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Infection may be acquired across the placenta (intrauterine infection)
or contracted during the process of birth or by direct contact
with maternal body fluids. Prolonged rupture of the membranes
predisposes to fetal infection. Infection can also be transmitted to
the neonate after birth from the mother or other contacts.
Jaundice associated with hepatitis is often the first sign of congenital
rubella. Haemolysis and thrombocytopenic purpura are also
common, as is a low-grade meningoencephalitis. Some babies have
evidence of metaphyseal dysplasia. Infected infants have low birthweight
and fail to attain their expected developmental milestones.
There is a high mortality in severely affected infants. Patent ductus
arteriosus, cataracts, deafness and retinal pigment dysplasia may
be present. Rubella IgM is positive and persists until the third
month of life.
The risk to the fetus from maternal infection during the first
trimester is more than 60% and some parents will opt for termination
of pregnancy. Later the risk is much lower (2% after 20 weeks)
and the balance between the chance of fetal damage and the desirability
of termination should be considered carefully.
Infection occurs in less than 1% of births, of which 1% are severely
affected. The risk of infection is highest during the first trimester.
It presents with prematurity, low birthweight, hepatomegaly,
splenomegaly, thrombocytopenia, prolonged jaundice, cerebral
irritability, fits and/or abnormal muscle tone or movement.
Microcephaly and sensorineural deafness are the most common
problems. Other problems include cerebral calcification, hemiplegia,
psychomotor retardation, chorioretinitis and myopathy.
Diagnosis depends on demonstrating IgM antibodies or cytomegalovirus
(CMV) excretion during the first 20 days of life.
Congenital and intrapartum herpes simplex infections
Primary herpes simplex infections may be accompanied by viraemia
when transplacental infection can occur. Infants born with
congenital infection tend to have severe disease, with pneumonitis,
meningoencephalitis, hepatosplenomegaly and cytopenias. Only a
few will demonstrate herpetic skin or mucosal lesions. Treatment
with aciclovir reduces mortality from 80-90% to 10-15% and
should not wait for laboratory confirmation.
Primary infection may be contracted at birth from maternal
genital herpes. Skin, conjunctival, oral or genital lesions develop
within a few days, with dissemination in 50% of cases. Treatment
is with intravenous aciclovir.
Varicella embryopathy follows maternal infection during the first
or second trimester of pregnancy; it is transmitted in less than
3% of infected pregnancies. Cicatricial contracture of a limb with
hypoplasia, microcephaly or microphthalmia may occur. Nonimmune
women exposed to chickenpox should be offered postexposure
prophylaxis with zoster immune globulin (ZIG) within 10
days of exposure.
Neonatal varicella occurs when the mother develops chickenpox
within 1 week of delivery. As neonatal mortality is up to 40%, the
neonate should be given ZIG within 48 h of birth if possible and
treated with aciclovir if infection develops. Normal immunoglobulin
given to the mother will not protect the infant. A vaccine is
entering clinical use in some countries.
Transplacental transmission of Listeria monocytogenes
during a maternal infection that is often not apparent. Infection
in early pregnancy often results in fetal death; later infection is
associated with premature labour. Severe bacteraemia, associated
with hepatosplenomegaly, meningoencephalitis, thrombocytopenia
and pneumonitis, usually complicates neonatal infection.
Intrapartum exposure may lead to neonatal infection during the
first 2 weeks of life, usually with meningitis and bacteraemia.
Blood, CSF, placental tissue and lochia should be cultured.
Infected mothers and infants may be a source of infections in the
postnatal ward and should be isolated. Ampicillin with or without
the addition of gentamicin (for 2-6 weeks) is the treatment of
Congenital infection is now rare as a result of antenatal screening.
Affected babies are feverish with features similar to secondary
syphilis: rash, condylomata and mucosal fissures. Osteochondritis
may cause pain. Persistent rhinitis ('snuffles') is common.
Diagnosis is confirmed by dark-ground microscopy of mucosal
or skin lesions. Specific IgM or antibodies persisting after 6 months
indicate infection. Late manifestations appear between 12 and 20
years: deafness, optic atrophy or paretic neurosyphilis. Other features
include bossing of the frontal bones, chronic tibial periostitis,
notching of the incisors, 'mulberry' deformity of the first permanent
molar and a high arched palate. The treatment of choice is
The incidence of toxoplasmosis varies internationally; it is uncommon
in the UK, but common in France. Transplacental infection
occurs in a third of affected pregnancies. Infection in the first and
second trimester is more likely to cause significant fetal disease:
the fetus may be stillborn, die soon after birth, or have cerebral
calcification, cerebral palsy or epilepsy. Chorioretinitis may not be
evident until after birth and may be the only feature. Maternal
toxoplasmosis is confirmed by specific IgM antibodies or by
seroconversion. IgM antibodies may also be demonstrated in
affected neonates. Treatment with spiramycin may reduce the risk
of transplacental infection but does not affect the outcome of fetal