Transcript Fetal Infection

Fetal Infection
Hesham Arab
Consultant Perinatologist
Jeddah, Saudi Arabia
Etiology of fetal death
 Sweden, May 2002: Extensive
evaluation of 188 cases (Dx. Established
in 91%)
 24% Fetal infection
 22% Placental Insuf./ IUGR
 19% Placental abruption
 12% Maternal disease
 10% Congenital anomalies
 09% Umbilical cord complications.
Suspected Pathogens
 Toxoplasma, and Syphilis
 CMV
 Rubella, Varicella
 Herpes simplex
 Parvovirus B19
 Hepatitis B & C
 HIV
Is The Fetus Infected?
 Maternal manifistation.
 Serologic Testing
 Ultrasound examination
 Fetal sampling for


Culture
Molecular genetics
Serologic Testing Problems
 IgG crosses placenta
 Is it maternal or fetal
 IgG takes time
 What if recent infec.?
 High or increased
 Not necessary fetal
IgG
 IgM does not cross
P. IgM appears after
one week for 30-90
days only
infection
 What if infection
transmitted outside
this window
Serologic testing
Serologic assays may be helpful,
but seldom are conclusive in
determining fetal infection.
“TORCH” is outdated!
 Originally used to increase awareness of
“similar” pathogens causing I U infection.
 Now it is misleading and outdated:




Cong. Infections are distinguishable
“O” is no longer Syphilis, but many others
Serologic testing of TORCH is
inappropriate in certain agents and may
need other assays
Focus Testing is more cost effective
Toxoplasmosis Cycle
oocytes
Tissue
cysts
Toxo. Screen..Yes/No ??
 Seroconversion in Stockholm (1998):
 Seroprevalence in pregnants 14%.
 When compared between 1969 & 1987
found majority of seropositive pregnants
today have had seroconversion before
entering childbearing age.
Toxoplasma in Saudi Arabia
 Al-Meshary (1989): 25%
 Abha (1991): 31%
 Riyadh (1993): 24%...Active in Preg.2%
 Abha (1994): 52% seroprevalence in
blood donors, and only 4% IgM.
 Al-Qurashi (SMJ,jan 2001):1st
Population-based study in S.A. found 5%
IgM in pregnancy (low).
To Screen, Or not to Screen?
 Incidence of primary toxoplasma
infection in Sweden is 5% susceptible
pregnancies.
 Prevalence of congenital infection in live
born children is 0.73/10000
 Sweden concluded: Incidence of
Toxoplasmosis in pregnancy is LOW and
screening program is NOT
recommended
The role of
ultrasound
examination
in Fetal infection
Limitations
Most infected fetuses are
sonographically normal
Ultrasound findings may
change with time
no correlation with infant
outcome
Cerebral Ventriculomegaly
 Measured at the posterior aspect of the choroid plexus
 Almost always symmetric
 5% of cases can be attributed to fetal infection
Intracranial Calcifications
 Intrauterine infection
 Periventricular hyperechoic
foci - the hallmark
 May be located in the
thalami and basal ganglia
 Small with no acoustic
shadowing
 Most frequently seen with
CMV and Toxoplasmosis
hydranencephaly
 Most severe : destructive process
 Cerebral hemispheres replaced by
fluid, brain stem preserved, falx
present, absent or deviated,
posterior fossa structures can be
identified
 reported in Herpes simplex,
Toxoplasmosis and CMV
Microcephaly
 Often with other CNS anomalies
 Diagnosed as three SD below the mean
for gestational age
 Abnormal HC/AC and HC/FL ratios
 Isolated microcephaly documented in
CMV, Rubella and Herpes simplex
Cardiac abnormalities
 Cardiomegaly,
mostly in CMV
 Cardiothoracic ratio
 VSD, ASD,
Pulmonic stenosis
and coaractation of
the aorta in Rubella
Hepatosplenomegaly
Documented in all fetal
infections
Often a transient finding
Normograms are available
Intra-abdominal:
Calcifications & Echogenic bowel
 Typical appearance:
echgenic foci with
acoustic shadowing
 Peritoneum, intestinal
lumen, organ
parenchyma, biliary tree
and vascular structures
 Echogenic bowel in CMV
and Toxoplasmosis
Hydrops, Placenta and
Amniotic fluid
 Hydrops reported in most cases but
may be transient
 Both Placentomegaly and small
placentae have been reported
 Hydramnios and oligohydramnios
have been reported with similar
frequency
Fetal growth restriction
Estimated weight below the
10th percentile
common feature with CMV,
Rubella, Herpes simplex and
Varicella
Usually not seen with
Toxoplasmosis and Syphylis
TOXOPLASMOSIS
 Ventriculomegaly is the most
frequently documented finding
 Intracranial calcifications,
placentomegaly, liver calcifications
and ascites
 hyper echoic bowel
 microcephaly never been reported
in utero
SYPHILIS
 Hepatomegaly and Placentomegaly
are the most frequent sonographic
manifestations
 Ascites, Hydrops and Hydramnios
are less commonly reported
 Resolution of sonographic signs
have been reported with maternal
antibiotic therapy
RUBELLA
 Incidence < 1:100,000 live birth
 Prenatal diagnosis by sonographic
findings have never been reported
 Potential detected abnormalities
include: cardiac anomalies,
microcephaly,
hepatosplenomegaly, FGR,
microphtalmia and cataract
CMV
 The most common congenital infection
affecting 1% of all live births
 10% of infected neonates demonstrate
clinical manifestations that potentially
could be identified by prenatal
sonography
 Ventriculomegaly, FGR, Intracranial
calcifications and oligohydramnios are
the most frequently reported findings
HERPES SIMPLEX
 HSV are usually acquired at birth
 Intrauterine infections resulting in clinical
signs has been reported in 100 cases
worldwide
 Hydranencephaly is the only sonographic sign
reported antenatally
 Microcephaly, intracranial calcifications and
FGR are potentially detectable
VARICELLA ZOSTER
The most common finding is
Hydramnios
Also reported: liver
calcifications, hepatomegaly,
hydrops, limb deformities,
ventriculomegaly and FGR
SUMMARY
Sonography is not a sensetive test
for fetal infection
Normal fetal anatomy survey
cannot predict a favorable outcome
Multiple organ systems are affected
in 50% of cases
Parvovirus B19
 Asymptomatic / erythema infectiosum
/fifth disease / slapped cheek syndrome
 Respiratory route. Incubation P. 1-3 wks.
 At risk: primary school teachers
 Infects erythroid precursors causing subclinical hemolytic anemia in normal
people
 In sicklers this causes aplastic crisis
 In immunocompromised: pancytopenia
Fetal infection by B19
 Transplacental transmission is 33-50%.
 1st half: 1. abortion (15% )

