Transcript Infections in Pregnancy

Infections in Pregnancy
CARIS – Public Health Wales
24.11.16
Dr Surabhi Nanda
Consultant Maternal Fetal Medicine
Honorary Senior Lecturer in Obstetrics
Case 1
a.30 G1P0
Low risk aneuploidy screen
20w anatomy scan-Echogenic bowel,
growth and liquor normal.
Parental blood for - negative
Amnio for karyotype – declined
Rescan – Persistent echogenic bowel
TORCH screen
Positive IgM and IgG for CMV
CMV IgM positive :
Through polyclonal stimulation of Rheumatoid factor of IgM class
Persistence from a remote infection
Reactivation of a previous infection
Primary or preconceptional infection with CMV
1. Check booking blood
2. Check avidity
3. Amniocentesis
Interpretation basics
IgM
IgG
No Exposure
-
-
Acute Infection
+
+/-
Past infection
-
+
IgG avidity
“Functional affinity” - the net antigen binding force of the populations of antibodies,
in response to an infection.
The anti-CMV IgG avidity test is currently the most reliable procedure to identify primary
infection in pregnant women- highly specific (100%) and sensitive (94.3%).
IgG avidity testing less
invasive than amniotic
fluid testing
IgG avidity index - low (0.57)
Amniocentesis
• Amniotic fluid CMV count = 4 million
• Booking bloods = CMV IgM & IgG
positive (cf:primary infection
occurred >6w previously)
• Fetal blood sample - positive for
virus
Detection in amniotic fluid does not
necessarily correlate with congenital
infection
If fetal blood still carrying virus >6 weeks
after primary infection then the risk to the
fetus is high
Counselling:
• Prevalence of CMV infection is around 0.5–1% of all live births
• Leading infectious cause of sensorineural hearing loss (SNHL) and
developmental delay (DD)
• 70% chance of DD
• Vertical transmission in ~ 30–40% following primary infection and 2–3%
following secondary infection
• ~only 5–10% of infected newborns will have symptoms at birth, 40-58% of
whom develop adverse outcomes, including cerebral palsy, SNHL and other
neurological problems.
• around 90% of congenitally infected infants are asymptomatic, although 5–15%
of them will develop SNHL
• Limited evidence about risk of transmission at different periods of gestation
Opted to continue pregnancy.
3 weekly scans - 33 weeks intra cranial anatomy normal.
Declined further FU Elective CS 39w Maternal Request
Early neonatal findings- mild ventriculomegaly on CT, and
unilateral deafness
Infant development- motor delay at 6 months, bilateral
deafness.
Currently antiviral treatment with GCV and
valganciclovir is only recommended for symptomatic
newborns (in the first 30 days of life) with severe
symptomatic focal organ disease, or CNS disease.
Case 2
20 week anomaly scan
a35, Para 1
Maternal APKD
Previous PIH
Low risk
Rhesus +
22 weeks - ascites
TORCH – CMV IgG- ; IgM+; Low Avidity
Booking Bloods – CMV IgG-; IgMAmniotic fluid CMV PCR 2.2x107
Acute Primary fetal CMV infection
Options – TOP Vs Expectant management
Opted for expectant
For review in 4 weeks and fetal MRI around 28-30 weeks
Symmetrical prominent horns of the
lateral ventricles. Otherwise normal
intracranial appearances.
Ascites resolved by 26 weeks
IOL 38 weeks
Admitted to NICU with tachypnoea,
pallor, petechial rash and
hepatomegaly. Ventilated
CRANIAL USS – NO VENTRICULOEMGALY
CMV results: High concentrations in
blood, lungs, urine and CSF
Platelets 35, Abnormal clotting.
1) Started valganciclovir
2) Audiology & Neurodevelopmental FU
Toxoplasma gondii
Usually self limiting maternal infection which does not
need treatment unless pregnancy or
immunocompromised.
T1
T2
T3
14%
41%
29%
8%
59%
~0%
Vertical transmission rate
Fetal severe sequele / Still birth
Toxoplasma infection
in HIV positive women
•
•
•
•
•
High incidence congenital toxoplasmosis (CT)
Late manifestations of latent CT
Common with CD4<500 or women on HAART
Ocular and CNS manifestations more common
All HIV+ women with or without HAART need
toxoplasma test +/- treatment in pregnancy
Diagnosis of acute infection
High titers of toxoplasmosis-specific IgM or IgA>95%
Toxoplasmosis-specific IgG and IgM rise in 1-2 weeks.
Toxoplasmosis-specific IgG peaks at about 2 months after infection.
Toxoplasmosis-specific IgA peak 4 weeks last about 7 months
USS findings associated with
congenital toxoplasmosis
• Ventriculomegaly
• Calcifications
• Intracerebral
• Periventricular
• Retinal
• Lenticulostriate
• Myocardial
• Hepatic
• Cataracts
• Microphthalmia
• Microcephaly
• Non-immune hydrops
• Ascites
• Pleural effusion
• Pericardial effusion
• Hepatosplenomegaly
• Placentomegaly
Case 3
a.30 Non English speaking traveller
HIV –ve
Toxo serology +ve of acute infection
Amniocentesis – High Toxo PCR
Diagnosis – Congenital Toxoplasmosis
Counselling – Risks and Sequale
Options – Treatment vs (Termination)
Commence
Pyrimethamine - 100 mg/d, then 25-50 mg/d
Sulfadiazine 1 gram QDS
Folinic Acid 5mg/d
Case 4
a.30 G1P0 Rh –ve
Admitted with vaginal bleeding at 19 weeks
Placenta low posterior
Incidental finding of fetal hydrops
Fetal anaemia – MCA Peak systolic velocity >1.5MoM
Intrauterine fetal blood transfusion
Normal PCR and karyotype
Fetal blood +ve Parvo DNA (PCR3.8X 10Log=9.6)
Mum seroconverted after booking to positive Parvo
IgG and IgM
Negative Toxo and CMV
1st transfusion 19w - Hb 2.3g/dL (14.6 / 25mls)
2nd transfusion 21w – Hb 5.3g/dL (14.4 /27mls)
Counselling
Cause for fetal anemia and hydrops is maternal
Parvovirus B19 infection. This causes bone
marrow suppression and is reversible. Until
baby's bone marrow starts working again, we
will have to support by giving adult
blood.
Parvovirus B19
Fetal implications more serious when maternal
infection occurs during the first two trimesters of
pregnancy
Spontaneous Miscarriage
<20w 14.8%
>20w 2.3%
2. Congenital anomalies
(No)association between
parvovirus infection in pregnancy and increased
risk of congenital anomalies in human fetus
(Case reports of some anomalies)
3. Hydrops
Non immune fetal hydrops secondary to anaemia
Myocarditis
Management of a pregnant woman with suspected or
diagnosed Parvovirus
Acknowledgements
Prof Z Alfirevic
Dr D Roberts
Mr U Agarwal
Ms Jackie Holian
Fetal Medicine Unit
LWHNHSFT
Thank you