INFECTIONS IN PREGNANCY

Dr. Irma Lee March 2, 2012

Transcribed by: Paula Siongco 3D-2013

Goals in Pregnancy:
Reduce risk of congenital structural
abnormalities/deformities
Optimize health care to minimize
effects of vertical transmission
Avoidance of horizontal transmission
to health care providers
Prevention

TORCH SYNDROME
T oxoplasma
O thers (Varicella zoster virus,
Hepatitis, Parvovirus, HIV, Group B
Streptococcus)
R ubella
C ytomegalovirus
H epatitis virus

TOXOPLASMOSIS
Acute toxoplasmosis during
pregnancy is rare
Acquired through ingestion of
encysted organisms in raw or
undercooked meat or through contact
with infected cat feces or
contaminated soil
Overall risk of having affected child
o 2% - 1
st
trimester
o 10% - 28 weeks
o 4% - at term

Diagnosis
Maternal signs and symptoms
o Non-tender posterior cervical
adenopathy and flu-like
symptoms
Serologic Test for Immunoglobulin
G and M antibodies
o IgG appears 1-2 weeks of
infection and peaks between 6-
8 weeks
o IgM - appears within 1
st
week
of infection then declines over
several months and may
persist for years
PCR testing of amniotic fluid
o Most accurate method to test
for fetal infection
o Done on 2
nd
trimester or 4
weeks after an acute maternal
infection

CONGENITAL TOXOPLASMOSIS
Sonographic abnormalities
o Ventricular dilatation (75%)
o Intracranial calcifications
(18%)
o Increased placental thickness
(32%)
o Hepatosplenomegaly (14%)
o Fetal ascites (15%)
o Pericardial or pleural effusions
o Microcephaly (5%)
At birth maculopapular rash,
hepatosplenomegaly, seizures,
convulsions
Blindness, deafness, mental
retardation

Treatment
Spiramycin (3-4 g/day)
o Concentrates in the placenta
o Given once maternal infection
is confirmed until delivery
Pyrimethamine (25-100mg PO QID)
and Sulfadiazine (1-1.5g PO QID)
and Solinic acid 10-25mcg
o Given once fetal infection is
confirmed
o Both are folic acid antagonists
and cross the placenta and
penetrate the fetal brain and
cerebrospinal fluid

RUBELLA
A mild viral illness with 30% of
mothers being asymptomatic or with a
mild 3-day rash with potential
auricular adenopathy
Transmission: Airborne
Diagnosis: Serologic testing of IgM or
IgG antibody titer which becomes
positive 4 weeks after exposure

CONGENITAL RUBELLA
Risk of major fetal damage varies with
the time of maternal infection:
o 80-90% - first 3 months
o 10% - >4 months
o 6% - >5 months
o No risk thereafter
Congenital heart (patent ductus
arteriosus), cataract, deafness
Microcephaly
Mental retardation

Prevention
MMR children 12-15 months of age
and at school age; non-pregnant
women and ALL women at
reproductive age group
NO TREATMENT



CYTOMEGALOVIRUS
Most common cause of viral
intrauterine infection affecting 0.5-
2.5% of all neonates
Infection can occur in-utero,
intrapartum and through breast milk
Transmission: Contact with body
fluids or sexual contact
40% of pregnant women with primary
infection CONGENITAL CMV
1-2% of newborn are CMV infected
from primary maternal CMV or
reactivation of prior infection

CONGENITAL CMV
85-90% of infected are asymptomatic
at birth
5-10% unilateral/bilateral hearing
impairment
Blueberry muffin baby
Other symptoms/signs:
o Jaundice, thrombocytopenia,
hepatosplenomegaly,
chorioretinitis, deafness,
microcephaly, mental
retardation, or death due to
DIC and sepsis

CMV INFECTION
4-8 weeks incubation period
Viremia between 3-12 months
Infected fetus shed virus up to 6 years
Viral transmission via primary or
recurrent maternal infection
Rate of transmission increases with
gestational age; highest at 3
rd

trimester
Severity of disease is inversely
proportional to gestational age
Neonatal CMV through breast milk
does not lead to visceral or
neurological sequelae

Primary Maternal Infection
(CMV IgM + or PCR +)


30-40% fetal infection (CMV PCR + in AF)
90% asymptomatic at birth 10-
15% develop abnormalities
10% symptomatic at birth 85-90%
develop abnormalities

RECURRENT INFECTION
Occur with immunosuppressive and
during pregnancy
Recurrent infection during pregnancy
are often asymptomatic and primarily
caused by reactivation of the
endogenous virus or low grade
chronic infection or reinfection by a
different strain of CMV
Risk of vertical transmission is 0.5-2%
Risk of CMV congenital infection is
only 0.5%
Neonates infected from recurrent
infection has <8% risk of hearing loss
and chorioretinitis

