequences
Abortion, stillbirth Prematurity Symptomatic congenital
infection
Developmental abnormalities/
birth defects
Neonatal disease
Fetal
CMV ϩ ϩ ϩϩ1
ϩϩϩ ϩ
Rubella ϩ Ϫ ϩϩϩ1
ϩϩϩ ϩ
Parvo BϪ19 ϩϪ Ϫ ϩ Ϫ Ϫ
LCV ϩ Ϫ ϩ ϩϩ ϩ
Mumps ϩϩ Ϫ Ϫ ϩ Ϫ
Materno-fetal
Measles ϩ ϩϩ Ϫ Ϫ ϩ
Neonatal
Coxsackie (mostly B1-B5
strains)
ϩ Ϫ Ϫ ϩ2
ϩϩ
Echovirus serotype 11 ϩ3
Ϫ Ϫ Ϫ ϩϩ4
Maternal-neonatal
Primary VZV Ϫϩ Ϫ5
Ϫ ϩ6
ϩϩϩ7
HSV Ϫ Ϫ ϩ8
Ϫ6
ϩϩ9
HPV Ϫ Ϫ Ϫ Ϫ ϩ10
Maternal
Influenza Ϫ Ϫ Ϫ Ϫ Ϫ
EBV11
Ϫ ϩ Ϫ Ϫ Ϫ
Ϫ No documented association.
ϩ Documented association but true incidence unknown.
ϩϩ Well-documented association (prospective, histopathologic correlation and/or molecular data).
ϩϩϩ Most clinically relevant association.
1
Risk of congenital disease in the baby may be significant enough to warrant counseling on continuation of pregnancy.
2
Congenital heart disease has been linked to coxsackie B3.
3
Stillbirths reported for echovirus 27 and 11. Symptomatic congenital infections reported for echoviruses 6, 7, 9, 11, 19, 27 and 33.
4
Neonatal sepsis-like syndrome and myocarditis associated with echovirus 11.
5
Prospective studies have shown conflicting results regarding prematurity for offspring of gestational VZV.
6
Congenital VZV syndrome is rare; risk is confined to maternal VZV in the first half of pregnancy (weeks 7–20).
7
Neonatal VZV develops in 24–50% of cases of maternal chickenpox within 4 weeks of delivery.
8
Intrauterine infection is extremely rare: 1/200,000 births.
9
Neonatal HSV affects 1/3200 births potentially resulting in permanent sequelae or death.
10
Incidence of JORRP in the offspring women with vaginal condyloma is 7/1000 versus 3.96/100,000 for the general pediatric population.
11
Mononucleosis-like syndromes must be investigated, as may be secondary to CMV, LCV or EBV.
CMV, cytomegalovirus; EBV, Epstein-Barr virus; HPV, human papilloma virus; HSV, herpes simplex virus; JORRP, juvenile-onset recurrent respiratory
papillomatosis; LCV, lymphocytic choriomeningitis virus; VZV, varicella-zoster virus.
and viral replication; viral antigens then are available to be
presented by HLA-I molecules to CD8ϩ T-cells (cytotoxic
T-cells (CTL)), resulting in production of virus-specific clones
of B-lymphocytes responsible for antibody production and
specific T-lymphocytes.
Innate immunity against viruses (Figure 17.2) is triggered
by viral destruction of cells, recognition of infected cells by
NK cells (which are able to recognize cells not expressing
HLA-I and otherwise evading immune surveillance) or direct
interaction of complement with virions, leading to cytokine
release, kinin and complement activation and recruitment of
monocytes and neutrophils. Normal pregnancy is character-
ized by generalized upregulation of granulocytes, monocytes
and complement [11]. NK cell cytotoxic function is reduced
in the peripheral maternal circulation, but NK cells are the
predominant leukocyte at the decidua.
de Swiet’s Medical Disorders in Obstetric Practice 5th edition 2010 p 433
Summary and characteristics of the laboratory tests
used for assessment of viral infections in pregnancy
Reproductive Toxicology 21 (2006) 350–382

26.03.2019
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Clinical syndromes associated with viral
infections in pregnancy and diagnostic tests
435
Table 17.2 Clinical syndromes associated with viral infections in pregnancy and diagnostic tests
Clinical syndrome Potential viral infections Direct viral detection Antibodies
Undifferentiated fever CMV, rubella1
, enteroviruses2,6
,
influenza, EBV, measles3
,
parvo B-19, WNV4
CMV, parvo B-195
NAAT blood
Nasopharyngeal wash for influenza
Throat swab for viral NAAT6
Urine for viral culture
Stool for viral culture6
Single serum:
CMV, EBV IgM, IgG7
WNV IgM
Monospot
Paired serum:
Rubella IgM, IgG8
Parvo B-19 IgM, IgG
Measles IgM, IgG
Fever and nonvesicular rash Rubella, measles, echoviruses2
,
EBV, parvo B-19, CMV
Throat swab for viral NAAT 6
Stool for viral culture 6
Parvo B-19 NAAT blood
EBV IgM, IgG
Monospot
Paired serum:
Rubella IgM, IgG
Parvo B-19 IgM, IgG
Measles IgM, IgG, CMV
Fever and arthritis Rubella, parvo B-19, enteroviruses2
Parvo B-19 IgM, IgG
Fever and neurologic signs HSV, WNV4
, polio WNV NAAT blood
CSF for HSV, polio, WNV NAAT
or viral culture
Vesicle fluid/scraping for HSV
Single serum:
WNV IgM, IgG
Vesicular rash VZV, HSV Vesicle fluid/scraping for VZV/HSV VZV IgM , IgG9
Genital ulcers HSV, VZV Vesicle fluid/scraping for HSV/VZV HSV type-specific serology
Hepatitis CMV, EBV, hepatitis A, B, C and E CMV NAAT blood CMV, EBV IgM, IgG
Monospot
HAV IgM
HBsAg10
anti-HBc IgM11
Anti-HCV
HEV IgM, IgG12
Mononucleosis-like illness
(recurrent fever, myalgias,
sore throat ϩ/Ϫ arthritis or
rash)
CMV, LCV, EBV, HIV13
CMV, EBV NAAT blood EBV IgM, IgG
Monospot
HIV IgG
Travelϩ/Ϫ any of the above Hepatitis E, Japanese encephalitis,
hemorrhagic fevers
Consultation with reference
laboratory advised
1
Direct viral isolation of rubella not routinely done as very difficult to culture and rapid methods are not widely available.
2
Enteroviruses – polio, coxsackie and echoviruses – to be considered particularly in the third trimester, during summer/fall season and/or in the context of
aseptic meningitis.
3
Direct viral isolation of measles not routinely done; in low-prevalence countries (USA/Canada) use paired acute and convalescent serum for anti-measles
IgM and IgG: a fourfold increase in anti-measles antibody titer is indicative of infection.
4
WNV to be considered in areas with known WNV transmission.
5
Parvo B-19 viremia by PCR is diagnostic of acute infection and precedes development of IgM by 7–10 days.
6
PCR for enteroviruses amplifies a highly conserved portion of the genome, allowing detection of most enteroviruses from throat swabs, blood, urine, and
stool; sampling multiple sites enhances likelihood of viral detection.
7
CMV IgG avidity test if available.
8
Take acute phase IgG as soon as possible after rash onset (ideally within 7 days) and convalescent phase IgG 10–14 days later.
9
Presence of IgG will rule out acute infection.
10
Hepatitis B surface antigen is positive for 95% of patients with acute hepatitis B.
11
Anti-hepatitis B core antibody particularly useful during “window” period when HbsAg disappears and anti-HB surface antibody appears.
12
Available in Europe, Asia, and Canada but not in the United States.
13
Diagnosis of HIV infection is routinely made only by serology.
CMV, cytomegalovirus; EBV, Epstein-Barr virus, HAV, hepatitis A virus; HSV, herpes simplex virus, LCV, lymphocytic choriomeningitis virus;
NAAT, nucleic acid amplification test (PCR is a type of NAAT); VZV, varicella-zoster virus; WNV, West Nile virus.
