Congenital Infections
TORCH
Toxoplasmosis
Other (syphilis)
Rubella
Cytomegalovirus (CMV)
Herpes simplex virus (HSV)
Varicella zoster (the chickenpox virus).
 Entroviruses
 Hepatitis B.
 Parvovirus.
 HIV (human immune deficiency virus).
 Chlamydia trachomatis.
 Mycoplasma.
 Group B streptococcus.
 Malaria
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COMMON CLINICAL FEATURES
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Low birth weight for
gestational age
Prematurity
Seizures
Chorio-retinitis
Cataracts
Purpura
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Cerebral calcification
Micro-ophthalmia
Jaundice
Anaemia
Hepatosplenomegaly
Pneumonitis
CONGENITAL CMV
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Caused by a DNA herpesvirus Cytomegalovirus
(CMV)
Most common congenital viral infection
The majority of congenital infections are
asymptomatic
severe neurologic morbidity occurs in 80 percent of
survivors
sequelae appear to be more severe when infection
is acquired earlier in pregnancy
PATHOGENESIS
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Neonatal
1.
Antenatal (in utero) - 80-96% of cases
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2.
3.
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Primary Maternal Infection
Recurrent Maternal Infection
Perinatal
Postnatal
Childhood
1. Horizontal Transmission

CMV excreted in saliva, urine, stool, tears
2. Organ Transplantation

kidney, marrow, heart, liver, blood (leukocytes)
CLINICAL FEATURES:
90% of infants with congenital CMV infection are clinically silent

CNS Manifestations
 70% - microcephaly
 60%
- intellectual impairment
 35% - sensorineural hearing loss
 seizures
 22%
- chorioretinitis
CLINICAL FEATURES:
 Systemic Manifestations
 Reticuloendothelial (Liver) - 65-75%
 70%
- hepatomegaly/splenomegaly
 68% - jaundice
 65% - thrombocytopenia (with petechiae
and purpura)
 hepatitis
 Others
65% - low birth weight (< 2500 gm)
2-5% - pneumonitis
INVESTIGATIONS
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Diagnostic
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Virology
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Serology
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PCR
Serum
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ELISA - CMV-specific IgM
of neonatal blood specimens, cord sampling
Others
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gold standard
of urine, saliva, blood, CSF, nasopharynx
CBC - anemia, thrombocytopenia
conjugated , unconjugated hyperbilirubinemia
elevated hepatic transaminases
CSF

elevated protein content
INVESTIGATIONS:
Imaging Studies
CT (Head)
 periventricular
calcifications

can be identified in
25-50% of
symptomatic infants
Prognosis
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Infants with signs of congenital CMV infection
80% have long-term sequelae:
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sensorineural hearing loss
neuromuscular problems
motor and intellectual retardation
seizures
chorioretinitis with visual deficits
Infants with silent congenital CMV infection
have a more favourable outcome
® Ganciclovir
CONGENITAL TOXOPLASMOSIS
caused by the protozoan Toxoplasma
gondii
 ocular, central nervous system (CNS)
 incidence: 0.3-1/1000 live births

Routes of Transmission
Neonatal (in utero)
Primary Maternal Infection
 acquired
by the ingestion of raw or undercooked
meat ( cattle), or of infectious oocysts in feces
(cats, birds)
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1st trimester - 17% - spontaneous abortion
2nd trimester - 25% - spontaneous abortion or severe
disease
3rd trimester - 65% - subclinical disease
CLINICAL FEATURES:
70% of infants with congenital toxoplasmosis infection are asymptomatic

Ocular Manifestations (76%)
 chorioretinitis
 optic
nerve atrophy
 microphthalmias
 blindness
CLINICAL FEATURES:

CNS Manifestations (52%)
hydrocephaly
 motor and intellectual retardation
 seizures
 sensorineuronal hearing loss

Systemic Manifestations
 classic triad of congenital toxoplasmosis :
chorioretinitis, hydrocephalus, and intracranial
calcifications.
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INVESTIGATIONS:
 Isolation
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of T. gondii from placenta or cord blood
Serology
 measures
IgG T. gondii antibody
 IgM fluorescent antibody test
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Imaging Studies
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CT (Head)
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intracranial calcifications (33%)
MANAGEMENT

combination of :
pyrimethamine
 sulphadiazine
 folinic acid is added
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
Spiramycin
Prevention
CONGENITAL RUBELLA
caused by an RNA Togavirus
 Vaccine-preventable disease
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Routes of Transmission
Antenatal (in utero)
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1st trimester - 75-90%
2nd trimester - 35-40%
3rd trimester - 25-50%
CLINICAL FEATURES:
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Neonatal Manifestations
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IUGR low birth weight - prematurity
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stillbirth - spontaneous abortion
Early Manifestations
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cloudy corneas
Cataracts
microcephaly
hepatomegaly splenomegaly
jaundice
pulmonary valve stenosis
patent ductus arteriosus
thrombocytopenia purpura
INVESTIGATIONS:

Virology
 from
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urine, naspharynx, CSF
Serology
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
fetal rubella-specific IgM
persistence of rubella-specific IgG after 8-12 months of age