Diagnosis
Usually asymptomatic or with
mononucleosis-like or flu-like
symptoms
Presence of symptoms or abnormal
laboratories highly suggestive of
primary infection
CMV screening not routinely
recommended
IgM and IgG screening at 8-12 weeks
AFP PCR for CMV to detect in-utero
infection

NEONATAL CMV INFECTION
CMV virus in AF by PCR at 21 weeks at
6 weeks interval
Ultrasound findings
o Ventriculomegaly
o Oligohydramnios
o Echogenic bowel
o Choroid plexus cyst
o Pleural effusion
o Brain/liver calcifications

Role of CMV specific Hyperimmune
Globulin
For mothers with primary CMV to
reduce maternal systemic or placental
viral loads
Reduce placental and fecal
inflammation in infected fetuses
increase fetal blood flow with
enhanced fetal nutrition and
oxygenation

Prevention
Hygiene avoid direct contact with
children, frequent hand washing,
glove use
Live-attenuated CMV vaccine
Glycoprotein B construct vaccine

HERPES SIMPLEX VIRUS
Recurrent STD caused by
o HSV-1: 90% oral, 10% genital
o HSV-2: 10% oral, 90% genital
Ulceration in genitalia with severe
local pain, dysuria, sacral paresthesia,
tender inguinal lymph nodes, fever,
malaise

PRIMARY FIRST EPISODE
HSV confirmed in a person without
prior HSV-1 or HSV-2 antibodies
2-4% of IgG negative women
seroconvert (acquire) to HSV-1 or
HSV-2 during pregnancy
No fetal consequences unless convert
shortly before labor and delivery

NON-PRIMARY FIRST EPISODE
HSV-2 confirmed with prior findings
of HSV-1 antibodies or vice-versa
1.5-2% of HSV-1 IgG + women
seroconvert to HSV-2
Risk of conversion from HSV-2 IgG +
to HSV-1 + <1%
Symptoms milder

RECURRENT GENITAL HERPES
Caused by reactivation of latent HSV
usually HSV-2
20-30% of pregnant women are IgG+
for HSV-2 with intermittent shedding
from vaginal mucosa
Virions travel from the skin or mucosa
to the sensory dorsal root ganglion
where latency established Viral
replication recurrent clinical
outbreaks
Trauma, UV radiation, extreme
temperature, stress, hormonal
fluctuations, immunosuppression

Risk of Fetal Transmission
Maternal-fetal transmission of HSV via
contact with infected genital
secretions
40-50% neonatal HSV infection if
delivery occurs during primary
infection
0-3% neonatal HSV infection occurs
during recurrent infection
Sites of intrapartum viral entry are the
fetal eye, nasopharynx, or break in the
skin

NEONATAL HSV INFECTION
First episode primary infection
microcephaly, ventriculomegaly,
spasticity, echogenic bowel,
hepatosplenomegaly, flexed
extremities
30% of infants die
40% neurogenic sequelae

Diagnosis
History
Maternal signs/symptoms
HSV culture 48-72 hours at
appearance of lesions
Serologic testing
PCR assay of genital lesions
Tzanck smear multinucleated giant
cells and viral inclusions

Prevention
Avoid sexual contact with infected
individuals
Condoms
Suppression decreases recurrent
genital lesions at term, and viral
shedding

Anti-viral Drugs
Acyclovir (Zovirax) inhibits viral
thymidine kinase, crosses placenta but
safe
Valacyclovir (Valtrex) prodrug of
acyclovir, better absorption, longer
half-life, decrease shedding
Fanciclovir prodrug of Penciclovir,
no specific studies in pregnancy

Management
1. Primary HSV
Analgesia
Hygiene
Antiviral Acyclovir 400mg PO
TID 7-14 days or Valacyclovir 1g
PO 7-14 days
Suppression Acyclovir 400mg PO
BID or Valacyclovir 500mg PO OD
at 36 weeks to delivery

2. First episode within 6-12 weeks of
delivery
IV Acyclovir intrapartum to both
mother and neonate
Daily Acyclovir or Valacyclovir
from 36 weeks until delivery

3. Complicated CMV infection
IV Acyclovir 5-10mg/kg BW q 8
hours until improved followed by
oral antiviral drug for 10 days

4. Recurrent HSV
Analgesia
Hygiene
Antiviral
Suppression therapy

Mode of Delivery
With active lesions at term CS
PPROM remote from term
Expectant
Cesarean delivery should not be
offered solely for a history of HSV


VARICELLA-ZOSTER VIRUS
A double-stranded DNA. Herpes virus
acquired in childhood
Primary infection manifests as
Varicella (chickenpox)
Herpes Zoster (shingles) is an
eruption from reactivation of latent
HSV infection of dorsal root ganglia
Transmission: Direct contact and
respiratory droplet