NAAT:nucleicacidamplificationtest
PCRisatypeofNAAT
Clinical syndromes associated with viral
infections in pregnancy and diagnostic tests
435
Table 17.2 Clinical syndromes associated with viral infections in pregnancy and diagnostic tests
Clinical syndrome Potential viral infections Direct viral detection Antibodies
Undifferentiated fever CMV, rubella1
, enteroviruses2,6
,
influenza, EBV, measles3
,
parvo B-19, WNV4
CMV, parvo B-195
NAAT blood
Nasopharyngeal wash for influenza
Urine for viral culture
Stool for viral culture6
Single serum:
CMV, EBV IgM, IgG7
WNV IgM
Monospot
Paired serum:
Rubella IgM, IgG8
Parvo B-19 IgM, IgG
Measles IgM, IgG
Fever and nonvesicular rash Rubella, measles, echoviruses2
,
EBV, parvo B-19, CMV
Throat swab for viral NAAT 6
EBV IgM, IgG
Monospot
Paired serum:
Rubella IgM, IgG
Parvo B-19 IgM, IgG
Measles IgM, IgG, CMV
Fever and arthritis Rubella, parvo B-19, enteroviruses2
Parvo B-19 IgM, IgG
Fever and neurologic signs HSV, WNV4
, polio WNV NAAT blood
CSF for HSV, polio, WNV NAAT
or viral culture
Vesicle fluid/scraping for HSV
Single serum:
WNV IgM, IgG
Vesicular rash VZV, HSV Vesicle fluid/scraping for VZV/HSV VZV IgM , IgG9
Genital ulcers HSV, VZV Vesicle fluid/scraping for HSV/VZV HSV type-specific serology
Hepatitis CMV, EBV, hepatitis A, B, C and E CMV NAAT blood CMV, EBV IgM, IgG
Monospot
HAV IgM
HBsAg10
anti-HBc IgM11
Anti-HCV
HEV IgM, IgG12
Mononucleosis-like illness
(recurrent fever, myalgias,
sore throat ϩ/Ϫ arthritis or
rash)
CMV, LCV, EBV, HIV13
CMV, EBV NAAT blood EBV IgM, IgG
Monospot
HIV IgG
Travelϩ/Ϫ any of the above Hepatitis E, Japanese encephalitis,
hemorrhagic fevers
Consultation with reference
laboratory advised
1
Direct viral isolation of rubella not routinely done as very difficult to culture and rapid methods are not widely available.
2
Enteroviruses – polio, coxsackie and echoviruses – to be considered particularly in the third trimester, during summer/fall season and/or in the context of
aseptic meningitis.
3
Direct viral isolation of measles not routinely done; in low-prevalence countries (USA/Canada) use paired acute and convalescent serum for anti-measles
IgM and IgG: a fourfold increase in anti-measles antibody titer is indicative of infection.
4
WNV to be considered in areas with known WNV transmission.
5
Parvo B-19 viremia by PCR is diagnostic of acute infection and precedes development of IgM by 7–10 days.
6
PCR for enteroviruses amplifies a highly conserved portion of the genome, allowing detection of most enteroviruses from throat swabs, blood, urine, and
stool; sampling multiple sites enhances likelihood of viral detection.
7
CMV IgG avidity test if available.
8
Take acute phase IgG as soon as possible after rash onset (ideally within 7 days) and convalescent phase IgG 10–14 days later.
9
Presence of IgG will rule out acute infection.
10
Hepatitis B surface antigen is positive for 95% of patients with acute hepatitis B.
11
Anti-hepatitis B core antibody particularly useful during “window” period when HbsAg disappears and anti-HB surface antibody appears.
12
Available in Europe, Asia, and Canada but not in the United States.
13
Diagnosis of HIV infection is routinely made only by serology.
CMV, cytomegalovirus; EBV, Epstein-Barr virus, HAV, hepatitis A virus; HSV, herpes simplex virus, LCV, lymphocytic choriomeningitis virus;
NAAT, nucleic acid amplification test (PCR is a type of NAAT); VZV, varicella-zoster virus; WNV, West Nile virus.
NAAT:nucleicacidamplificationtest
PCRisatypeofNAAT
Investigation and management of symptomatic
infective illness during pregnancy
MJA 2002; 176: 229–236
Investigation and management of symptomatic
infective illness during pregnancy
MJA 2002; 176: 229–236

26.03.2019
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Common prenatal ultrasound findings of
certain viral infections
CHAPTER 17
436
Traditionally, TORCH serology has been used to aid in
the diagnosis of fetal manifestations of disease like IUGR or
malformations, but given its poor yield and high cost, it is
not widely recommended [16,17]. TORCH testing is an acro-
nym and refers to obtaining antibody titers for Toxoplasma,
syphyllis, HBV, Rubella, CMV and HSV.
Fetal ultrasound is used to follow pregnancies with con-
firmed maternal viral infections or to detect findings suspi-
cious for infection (see Table 17.3). Sequential ultrasound
assessment is crucial for confirmed or suspected infections,
even if initial assessment is normal, to assess fetal growth and
because structural abnormalities may become apparent only
with further development.
Viral infections of predominantly
maternal impact
Influenza A and B
Influenza is a vaccine-preventable febrile respiratory illness,
which affects 10–40% of the general population over a 6-week
period every winter in temperate climates, but year round in
the tropics. Pregnant patients are more susceptible to develop-
ing influenza complications, particularly pneumonia. Although
influenza vaccine is widely recommended for all pregnant
women throughout the flu season, vaccination rates remain low.
Virology
Influenza A and B are single-stranded RNA viruses that rou-
tinely affect humans every year (seasonal influenza). Influenza
A also affects other species like swine and avian. Influenza
viruses undergo frequent variations in their capsular antigens,
resulting in new circulating strains every year. Small, gradual
changes resulting in new strains of an existing influenza sub-
type are called antigenic drifts. Abrupt, major changes result-
ing in new influenza subtypes are called antigenic shifts; these
may arise from recombination of human and animal Influenza
A viruses, i.e. 2009 novel H1N1 Influenza A. These antigenic
changes are responsible for the yearly influenza season and
major pandemics as the population has little or no immunity
against new circulating strains or subtypes.
Pathogenesis
Influenza is acquired by aspiration of small-particle aerosols
(Ͻ10 ␮m) created by sneezing, coughing, and talking [18,19].
The incubation period varies from 18 to 72 hours.
Clinical presentation
The most common clinical course is abrupt onset of fever,
malaise, headache, severe myalgias and cough. Fever typically
lasts 3 days and most people recover within a week. Influenza
pneumonia is more common among patients with pre-existing
Table 17.3 Common prenatal ultrasound findings of certain viral infections
Virus CNS Cardiac Abdominal Placenta Other
CMV Ventriculomegaly
Calcifications
Microcephaly
Cerebellar aplasia
Cardiomegaly
Septal defects
Calcifications
Hepatomegaly
Splenomegaly
Calcifications
Ascites
Echogenic bowel
Placentomegaly IUGR
Hydrops
Demise
Oligohydramnios
Rubella Calcifications
Encephalocele
Microcephaly
Microphthalmia
Ventriculomegaly
Septal defects
Pulmonic stenosis
Coarctation of aorta
Hepatomegaly
Hepatic Calcifications
Splenomegaly
Meconium peritonitis
Calcifications IUGR
Cleft palate
VZV Ventriculomegaly
Calcifications
Microphthalmia
Retinal Calcifications
– Hepatomegaly
Calcifications
Ascites
Small placenta
Calcifications
IUGR
Limb deformities
Oligohydramnios
HSV Hydranencephaly
Ventriculomegaly
Calcifications
Microcephaly
Microphthalmia
– Hepatomegaly
Splenomegaly
Calcifications IUGR
Limb hypoplasia
Parvo B-19 – – – – Hydrops
Polyhydramnios
Increase in MCA-
Doppler velocity
CMV, cytomegalovirus; CNS, central nervous system; HSV, herpes simplex virus; IUGR, intrauterine growth retardation; VZV, varicella-zoster virus.