2. hydrops fetalis (3%)
 2nd half: IUFD (9%)
 No intervention or screening unless hydrops
developed then treat (blood Tx)
 But still mechanisms other than anemia and
cardiac decompensation could be the cause
The killer ..( B 19 )
 Parvovirus B19 DNA tested +ve by PCR:
 15% of Stillbirths
 0% of live births
 Majority of late fetal deaths are non-
hydropic and are due to B 19.
Outcome from hydrops fetalis
 B19 implicated in 5-15% of cases NIHF
 Depending on severity any of this
happen



Spontaneous resolution (1/3 of case)
IUFD (1/3 of cases)
Intrauterine transfusion(1/3), 80% success
Fetal blood flow in Anemia
Fetus with hemolytic anemia shows
characteristic hemodynamic changes.
This is thought to be due to fetal
compensatory mechanisms in response to the
decreased blood oxygen content, leading to
increased cardiac output.
Furthermore, low hemoglobin and albumin
levels lead to decreased viscosity and thus to
higher blood flow velocities, and the fetus is
rendered ‘hyperdynamic’.
Middle Cerebral Artery
Flow velocity waveform in the fetal middle cerebral artery in a
severely anemic fetus at 22 weeks (left) and in a normal fetus
(right). In fetal anemia, blood velocity is increased
Ultrasonographic Surviellance
 Size of the right lobe of the liver
 Middle cerebral artery peak velocity
 This strategy avoid invasive procedures
and so:




Reduced fetal loss & preterm del. by 7%
Reduced Mat-fetal hemorrhage by 40%
BUT you need to do it weekly
AND further critical evaluation is on the
way
Treatment implications



Rx heart failure (antiarrythmics)
Rx anemia (transfusions)
Drainage of hydrothorax
Intrauterine Transfusion
Case of Hydrops Fetalis