The virus disrupts mitosis, retarding cellular division and causing vascular damage. Major malformations are most likely during organogenesis with severity decreasing with advancing gestation (Table 4.1). Defects include:
Sensorineural deafness.
Cardiac abnormalities including VSD and patent ductus arteriosus (PDA).
Eye lesions (congenital cataracts, microphthalmia, and glaucoma).
Microcephaly and mental retardation.
Gestation | Risk of transmission | Risk of congenital abnormality | Treatment |
<13wks | 80% | Almost all infected fetuses | TOP may be offered without invasive prenatal diagnosis |
13–16wks | 50% | About 35% of those infected (mainly deafness) | Fetal blood sampling may be later offered to confirm infection |
>16wks | 25% | Rarely causes defects | Reassurance |
Gestation | Risk of transmission | Risk of congenital abnormality | Treatment |
<13wks | 80% | Almost all infected fetuses | TOP may be offered without invasive prenatal diagnosis |
13–16wks | 50% | About 35% of those infected (mainly deafness) | Fetal blood sampling may be later offered to confirm infection |
>16wks | 25% | Rarely causes defects | Reassurance |
Late-developing sequelae include:
Diabetes.
Thyroid disorders.
Progressive panencephalitis.
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