Infant outcome following cytomegalovirus
(CMV) maternal infection in pregnancy506 SECTION FOUR • Infection
additional training.68
In a different study, only 14% of
women had heard of CMV, indicating the potential of pre-
ventional behavior education.77
Management Options
Treatment of acute, symptomatic CMV infection in the
immunocompetent normal individual is palliative. The vast
majority of infections are asymptomatic; the remainder are
mild. Currently, eradication of the virus is beyond the capac-
ity of modern medicine. In the patient with compromised
immunity, such as the transplant patient or the patient with
AIDS, the antiviral drug ganciclovir provides temporary relief
from such severe effects as retinitis.13
To date, there is no
accepted therapy for acute maternal or neonatal infection.78
There is progress in the development of a specific CMV
vaccine,79
although a number of real and theoretical obsta-
cles remain.80
Even though complete eradication of the virus
may appear unlikely, antibody presence similar to that after
primary human infection could reduce the rate of congenital
fetal infection and its sequelae. Thus, an effective CMV
vaccine will be a significant step forward. Passive immuniza-
tion with specific anti-CMV immunoglobulins appears to be
useful as prophylaxis in cases of renal and marrow transplan-
tation.81
Thus, prevention of maternal infection is clearly the
strategy to avert intrauterine infection. Three different areas
offer potential to reduce the likelihood of maternal CMV
infection in pregnancy: patient education, physician educa-
tion, and vaccine development. CMV is typically spread by
interpersonal contact with transmission of infected secre-
tions from person to person, so, in particular, pregnant
women working in high risk situations (e.g., daycare centers)
should be counseled to wash their hands carefully after
changing diapers and after any contact with children’s secre-
tions (e.g., saliva).78,82
Mouth-to-mouth kissing with children
should be discouraged. Physicians need to be aware of the
risk of transfusion-related CMV transmission.83
Thus, when
transfusing women of childbearing age who could poten-
tially be or soon become pregnant, CMV-negative blood
products should be used whenever possible. Any fetal trans-
fusion in utero must use CMV-negative washed packed cells
to avoid fetal CMV contamination. It is not appropriate,
however, to screen all pregnant women for either anti-CMV
IgG or viral excretion with the aim of isolating them for the
duration of the pregnancy. The most reasonable course is to
serologically screen all women in high risk areas (e.g.,
daycare workers) and recommend to susceptible individuals
Pregnant women of
higher income group
55%
immune
45%
susceptible
0.15%
congenital
infection (recurrent
maternal infection)
1–4%
primary infection
0–1%
infected infants may
have clinically apparent
disease or sequelae
10–15%
disease (mild to severe)
0–1%
disease or sequelae
0.5–1%
congenital
maternal infection)
85–90%
infected infants
are asymptomatic
40%
transmit
infection to fetus
10%
develop normally
90%
develop sequelae
5–15%
develop sequelae
85–95%
develop normally
Pregnant women of
lower income group
85%
immune
15%
susceptible
FIGURE 30–1
(CMV) maternal infection in pregnancy.
(Adapted from Stagno S: Cytomegalovirus. In
Remington JS, Klein JO (eds): Infectious
Diseases of the Fetus and Newborn Infant, 4th
ed. Philadelphia, Saunders, 1995, p 322.)
T A B L E 3 0 – 1
Sequelae in Children with Congenital
Cytomegalovirus Infection According to Type of
Maternal Infection
PRIMARY RECURRENT
Symptomatic disease at birth 24/132 (18%) 0/65 (0%)
Any sequelae 31/125 (25%) 5/64 (8%)
More than one sequela 7/125 (6%) 0/64 (0%)
Sensorineural hearing loss 18/120 (15%) 3/56 (5%)
Bilateral hearing loss 10/120 (8%) 0/56 (0%)
Microcephaly 6/125 (5%) 1/64 (2%)
Seizures 6/125 (5%) 0/64 (0%)
IQ < 70 9/68 (13%) 0/32 (0%)
Death 3/125 (2%) 0/64 (0%)
From Fowler KB, Stagno S, Pass RF, et al: The outcome of congenital cyto-
megalovirus infection in relation to maternal antibody status. N Engl J Med
1992;326:663–667.
506 SECTION FOUR • Infection
additional training.68
In a different study, only 14% of
women had heard of CMV, indicating the potential of pre-
ventional behavior education.77
Management Options
Treatment of acute, symptomatic CMV infection in the
immunocompetent normal individual is palliative. The vast
majority of infections are asymptomatic; the remainder are
mild. Currently, eradication of the virus is beyond the capac-
ity of modern medicine. In the patient with compromised
immunity, such as the transplant patient or the patient with
AIDS, the antiviral drug ganciclovir provides temporary relief
from such severe effects as retinitis.13
To date, there is no
accepted therapy for acute maternal or neonatal infection.78
There is progress in the development of a specific CMV
vaccine,79
although a number of real and theoretical obsta-
cles remain.80
Even though complete eradication of the virus
may appear unlikely, antibody presence similar to that after
primary human infection could reduce the rate of congenital
fetal infection and its sequelae. Thus, an effective CMV
vaccine will be a significant step forward. Passive immuniza-
tion with specific anti-CMV immunoglobulins appears to be
useful as prophylaxis in cases of renal and marrow transplan-
tation.81
Thus, prevention of maternal infection is clearly the
strategy to avert intrauterine infection. Three different areas
offer potential to reduce the likelihood of maternal CMV
infection in pregnancy: patient education, physician educa-
tion, and vaccine development. CMV is typically spread by
interpersonal contact with transmission of infected secre-
tions from person to person, so, in particular, pregnant
women working in high risk situations (e.g., daycare centers)
should be counseled to wash their hands carefully after
changing diapers and after any contact with children’s secre-
tions (e.g., saliva).78,82
Mouth-to-mouth kissing with children
should be discouraged. Physicians need to be aware of the
risk of transfusion-related CMV transmission.83
Thus, when
transfusing women of childbearing age who could poten-
tially be or soon become pregnant, CMV-negative blood
products should be used whenever possible. Any fetal trans-
fusion in utero must use CMV-negative washed packed cells
to avoid fetal CMV contamination. It is not appropriate,
however, to screen all pregnant women for either anti-CMV
IgG or viral excretion with the aim of isolating them for the
duration of the pregnancy. The most reasonable course is to
serologically screen all women in high risk areas (e.g.,
daycare workers) and recommend to susceptible individuals
Pregnant women of
higher income group
55%
immune
45%
susceptible
0.15%
congenital
maternal infection)
1–4%
primary infection
0–1%
disease or sequelae
10–15%
disease (mild to severe)
0–1%
disease or sequelae
0.5–1%
congenital
maternal infection)
85–90%
infected infants
are asymptomatic
40%
transmit
infection to fetus
10%
develop normally
90%
develop sequelae
5–15%
develop sequelae
85–95%
develop normally
Pregnant women of
lower income group
85%
immune
15%
susceptible
FIGURE 30–1
(CMV) maternal infection in pregnancy.
(Adapted from Stagno S: Cytomegalovirus. In
Remington JS, Klein JO (eds): Infectious
Diseases of the Fetus and Newborn Infant, 4th
ed. Philadelphia, Saunders, 1995, p 322.)
T A B L E 3 0 – 1
Sequelae in Children with Congenital
Cytomegalovirus Infection According to Type of
Maternal Infection
PRIMARY RECURRENT
Symptomatic disease at birth 24/132 (18%) 0/65 (0%)
Any sequelae 31/125 (25%) 5/64 (8%)
More than one sequela 7/125 (6%) 0/64 (0%)
Sensorineural hearing loss 18/120 (15%) 3/56 (5%)
Bilateral hearing loss 10/120 (8%) 0/56 (0%)
Microcephaly 6/125 (5%) 1/64 (2%)
Seizures 6/125 (5%) 0/64 (0%)
IQ < 70 9/68 (13%) 0/32 (0%)
Death 3/125 (2%) 0/64 (0%)
From Fowler KB, Stagno S, Pass RF, et al: The outcome of congenital cyto-
megalovirus infection in relation to maternal antibody status. N Engl J Med
1992;326:663–667.
High risk pregnancy : management options 5th edition 2011 p. 506
CMV
Cytomegalovirus
Relative changes in CMV IgM, IgG, and IgG avidity levels
over time following primary CMV infection.
IgM pattern A represents the typical IgM response
pattern, whereas IgM pattern B represents long-term
IgM persistence.
In a CMV IgG-positive individual, an IgM-positive result
of 20 indicates infection around 3 months previously if
the individual exhibits IgM pattern A but around 6
months previously if the individual exhibits IgM pattern
B.
By employing CMV IgG avidity testing, the correct time
since infection can be determined;
a low-avidity result (expected to be about 30 based on
this figure) indicates primary infection about 3 months
previously,
whereas a high-avidity result (expected to be about 70)
indicates primary infection more than 6 months
previously.
CMV
Algorithm for assessment of CMV infection in pregnancy

26.03.2019
4
Cytomegalovirus
CMV
VZV in pregnancy: treatment and prevention
CHAPTER 17
448
VZV pneumonia
A high index of suspicion is required in the presence of risk
factors for development of VZV pneumonia, including third
trimester, smoking, co-morbidities (asthma/COPD, transplant
recipients) and severe rash. Respiratory symptoms should
prompt hospitalization, assessment with chest X-rays, trans-
cutaneous oxygen saturation and treatment with intravenous
acyclovir 10 mg/kg every 8 hours.