Diagnosis
Varicella Maculopapular vesicular
pruritic lesions
Herpes Zoster Painful lesions over
sensory nerve root distribution
Laboratory diagnosis:
o ELISA VZV IgI titer
o Tissue culture
o Tzanck smear
o Direct fluorescent antibody test
o Nucleic acid amplification test

MATERNAL PRIMARY VARICELLA
Pneumonitis
Bacterial superinfection (cellulitis,
abscess formation)

CONGENITAL VARICELLA SYNDROME
Occurs in 2% when mothers have the
infection <20 weeks
Varicella Embryopathy (cutaneous
scar, denuded skin, limb hypoplasia,
muscle atrophy, rudimentary digits,
microcalcephaly, intracranial
calcification, cortical atrophy,
cataracts, chorioretinitis,
mocrophthalmia, psychomotor
retardation)

NEONATAL VZV INFECTION
Fetal exposure just before or during
delivery result in 25-50% of cases
Varicella Zoster Immune Globulin
to neonates whose mother developed
Varicella 5 days before to up to 2 days
post delivery

Treatment
Supportive care
Acyclovir 500mg q8 hours for
complicated varicella or
immunocompromised
Varicella Zoster Immune globulin
up to 96 hours post exposure

Prevention
Varivax not recommended to
pregnant women

HEPATITIS A
Caused by RNA virus transmitted by
fecal-oral route
Average incubation period is 28 days
with symptoms lasting 2 to 6 months
Children are usually asymptomatic in
contrast to adults who are always
symptomatic
Prevalent in areas with poor
sanitation and closed-living conditions
Occurs in <1:1000 pregnancies

Risks of acquiring HAV
Travel to prevalent countries
Homosexuals
IV drug users
Working with non-human primates
Chronic liver disease

Management in Pregnancy
Supportive
No perinatal transmission

HEPATITIS B
Most common form of viral hepatitis
in pregnancy
Caused by DNA virus transmitted
parenterally and sexual contact
Acute hepatitis occurs in 1-2:1000
pregnancies in the US
Chronic carrier state occurs in 6-
10:1000 pregnancies
Incubation period is 60 to 90 days

Risk Factors
Perinatal transmission highest risk
of chronic HBV infection
Sexual contact
IV drug users
STDs
Multiple sexual partners
House contacts
Mental institutions/prisons
Acupuncture
HBV infected at high risk of HIV and
HCV infections

Pathophysiology
Incubation period depends on viral
exposure than laboratory changes
Antigens
o S Surface infected if present
>6 months; Chronic HBV
infection
o c Core
o e Infectious
Antibodies
o S Immune
o C covers window period,
usually precedes HbsAb
conversion

Pregnancy Considerations
Vertical transmission is high when
laboratory is as follows:
o HbsAg + 10-20%
o HbsAg + HbeAg + 80-90%
Vertical transmission is trimester
related
o 10% first trimester
o 80-90% third trimester
Only 10% is transmitted
transplacental, hematogenous or thru
breastfeeding

ACUTE HEPATITIS B IN PREGNANCY
Document conversion of HBsAg to +
Outpatient supportive therapy
If with co-morbidities like bilirubin
15mg/dL
Vit K 10mg/IM q8 hrs for 3 doses
Consider interferon

Exposure to HBV during Pregnancy
If HBsAg (-) and HBsAb (-) HBIg
and HB vaccine (prevents .5% of
transmission)
HBIg must be given within 14 days of
exposure

Vertical Transmission Prevention
All newborns of mothers HBsAg+
should receive HBIg and HB vaccine
within 12 hours of birth
95% prevention of neonatal HBV

HEPATITIS C
Caused by RNA virus acquired via
infected blood, sexual contact or
mother-to-infant (vertical
transmission)
Incubation period: 30 to 60 days
Complications: Cirrhosis and
Hepatocellular Carcinoma

Definition of types of HCV infection
HCV: HCVAb (+)
Chronic HCV: HCVAb (+) and HCV
RNA (+)
Chronic Active HCV: HCVAb (+) and
HCV RNA (+) and increased LFTs

Risk factors for HCV infection
BT or exposure to blood products
IV drug users
Multiple sexually transmitted disease
HIV infection
Multiple sexual partners
History of body piercing or tattooing
Organ transplant: Berone 1992
Unexplained elevated transaminases
Patient or staff involved in chronic
dialysis programs
Participant in in-vitro fertilization
program from anonymous donors

Prevention
Avoid risk factors
Prevent complications by avoiding
alcohol and hepatotoxic medicine and
foods

Effects of Pregnancy on Hepatitis C
Pregnancy DOES NOT affect the
clinical course of acute or chronic
Hepatitis C
Linear increase in HCV viremia
throughout pregnancy
Chronic Hepatitis C associated with
increased preterm delivery and IUGR
Long term effects cirrhosis, cancer,
death

Therapy
No approved treatment of HCV
infection during pregnancy
No HCV vaccine or Ig
Pegylated interferon and ribavirin
eradicated virus >50% in non-
pregnant women