Perinatal Infections Flashcards
What is the pathogenesis of listeriosis and why is it more common among pregnant women
Listeria monocytogenes is a facultative anaerobic gram- positive bacillus. It can grow and survive within host cells. The body’s main defence mechanism against listeria is cell- mediated immunity.
Pregnancy is a state of suppressed immune response, in particular cell- mediated immunity, leading to pregnant women being more susceptible to listeria
What is the pathogenesis of parvovirus fetal disease
Parvovirus B19 has an affinity for progenitor erythroid cells and prevent them from reproducing. From the second trimester, there is an increased demand for RBCs so this coupled with parvovirus infection can lead to severe fetal anaemia.
Fetal anaemia can spontaneously resolve or progress to hydrops fetal is by 2 mechanisms:
- high output cardiac failure
- injury to myocardial cells causing myocarditis
Perinatal effects of listeriosis
Dependent on timing of infection
Miscarriage
Preterm delivery
Stillbirth (particularly if acquired in second and third trimesters)
Features of early- onset listeriosis
Onset within 7 days of birth
Severe sepsis
Associated with preterm babies
High mortality
Features of late- onset listeriosis
Onset from 7 days to 6 weeks from birth
Meningitis
Non- specific sepsis
Associated with term babies
Risk of fetal varicella syndrome
Depends on timing of maternal infection:
<12 weeks: 0.55%
12-28 weeks: 1.4%
> 28 weeks: no cases of FVS reported
How do you diagnose fetal varicella syndrome?
Detailed fetal ultrasound to assess for anomalies at least 5 weeks after primary infection.
Amniocentesis for VZV PCR not routinely advised if normal ultrasound.
If VZV positive but normal ultrasound at 17-21 weeks risk is low.
Fetal Varicella syndrome manifestations
Skin scars 78%
Limb abnormalities 68%
Eye abnormalities 60%
Prematurity, low birth weight 50%
Mental retardation 46%
Incontinence 32%
Early death 29%
Risk of fetal toxoplasmosis with mother contracting toxoplasmosis in pregnancy
Depends in trimester:
First trimester: fetal infection low risk (4-15%) but high risk of damage if infected (34- 85%)
Second trimester: fetal infection intermediate risk (25- 44%) with intermediate risk of damage if infected (18- 33%)
Third trimester: fetal infection high risk (30- 75%) but low risk of damage if infected (4- 17%), usually asymptomatic
Diagnosis of intrauterine toxoplasmosis
Ultrasound features +/- MRI- limited sensitivity + specificity
T gondii PCR on amniotic fluid at 18-20 weeks or at least 4 weeks post- maternal infection
If T gondii PCR and USS negative = fetus not infected
If T gondii PCR positive, regardless of USS= congenital toxoplasmosis
Treatment of congenital toxoplasmosis
Consider termination
Treat mother with pyrimethamine + sulfadiazine + folinic acid
Confirm diagnosis at birth
Treatment of maternal toxoplasmosis
<18 weeks + T gondii PCR negative: spiramycin alone. Spiramycin doesn’t cross placenta so doesn’t treat fetus
> 18 weeks + T gondii PCR positive: pyrimethamine + sulfadiazine + folinic acid
Ultrasound features of congenital toxoplasmosis
Hydrocephalus
Brain or hepatic calcifications
Ascites
Splenomegaly
Stigmata of congenital CMV infection
IUGR
Cerebral ventriculomegaly/ periventricular echogenicity
Microcephaly
Intracranial calcifications
Echogenic fetal bowel
Abdo calcification
Hepatosplenomegaly +/- liver calcifications
Hydrops- ascites/ pleural effusion/ placentomegaly/ poly
Oligo
Risk of vertical transmission with CMV infection
Increases with gestational age:
1st tri- 36%
2nd tri- 40%
3rd tri- 65%
Severity and sequelae decreases with gestational age