Table 17.4 VZV in pregnancy: treatment and prevention
Clinical situation Maternal intervention Fetal surveillance Intervention for newborn
Susceptible mother with close
exposure at any point in
pregnancy
• Confirm susceptible status:
VZV serology
• If susceptible, consider
administration of VZ IG
(presently only available in the
US as lyophilized purified
varicella immune globulin
(VariZIG™) or immune
globulin (IVIG)) within 96 hours
of exposure
• No intervention necessary if
mother not susceptible or
mother does not develop
clinical syndrome
• No intervention necessary if mother
not susceptible or mother does not
develop clinical syndrome
Uncomplicated maternal
chickenpox in the first 20 weeks
of pregnancy
• Symptom control for fever,
pruritus and volume depletion
• May consider oral acyclovir
800 mg 5 times/day for 7 days
to reduce duration of rash and
number of lesions
• Contact (gloves, gowns) and
air-borne precautions if
in hospital
• Discussion on risk of
congenital varicella syndrome
(CVS) and continuation of
pregnancy is warranted
• Level II ultrasound
at 18–20 weeks and/or 5 weeks
after onset of maternal rash, plus
• Sequential ultrasound over the
course of pregnancy to detect
features of in utero recurrent
fetal infection
• Consider fetal MRI for CNS
abnormalities not seen on
ultrasound
• Ophthalmologic exam at birth
highly recommended
chickenpox any time between
20 weeks of gestation to 5 days
prior to delivery
number of lesions
air-borne precautions if in
hospital
• Not an indication for
termination of pregnancy as
risk of CVS is extremely low
• Level II ultrasound at
18–20 weeks and/or 5 weeks
after onset of maternal rash
chickenpox 5 days before
delivery or 2 days post partum
As above No special monitoring required • VZ IG at birth or as soon as
maternal rash is recognized
• IV acyclovir if severe illness
• Contact (gloves, gowns) and air-
borne precautions in the nursery
Complicated maternal
chickenpox (pneumonia, CNS
disease) or disseminated zoster
• Admit to hospital: respiratory
support may be required
• IV Acyclovir
• Consider IV antibiotics for
pneumonia superinfection
• Contact and air-borne
precautions
As above for relevant
gestational age
As above for relevant gestational age
Maternal zoster in late
pregnancy
• Confirm diagnosis if
lumbosacral area with PCR
or DFA
• Consider use of acyclovir
800 mg PO 5 times/day within
first 72 hours of rash appearing
No special monitoring required Contact (gloves, gowns) and air-borne
precautions in the nursery if zoster
confirmed
VZV
VZV in pregnancy: treatment and prevention
CHAPTER 17
448
VZV pneumonia
A high index of suspicion is required in the presence of risk
factors for development of VZV pneumonia, including third
trimester, smoking, co-morbidities (asthma/COPD, transplant
recipients) and severe rash. Respiratory symptoms should
prompt hospitalization, assessment with chest X-rays, trans-
cutaneous oxygen saturation and treatment with intravenous
acyclovir 10 mg/kg every 8 hours.
Table 17.4 VZV in pregnancy: treatment and prevention
Clinical situation Maternal intervention Fetal surveillance Intervention for newborn
Susceptible mother with close
exposure at any point in
pregnancy
• Confirm susceptible status:
VZV serology
• If susceptible, consider
administration of VZ IG
(presently only available in the
US as lyophilized purified
varicella immune globulin
(VariZIG™) or immune
globulin (IVIG)) within 96 hours
of exposure
• No intervention necessary if
mother not susceptible or
mother does not develop
clinical syndrome
• No intervention necessary if mother
not susceptible or mother does not
develop clinical syndrome
chickenpox in the first 20 weeks
of pregnancy
number of lesions
air-borne precautions if
in hospital
• Discussion on risk of
congenital varicella syndrome
(CVS) and continuation of
pregnancy is warranted
• Level II ultrasound
at 18–20 weeks and/or 5 weeks
after onset of maternal rash, plus
• Sequential ultrasound over the
course of pregnancy to detect
features of in utero recurrent
fetal infection
• Consider fetal MRI for CNS
abnormalities not seen on
ultrasound
highly recommended
chickenpox any time between
20 weeks of gestation to 5 days
prior to delivery
number of lesions
air-borne precautions if in
hospital
• Not an indication for
termination of pregnancy as
risk of CVS is extremely low
• Level II ultrasound at
18–20 weeks and/or 5 weeks
after onset of maternal rash
chickenpox 5 days before
delivery or 2 days post partum
As above No special monitoring required • VZ IG at birth or as soon as
maternal rash is recognized
• IV acyclovir if severe illness
• Contact (gloves, gowns) and air-
borne precautions in the nursery
Complicated maternal
chickenpox (pneumonia, CNS
disease) or disseminated zoster
• Admit to hospital: respiratory
support may be required
• IV Acyclovir
• Consider IV antibiotics for
pneumonia superinfection
• Contact and air-borne
precautions
As above for relevant
gestational age
As above for relevant gestational age
Maternal zoster in late
pregnancy
• Confirm diagnosis if
lumbosacral area with PCR
or DFA
• Consider use of acyclovir
800 mg PO 5 times/day within
first 72 hours of rash appearing
No special monitoring required Contact (gloves, gowns) and air-borne
precautions in the nursery if zoster
confirmed
VZV
Management of pregnant women with VZV
exposure and infection.
CHAPTER 17
lymphocyte transformation after stimulation with different
VZV antigens.24
Treatment and prevention
In adults and children, acute infection with VZV is self-limited
and treatment is generally directed at the symptoms. Table
17.7 summarizes the management of pregnant women who
have been exposed to, or who develop, acute chickenpox.
Pregnant women exposed to chickenpox should have their
immune status identified; within 96h of exposure, those found
to be susceptible should receive varicella zoster immunoglob-
ulin (VZIG) at a dose of 0.125mg/kg of body weight. Of preg-
nant women exposed to VZV who were administered VZIG,
only 20% developed primary varicella compared with 89% of
patients who did not receive VZIG.18
When administered more
than 96 h after exposure, the efficacy of VZIG is questionable.
Infants born to women who develop chickenpox from 5 days
before and up to 2 days after delivery should be given VZIG.
Both pregnant and nonpregnant patients with herpes zoster
benefit from a short course of antiviral therapy to shorten the
duration of postherpetic neuralgia. These antiviral agents
include acyclovir, valaciclovir, and famciclovir.
The VZV vaccine is the Oka strain of a live attenuated virus
obtained from a child in Japan with a natural chickenpox
infection, which was introduced into human embryonic lung
cell cultures, and propagated in human diploid cell cultures.
The vaccine was first introduced to high-risk children in
Europe in 1984, in Japan in 1986, and in Korea in 1988; it
was subsequently licensed in the USA in 1995. Seroimmunity
is conferred 4–6 weeks after vaccination in 97% of suscepti-
ble children. The reported annual attack rate of chickenpox
among vaccinated children is 0.2–1.0%, compared with 8–9%
254
Table 17.6 Clinical manifestations of VZV infection in newborns
and adults.
Birth defects
General: spontaneous abortion, fetal demise, premature delivery,
low birthweight
Congenital varicella syndrome, which includes any of the following
findings:
Neurological: cerebral cortical atrophy, microcephaly, encephalitis,
seizures, mental retardation, intracranial calcifications, bulbar
palsy, cerebellar hypoplasia, ventriculomegaly,
neurodevelopmental delay, nystagmus
Ophthalmological: microphthalmia, optic atrophy, cataracts,
chorioretinitis, anisocoria, corneal opacification, hydrocephalus,
meningocele
Dermatological: cicatricial scarring of limb, vesicular lesions over
dermatomal pattern
Limb disorder: limb hypoplasia ipsilateral to skin scarring, limb
paresis, hypotonia, areflexia, flexion contracture deformities
Gastrointestinal: duodenal stenosis, colon atresia
Miscellaneous: Horner syndrome, hydroureter
Clinical findings
Mother: chickenpox, pneumonia, encephalitis, Reye syndrome,
aseptic meningitis, Guillain–Barré syndrome, ophthalmological
complications (conjunctivitis, uveitis), hepatitis, shingles (zoster),
pneumonitis, esophagitis, myocarditis, herpes gangrenosum;
laboratory diagnoses include VZV-specific IgG and IgM, virus
culture, viral antigen, detection of viral DNA using PCR
Infant: four distinct clinical presentations:
(1) Congenital varicella syndrome
(2) Disseminated varicella; generalized lesions, pneumonia,
hepatitis, viremia
(3) Neonatal varicella
(4) Neonatal zoster (shingles)
Laboratory diagnoses include VZV-specific IgG and IgM, virus
culture, detection of viral DNA using PCR
Table 17.7 Management of pregnant women with VZV exposure
and infection.
Pregnant women with VZV exposure, within 96h of exposure
Test for VZV IgG
If IgG positive, confirms previous immunity, discontinue evaluation
If IgG negative, administer VZIG, 0.125mg/kg i.m.
Observe for symptoms of chickenpox
Pregnant women with VZV exposure, more than 96h after
exposure
Test for VZV IgG
If IgG negative, efficacy of VZIG questionable, weigh risks and
benefits of vaccine administration
Pregnant women with primary chickenpox
Isolate from susceptible persons
Test for VZV IgG
Treat symptoms
Infection within the first 20 weeks of gestation:
Counsel approximately 2–5% risk of congenital varicella
syndrome, miscarriage, prematurity, low birthweight
Observe for complications (e.g., varicella pneumonia)
Consider acyclovir for pneumonia
VZIG not necessary
Infection from 20 to 5 days before delivery:
Counsel about risk for neonatal chickenpox
Observe infant for chickenpox
VZIG not necessary
Infection from 5 days before and up to 2 days after delivery
Counsel approximately 30% risk of disseminated varicella
Observe infant for disseminated varicella
Administer VZIG to infant at birth, 1.25–2mL i.m.
Consider acyclovir for symptomatic infant
Consider delaying birth until mother recovers from acute
infection
Pregnant women with herpes zoster (shingles)
Counsel theoretical risk of neonatal infection
Isolate from susceptible persons (vesicular fluid is infectious)
Treat symptoms
Administer famciclovir for postherpetic neuralgia
TCO17 9/13/06 4:58 PM Page 254
CHAPTER 17
lymphocyte transformation after stimulation with different
VZV antigens.24
Treatment and prevention
In adults and children, acute infection with VZV is self-limited
and treatment is generally directed at the symptoms. Table
17.7 summarizes the management of pregnant women who
have been exposed to, or who develop, acute chickenpox.
Pregnant women exposed to chickenpox should have their
immune status identified; within 96h of exposure, those found
to be susceptible should receive varicella zoster immunoglob-
ulin (VZIG) at a dose of 0.125mg/kg of body weight. Of preg-
nant women exposed to VZV who were administered VZIG,
only 20% developed primary varicella compared with 89% of
patients who did not receive VZIG.18
When administered more
than 96 h after exposure, the efficacy of VZIG is questionable.
Infants born to women who develop chickenpox from 5 days
before and up to 2 days after delivery should be given VZIG.
Both pregnant and nonpregnant patients with herpes zoster
benefit from a short course of antiviral therapy to shorten the
duration of postherpetic neuralgia. These antiviral agents
include acyclovir, valaciclovir, and famciclovir.
The VZV vaccine is the Oka strain of a live attenuated virus
obtained from a child in Japan with a natural chickenpox
infection, which was introduced into human embryonic lung
cell cultures, and propagated in human diploid cell cultures.
The vaccine was first introduced to high-risk children in
Europe in 1984, in Japan in 1986, and in Korea in 1988; it
was subsequently licensed in the USA in 1995. Seroimmunity
is conferred 4–6 weeks after vaccination in 97% of suscepti-
ble children. The reported annual attack rate of chickenpox
among vaccinated children is 0.2–1.0%, compared with 8–9%
254
Table 17.6 Clinical manifestations of VZV infection in newborns
and adults.
Birth defects
General: spontaneous abortion, fetal demise, premature delivery,
low birthweight
Congenital varicella syndrome, which includes any of the following
findings:
Neurological: cerebral cortical atrophy, microcephaly, encephalitis,
seizures, mental retardation, intracranial calcifications, bulbar
palsy, cerebellar hypoplasia, ventriculomegaly,
neurodevelopmental delay, nystagmus
Ophthalmological: microphthalmia, optic atrophy, cataracts,
chorioretinitis, anisocoria, corneal opacification, hydrocephalus,
meningocele
Dermatological: cicatricial scarring of limb, vesicular lesions over
dermatomal pattern
Limb disorder: limb hypoplasia ipsilateral to skin scarring, limb
paresis, hypotonia, areflexia, flexion contracture deformities
Gastrointestinal: duodenal stenosis, colon atresia
Miscellaneous: Horner syndrome, hydroureter
Clinical findings
Mother: chickenpox, pneumonia, encephalitis, Reye syndrome,
aseptic meningitis, Guillain–Barré syndrome, ophthalmological
complications (conjunctivitis, uveitis), hepatitis, shingles (zoster),
pneumonitis, esophagitis, myocarditis, herpes gangrenosum;
laboratory diagnoses include VZV-specific IgG and IgM, virus
culture, viral antigen, detection of viral DNA using PCR
Infant: four distinct clinical presentations:
(1) Congenital varicella syndrome
(2) Disseminated varicella; generalized lesions, pneumonia,
hepatitis, viremia
(3) Neonatal varicella
(4) Neonatal zoster (shingles)
Laboratory diagnoses include VZV-specific IgG and IgM, virus
culture, detection of viral DNA using PCR
Table 17.7 Management of pregnant women with VZV exposure
and infection.
Pregnant women with VZV exposure, within 96h of exposure
Test for VZV IgG
If IgG positive, confirms previous immunity, discontinue evaluation
If IgG negative, administer VZIG, 0.125mg/kg i.m.
Pregnant women with VZV exposure, more than 96h after
exposure
Test for VZV IgG
If IgG negative, efficacy of VZIG questionable, weigh risks and
benefits of vaccine administration
Pregnant women with primary chickenpox
Isolate from susceptible persons
Test for VZV IgG
Treat symptoms
Infection within the first 20 weeks of gestation:
Counsel approximately 2–5% risk of congenital varicella
syndrome, miscarriage, prematurity, low birthweight
Observe for complications (e.g., varicella pneumonia)
Consider acyclovir for pneumonia
VZIG not necessary
Infection from 20 to 5 days before delivery:
Counsel about risk for neonatal chickenpox
Observe infant for chickenpox
VZIG not necessary
Infection from 5 days before and up to 2 days after delivery
Counsel approximately 30% risk of disseminated varicella
Observe infant for disseminated varicella
Administer VZIG to infant at birth, 1.25–2mL i.m.
Consider acyclovir for symptomatic infant
Consider delaying birth until mother recovers from acute
infection
Pregnant women with herpes zoster (shingles)
Counsel theoretical risk of neonatal infection
Isolate from susceptible persons (vesicular fluid is infectious)
Treat symptoms
Administer famciclovir for postherpetic neuralgia
TCO17 9/13/06 4:58 PM Page 254
VZV
Algorithm for assessment of VZV infection in pregnancy
Rubella
T A B L E 2 9 – 1
Abnormalities in Congenital Rubella: Triad
of Gregg
ABNORMALITY DESCRIPTION
Eye
Cataract Usually bilateral and present at
birth.
Retinopathy “Salt and pepper” appearance, may
have a delayed onset, frequently
bilateral, visual acuity is not
affected.
Microphthalmia Often associated with cataract.
Glaucoma Rare but leads to blindness if not
recognized.
Heart
Patent ductus arteriosus Common, often associated with
persistence of the foramen ovale.
Pulmonary valvular stenosis Common, due to intimal
proliferation and arterial elastic
hypertrophy.
Pulmonary artery stenosis
Coarctation of the aorta Infrequent.
Ventricular septal defects Rare.
Atrial septal defects Rare.
Ear
Commonly damaged Injury of cells of the middle ear
leading to sensorineural deafness
may also have a central origin.
Bilateral and progressive May be present at birth or develop
later in childhood. Severe enough
for the child to need education at a
special school; rare when maternal
rubella occurs after the fourth mo of
pregnancy.
Adapted from Freij BJ, South MA, Sever JL, et al: Maternal rubella and the
congenital rubella syndrome. Clin Perinatol 1988;15:247–257.
pregnant women. However, the Centers for Disease Control
and Prevention (CDC) have monitored inadvertent rubella
vaccination during pregnancy, collecting over 500 cases. No
case of CRS due to vaccination was documented, although
virus was isolated from the conceptus in several cases.17
Thus, patients inadvertently vaccinated during pregnancy,
or becoming pregnant shortly after vaccination, should be
reassured and counseled that the risk of fetal infection is
negligible.18,19
Furthermore, follow-up studies on fetuses
inadvertently exposed to rubella vaccine RA27/3 in preg-
nancy in Costa Rica did not have increased rates of miscar-
riage or stillbirth.20
Prenatal
A pregnant woman infected with rubella is at little risk.
However, depending on the gestational age at infection, the
fetus may be at great risk for congenital anomalies. Methods
for in utero diagnosis include fetal blood sampling measure-
ment of rubella-specific IgM,21
rubella-specific reverse tran-
scriptase polymerase chain reaction (RT-PCR), and virus
isolation from amniotic fluid or products of conception.22,23
RT-PCR can detect the presence of viral RNA even when
the fetal rubella virus–specific IgM obtained by fetal blood
sampling is negative.24
Although these tests may indicate
fetal infection, the counseling is largely based on the gesta-
tional age–related risk of congenital abnormalities due to
CRS. No treatment other than pregnancy termination is
available.
Treatment for acute maternal rubella is generally symp-
tomatic. Rarely, patients who develop thrombocytopenia or
encephalitis may benefit from glucocorticoids or platelet
transfusion. Immunoglobulin for pregnant women with
acute infection is controversial. Furthermore, no data suggest
that immunoglobulin will prevent fetal anomalies.
Labor, Delivery, and Postnatal
Acute infection during these time periods is unlikely. If sus-
pected, appropriate infection control measures should be
instituted. The neonate should be evaluated for infection
following birth.
T A B L E 2 9 – 2
Fetal Consequences of Symptomatic Maternal Rubella during Pregnancy
INFECTION DEFECTS
STAGE OF
PREGNANCY (WK) NO. TESTED NO. POSITIVE NO. FOLLOWED RATE (%)
OVERALL RISK OF DEFECT (RATE OF
INFECTION × RATE OF DEFECTS) (%)
<11 10 9 (90%) 9 100 90
11–12 6 4 (67%) 4 50 33
13–14 18 12 (67%) 12 17 11
15–16 36 17 (47%) 14 50 24
17–18 33 13 (39%) 10 0 0
19–22 59 20 (34%)
23–26 32 8 (25%)
27–30 31 11 (35%)
31–36 25 15 (60%) 53 0 0
>36 8 8 (100%)
Total 258 117 (45%) 102 20 9
From Miller E, Cradock-Watson JE, Pollock TM: Consequences of confirmed maternal rubella at successive stages of pregnancy. Lancet 1982;2:781–784.
T A B L E 2 9 – 1
Abnormalities in Congenital Rubella: Triad
of Gregg
ABNORMALITY DESCRIPTION
Eye
Cataract Usually bilateral and present at
birth.
Retinopathy “Salt and pepper” appearance, may
have a delayed onset, frequently
bilateral, visual acuity is not
affected.
Microphthalmia Often associated with cataract.
Glaucoma Rare but leads to blindness if not
recognized.
Heart
Patent ductus arteriosus Common, often associated with
persistence of the foramen ovale.
Pulmonary valvular stenosis Common, due to intimal
proliferation and arterial elastic
hypertrophy.
Pulmonary artery stenosis
Coarctation of the aorta Infrequent.
Ventricular septal defects Rare.
Atrial septal defects Rare.
Ear
Commonly damaged Injury of cells of the middle ear
leading to sensorineural deafness
may also have a central origin.
Bilateral and progressive May be present at birth or develop
later in childhood. Severe enough
for the child to need education at a
special school; rare when maternal
rubella occurs after the fourth mo of
pregnancy.
Adapted from Freij BJ, South MA, Sever JL, et al: Maternal rubella and the
congenital rubella syndrome. Clin Perinatol 1988;15:247–257.
pregnant women. However, the Centers
and Prevention (CDC) have monitored
vaccination during pregnancy, collectin
case of CRS due to vaccination was do
virus was isolated from the conceptu
Thus, patients inadvertently vaccinate
or becoming pregnant shortly after va
reassured and counseled that the risk
negligible.18,19
Furthermore, follow-up
inadvertently exposed to rubella vacci
nancy in Costa Rica did not have incre
riage or stillbirth.20
Prenatal
A pregnant woman infected with rub
However, depending on the gestational
fetus may be at great risk for congenital
for in utero diagnosis include fetal bloo
ment of rubella-specific IgM,21
rubella-
scriptase polymerase chain reaction (
isolation from amniotic fluid or produc
RT-PCR can detect the presence of vi
the fetal rubella virus–specific IgM obt
sampling is negative.24
Although these
fetal infection, the counseling is largely
tional age–related risk of congenital a
CRS. No treatment other than pregn
available.
Treatment for acute maternal rubella
tomatic. Rarely, patients who develop t
encephalitis may benefit from glucoc
transfusion. Immunoglobulin for pre
acute infection is controversial. Furtherm
that immunoglobulin will prevent fetal
Acute infection during these time perio
pected, appropriate infection control
instituted. The neonate should be eva
following birth.
T A B L E 2 9 – 2
Fetal Consequences of Symptomatic Maternal Rubella during Pregnancy
INFECTION DEFECTS
STAGE OF
PREGNANCY (WK) NO. TESTED NO. POSITIVE NO. FOLLOWED RATE (%)
OVERALL RISK
INFECTION ×
<11 10 9 (90%) 9 100
11–12 6 4 (67%) 4 50
13–14 18 12 (67%) 12 17
15–16 36 17 (47%) 14 50
17–18 33 13 (39%) 10 0
19–22 59 20 (34%)
23–26 32 8 (25%)
27–30 31 11 (35%)
31–36 25 15 (60%) 53 0
>36 8 8 (100%)
Total 258 117 (45%) 102 20
From Miller E, Cradock-Watson JE, Pollock TM: Consequences of confirmed maternal rubella at successive stages of pregnancy. Lance
Rubella

26.03.2019
5
Rubella
Rubella
Rubella
Rubella
Algorithm for assessment of rubella infection in pregnancy
Herpes Simplex Virus
HSV
HSV

26.03.2019
6
HSV
Algorithm for assessment of HSV infection in pregnancy
and in neonates
Risk factors for transmission of HSV from
mother to infant.
CHAPTER 17
of clinical manifestations. Infants infected transplacentally
present with symptoms within the first 24–48h of life. In
contrast, infants who acquire HSV at the time of birth
become clinically symptomatic within 1–2 weeks. One-half of
the infants with CNS manifestations will also have SEM
characteristics. CNS complications in infants, such as herpes
encephalitis, can be life-threatening and carry a mortality rate
of approximately 50%. Disseminated HSV with encephalitis
carries the worst prognosis for infants, with a mortality rate
of approximately 80%.
Diagnosis
In adults and adolescents, genital infections with HSV are
usually diagnosed clinically. Up to one-fourth of patients who
present with a first-episode infection show serological evidence
of a previous infection; these patients are, in fact, experienc-
ing a recurrent infection. Commercial assays for HSV2-
specific antibodies are useful in confirming a previous
infection; however, cross-reactivity with HSV1 antibodies is
possible. HSV2-specific IgG is detectable 2–12 weeks after
exposure, with a mean seroconversion time of 22 days.29
Therefore, many patients with primary infections do not
demonstrate serological evidence of infection at the time of
symptomatic clinical presentation. Virus isolation from vesicle
fluid obtained from fresh lesions or from the cervix is the most
specific laboratory method for detection of HSV.
Diagnosis of neonatal herpes includes a maternal history of
HSV infection (primary or recurrent), clinical symptoms in the
256
Table 17.8 Risk factors for transmission of HSV from mother to
infant.
Incidence of neonatal HSV 1/3000–1/20000 live births
Primary methods of infection
Transplacental (in utero) 5%
Intrapartum 85%
Postpartum 10%
Risk of perinatal transmission
Primary infection 30–50%
Nonprimary first episode 33%
Recurrent < 5%
Percentage of infants with clinical syndrome at birth
SEM disease 30%
CNS disease only 30%
Disseminated HSV 30%
SEM, neonatal herpes involving skin, eyes, and mouth.
Table 17.9 Clinical manifestations HSV infection in infants.
Site Early symptoms Late symptoms
Skin Vesicles Recurrent cutaneous lesions
Exanthem
Skin scarring
Eye Chorioretinitis Chorioretinitis
Keratoconjunctivitis Blindness
Microphthalmia Cataracts
Cataracts Retinal dysplasia
Mouth Oral ulcerations
CNS Microcephaly Microcephaly
Cerebral atrophy Psychomotor retardation
Hydrancephaly Learning disability
Intracranial calcifications Spasticity
Encephalitis (bulging fontanelles, pyramidal Seizures
tract signs, poor feeding, temperature Porencephalic cysts
instability) Hydrancephaly
Disseminated Shock
HSV Disseminated intravascular coagulopathy
Jaundice
Respiratory distress
Seizures
Irritability
Thrombocytopenia
Miscellaneous Hepatosplenomegaly Hearing loss
Pneumonitis Dental anomalies
Purpura/petechiae Pneumonitis
TCO17 9/13/06 4:58 PM Page 256
HSV
Antiviral treatment options for HSV infection
in adults
TERATOGENIC VIRUSES
infant (Table 17.9), and laboratory evidence of infection in
both mother and infant. Because viral shedding may be asymp-
tomatic in the cervix of pregnant women, symptomatic disease
in the mother is not a requisite for the diagnosis of infection
in the newborn. Detection of HSV1- and HSV2-specific
IgM in the newborn may be helpful in the diagnosis of con-
genital infection. As in adults, virus isolation from skin vesi-
cles, conjunctiva, nasopharynx, and cerebrospinal fluid
remains the gold standard in the diagnosis of HSV in infants.
Unfortunately, however, virus isolation carries a false-negative
rate as high as 20% in primary infection and even higher in
recurrent disease. Recent data on the detection of viral DNA
using PCR show that this technique has greater specificity and
sensitivity than classical virus isolation techniques.34
Treatment
HSV infections in adults and adolescents are treated sympto-
matically. Antiviral therapy with aciclovir has been shown to
be effective in: (1) reducing both the severity and duration
of symptoms in primary infection; (2) preventing the occur-
rence and reducing the frequency of recurrent outbreaks; and
(3) treating fulminant, disseminated HSV in adults and
infants.
Aciclovir is a synthetic thymidine analog that acts as a com-
petitive inhibitor of HSV1 and HSV2 DNA polymerase. The
drug has also been shown to have in vitro and in vivo antivi-
ral activity against CMV, VZV, and Epstein–Barr virus. HSV
thymidine kinase phosphorylates aciclovir and the resulting
triphosphate derivative terminates the elongating chain, thus
inhibiting further viral replication. Second-generation thymi-
dine analogs (famciclovir and valaciclovir) are also approved
treatments for HSV; in vivo, valaciclovir is converted to aci-
clovir, while the active antiviral agent in famciclovir is penci-
clovir. Table 17.11 summarizes treatment options using these
three antiviral drugs. Topical treatments for both genital and
oral lesions have not been shown to be effective.
Acyclovir has been shown to be effective in the treatment
of neonatal HSV infections. Vidarabine, another nucleoside
257
Table 17.10 Clinical manifestations of HSV infection in mothers
and infants.
Birth defects
General: miscarriage, preterm delivery
Early and late symptoms: see Table 17.9
Clinical findings
Mother: mostly asymptomatic; when symptoms are present, genital
and extragenital lesions (painful, vesicular to ulcerative lesions),
gingivostomatitis, pharyngitis, herpetic whitlow, keratitis,
penumonitis, hepatitis; disseminated HSV; laboratory diagnoses
include HSV1- and HSV2-specific IgG and IgM, viral antigen,
virus isolation, detection of viral DNA using PCR
Infant: see Table 17.9; laboratory diagnoses include HSV1- and
HSV2-specific IgG and IgM, virus isolation, detection of viral
DNA using PCR
Table 17.11 Antiviral treatment options for HSV infection in adults.29
Type of infection Drug Dosage Pregnancy category
First episode (primary or nonprimary)
Treat for 7–10 days Acyclovir 400mg p.o. t.i.d. B
Acyclovir 200mg p.o. 5 × /day
Valaciclovir 1g p.o. b.i.d. B
Famciclovir 250mg p.o. t.i.d. B
Recurrent disease
Treat for 5 days Acyclovir 400mg p.o. t.i.d.
Acyclovir 200mg p.o. 5 × /day
Valaciclovir 500mg p.o. b.i.d.
Valaciclovir 1g po q.d.
Famciclovir 125mg p.o. b.i.d.
Suppressive therapy
May be given for several years Acyclovir 400mg p.o. b.i.d.
Valaciclovir 0.5–1g p.o. b.i.d.
Famciclovir 250mg p.o. b.i.d.
Herpes zoster (recurrent VZV)
Treat for 7–10 days Acyclovir 800mg p.o. 5 × /day
Valaciclovir 1g p.o. t.i.d.
Famciclovir 500mg p.o. t.i.d.
TCO17 9/13/06 4:58 PM Page 257
HSV
Parvovirus B19
Algorithm for assessment of parvovirus B19 infection in
pregnancy

26.03.2019
7
Hepatitis A
Hepatitis A
Hepatitis B
Hepatitis B
Hepatitis C
Hepatitis C
Hepatitis
CREASY AND RESNIK’S MATERNAL-FETAL MEDICINE: PRINCIPLES AND PRACTICE, SIXTH EDITION
2009 p738
HSV
Human Immunodeficiency Virus
CHAPTER 28 • Human Immunodeficiency Virus 489
Management Options
Evidence Quality and
Recommendation References
Recommend against conception until HIV RNA level
undetectable and no indication for opportunistic
infection prophylaxis (CD4+ cell count >200/mm3
for >6 mo).
IIa/B 29,79
Complete other routine preconception assessments
such as genetic screening, evaluation for other
medical conditions.
IIa/B 29
If partner is HIV-negative, discuss methods to avoid
unprotected intercourse: male condoms for all
intercourse and artificial insemination for
conception.
GPP
Recommend folate supplementation. Ia/A 29
Prenatal Screening Policy
Offer opt-out testing for HIV to all pregnant women,
rescreen in third trimester in high-prevalence areas
and in women with ongoing risk.
—/GPP —
Prenatal HIV-positive Patients
Assess immunization status and update as needed
for pneumococcus, influenza, hepatitis A and B,
tetanus.
Ia/A 79
Assess antibody status to hepatitis C, Toxoplasma
gondii, and CMV if not previously documented.
IIa/B 79
Perform tuberculin skin test if not done in past year. Ia/A 79
Counsel regarding risk of transmission, methods to
minimize risk (antiretroviral therapy with scheduled
cesarean delivery if HIV RNA >1000 copies/mL after
34 wk), lack of impact of pregnancy on maternal
disease progression, symptoms of drug toxicity,
possible effects of therapy on infant, evaluation of
infant after birth for HIV status.
Ia/A 29
Assess indications for antiretroviral therapy and
opportunistic infection prophylaxis with HIV RNA
level, CD4+ lymphocyte count. For women already
on therapy, discuss risks/benefits of continuing or
stopping. Modify regimen if first trimester and on
efavirenz. If not on therapy, recommend highly
active antiretroviral regimen including zidovudine for
all women starting after first trimester, regardless of
HIV RNA and CD4+ cell count. Provide opportunistic
infection prophylaxis according to adult guidelines.
Ia/A 29,79
Monitor HIV RNA levels monthly after changing or
initiating therapy. Level should drop by ≥1 log in
II/B 28
HIV
Management Options
for >6 mo).
IIa/B 29,79
medical conditions.
IIa/B 29
conception.
GPP
—/GPP —
tetanus.
Ia/A 79
IIa/B 79
Ia/A 29
Ia/A 29,79
first 4–8 wk.
II/B 28
Monitor CD4+ lymphocyte counts each trimester. Ia/B 29
Perform complete blood count, liver enzymes, renal
function frequently (every 2–4 wk) on new regimen,
monthly in third trimester.
Ia/A 29
Perform HIV resistance testing for women with
detectable HIV RNA levels before initiating therapy
or if not responding appropriately to therapy or if
rebound from undetectable.
II/B 28,82
Perform ultrasound at 18–20 wk’ gestation to rule
out anomalies and confirm dates
—/GPP —
Discuss risks versus benefits of scheduled
cesarean delivery. Recommend for HIV RNA levels
>1000 copies/mL after 34 wk. Schedule at or after
38 wk’ gestation if dating criteria adequate. Perform
vaginal delivery only if on antiretroviral therapy with
undetectable HIV RNA.
Ia/A 29,86
HIV

26.03.2019
8
Management Options
for >6 mo).
IIa/B 29,79
medical conditions.
IIa/B 29
conception.
GPP
—/GPP —
tetanus.
Ia/A 79
IIa/B 79
Ia/A 29
Ia/A 29,79
first 4–8 wk.
II/B 28
Ia/A 29
II/B 28,82
—/GPP —
Ia/A 29,86High risk pregnancy : management options 5th edition 2011 p. 489
HIV
—/GPP —
tetanus.
Ia/A 79
IIa/B 79
Ia/A 29
Ia/A 29,79
first 4–8 wk.
II/B 28
Ia/A 29
II/B 28,82
—/GPP —
Ia/A 29,86
HIV
HIV
Algorithm for assessment of HIV infection in pregnancy
and in newborns to infected mothers
Rubeola
CHAPTER 29 • Rubella, Measles, Mumps, Varicella, and Parvovirus 497
Management Options
Prenatal
Treat acute infection symptomatically. —/GPP —
Antibiotics are given if secondary bacterial infection is suspected. —/GPP —
Immunoglobulin should be considered for the susceptible woman
exposed to the infection.
III/B 13
Inadvertent vaccination is not an indication for termination. III/B 13
Appropriate isolation precautions must be taken when in
hospital.
—/GPP —
GPP, good practice point.
MUMPS
Maternal and Fetal Risks
Mumps is a contagious acute viral illness caused by a para-
myxovirus, primarily infecting children and young adults.
Human beings are the only recognized natural host for this
pathogen. The classic presenting symptom for mumps is
either unilateral or bilateral parotitis, which usually develops
14 to 18 days after exposure. Respiratory droplets typically
transmit the virus. Prodromal symptoms include fever, chills,
malaise, and myalgias. The disease can also remain asymp-
tomatic in 20% of cases. Persons are considered infectious
from 2 days before the onset of symptoms to approximately
9 days after the parotitis is noted.
Although generally a self-limited disease with symptoms
resolving within 5 to 7 days, mumps can result in significant
complications, particularly in the adult population. Orchitis
occurs in up to 38% of cases in postpuberal males and may
lead to infertility.13
Conversely, mastitis and oophoritis have
been reported in women, but infertility is rare.38
Other com-
plications include aseptic meningitis, pancreatitis, and thy-
roiditis. Mumps meningoencephalitis can cause permanent
sequelae such as sensorineural hearing loss, seizures, nerve
palsies, and hydrocephalus.13
There are limited data on mumps in pregnancy. In a
cohort study of measles, mumps, and rubella, Siegel39
reported an increased incidence of first-trimester pregnancy
loss with acute mumps infection. No data suggest mumps
specifically increases the incidence of stillbirths or preterm
which were enacted in 1989, include a second dose of MMR
vaccine given at age 6 years. This practice has resulted in a
further decline in mumps infection.43
A remaining concern
is that only 38% of countries worldwide use routine mumps
vaccination. Still, outbreaks occur intermittently such as the
outbreak in Iowa among 605 18- to 25-year-olds in which
the source is unknown but the G genotype of mumps was
isolated. The latter is the same strain found in a large out-
break (>70,000 cases over 3 yr) in the United Kingdom.44
The importation of mumps into previously protected com-
munities has become increasingly recognized.
Diagnosis
The diagnosis of mumps is usually suspected based on pre-
senting features of the disease in the appropriate clinical
setting. Although the virus can be isolated in culture or by
RT-PCR detection from a clinical specimen (saliva, cerebro-
spinal fluid, urine, or other infected organ system), the diag-
nosis is more typically established by serologic techniques.
Enzyme immunoassay (EIA) is the most widely used meth-
odology and is more sensitive than complement fixation or
hemagglutination inhibition. Both IgM and IgG antibody
testing is available. A positive mumps-specific IgM result
from a reliable laboratory or a significant rise between acute
and convalescent titers of IgG antibody helps establish the
diagnosis of acute infection. After acute infection, it is pre-
sumed that one has lifelong immunity and persistent IgG
titers.
High risk pregnancy : management options 5th edition 2011 p. 496-7
Rubeola
Mumps
Mumps

26.03.2019
9
Adenovirus
Coxsackievirus
Human Papilloma Virus
HPV
Immunization: pregnancy and breastfeeding
recommendations
CHAPTER 17
456
Table 17.5 Immunization: pregnancy and breastfeeding recommendations
Product
(type & schedule)
Pregnancy Post partum Breastfeeding Comments
Varicella
• Live
• 2 doses (0, 4–8 weeks)
Contraindicated Immunize susceptible women
post partum before hospital
discharge or shortly thereafter
whether or not they intend to
breastfeed
Breastfeeding is not a
contraindication or
precaution to vaccination
Inadvertent use in pregnancy
has not resulted in fetal or
neonatal disease; not a reason
for termination of pregnancy.
Pregnancy to be avoided until
28 days after vaccination
Measles, mumps, rubella
• Live
• 1 dose
breastfeed
contraindication or
Vaccinia (smallpox)
• Live
• 1 dose
Contraindicated Contraindicated if intention to
breastfeed
Contraindicated Has been reported to cause
fetal and neonatal infection
Poliomyelitis (aka IPV
or Salk vaccine)
• Live attenuated
• 3 doses (0, 1, 6 months)
Precaution: consider if
pregnant woman needs
immediate protection
(high-risk situation, travel)
Immunize susceptible women
breastfeed as per routine adult
immunization schedule
contraindication or
No known fetal effects.
Ideally defer vaccination until
after 12 weeks gestation
Yellow fever
• Live attenuated
• 1 dose
Precaution: vaccinate
during pregnancy in cases
of unavoidable travel to area
where exposure is likely
Precaution if intention to
breastfeed due to lack of data
Breastfeeding is a
precaution due to lack of
data
Very limited data on
pregnancy: has not resulted in
fetal disease; not a reason for
termination of pregnancy
Rabies
• Live attenuated
• 5 doses (0, 3, 7, 14 &
28 days)
Precaution: vaccinate during
pregnancy only after possible
exposure (postexposure
prophylaxis)
Immunize women post
partum at any time, whether
or not they intend to
breastfeed, as per routine
recommendations:
pre-exposure prophylaxis
contraindication or
Prudent to delay pre-
exposure immunization unless
substantial risk of exposure
Influenza
• Inactivated
• 1 dose annually
Recommended: for all
pregnant women during the
flu season, and all pregnant
women as per routine
recommendations based on
co-morbidities or occupation
(see text)
Immunize women post
(see text)
contraindication or
Hepatitis A
• Inactivated
• 2 doses (0, 6 months)
pregnancy if unavoidable
travel to area where exposure
is likely to happen
whether or not they intend
to breastfeed as per routine
adult immunization
schedule
contraindication or
Hepatitis B
• Recombinant inactivated
Precaution: recommended
only for pregnant women
at risk
adult immunization
schedule
contraindication or
• Recombinant
Precaution: not recommended
in pregnancy but inadvertent
use has not resulted in adverse
outcomes
Immunize as per adult
Breastfeeding is not
a contraindication or
has not resulted on fetal or
neonatal disease
Immunization: pregnancy and breastfeeding
recommendations
CHAPTER 17
456
Table 17.5 Immunization: pregnancy and breastfeeding recommendations
Product
(type & schedule)
Pregnancy Post partum Breastfeeding Comments
Varicella
• Live
• 2 doses (0, 4–8 weeks)
breastfeed
contraindication or
Measles, mumps, rubella
• Live
• 1 dose
breastfeed
contraindication or
Vaccinia (smallpox)
• Live
• 1 dose
Contraindicated Contraindicated if intention to
breastfeed
Contraindicated Has been reported to cause
fetal and neonatal infection
Poliomyelitis (aka IPV
or Salk vaccine)
• Live attenuated
Precaution: consider if
pregnant woman needs
immediate protection
(high-risk situation, travel)
breastfeed as per routine adult
contraindication or
No known fetal effects.
Ideally defer vaccination until
after 12 weeks gestation
Yellow fever
• Live attenuated
• 1 dose
Precaution: vaccinate
during pregnancy in cases
of unavoidable travel to area
where exposure is likely
Precaution if intention to
breastfeed due to lack of data
Breastfeeding is a
precaution due to lack of
data
Very limited data on
pregnancy: has not resulted in
fetal disease; not a reason for
termination of pregnancy
Rabies
• Live attenuated
• 5 doses (0, 3, 7, 14 &
28 days)
pregnancy only after possible
exposure (postexposure
prophylaxis)
Immunize women post
recommendations:
pre-exposure prophylaxis
contraindication or
Prudent to delay pre-
exposure immunization unless
substantial risk of exposure
Influenza
• Inactivated
• 1 dose annually
Recommended: for all
pregnant women during the
flu season, and all pregnant
women as per routine
(see text)
Immunize women post
(see text)
contraindication or
Hepatitis A
• Inactivated
• 2 doses (0, 6 months)
pregnancy if unavoidable
travel to area where exposure
is likely to happen
adult immunization
schedule
contraindication or
Hepatitis B
• Recombinant inactivated
Precaution: recommended
only for pregnant women
at risk
adult immunization
schedule
contraindication or
• Recombinant
Precaution: not recommended
in pregnancy but inadvertent
use has not resulted in adverse
outcomes
Immunize as per adult
Breastfeeding is not
a contraindication or
has not resulted on fetal or
neonatal disease

Fetal viral infections

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