Congenital rubella syndrome (CRS) occurs in a developing fetus of a pregnant woman who has contracted rubella, usually in the 1st trimester.

• Molecular basis for the causation of CRS isn't yet completely clear, but in vitro studies with cell lines showed that rubella virus has an apoptotic effect on certain cell types
• There is evidence for a p53-dependent mechanism

• Classical triad, including:
  • Sensorineural deafness (58%)
  • Eye abnormalities (43%), especially retinopathy, cataract, and microphthalmia
  • Congenital heart disease (50%), especially pulmonary artery stenosis, and patent ductus arteriosus
• Spleen, liver, or bone marrow problems (some of which may disappear shortly after birth)
• Intellectual disability
• Microcephaly (small head size)
• Eye defects
• Low birth weight
• Thrombocytopenic purpura
• Extramedullary hematopoiesis (characteristic blueberry muffin rash)
• Hepatomegaly
• Micrognathia

Children exposed to rubella in the womb should be watched closely as they age for any indication of:

• Developmental delay
• Autism
• Schizophrenia
• Growth retardation
• Learning disabilities
• Diabetes mellitus
• Glaucoma

• If infection occurs 0-28 days BEFORE conception, the infant has a 43% chance of being affected
• If infection occurs 0-12 weeks AFTER conception, the chance increases to 51% <-- i.e. greatest risk here!!
• If infection occurs 13-26 weeks after conception, the chance is 23% of the infant being affected by the disease
• Infants are not generally affected if rubella is contracted during the 3rd trimester, or 26-40 weeks after conception
• Problems rarely occur when rubella is contracted by the mother >20 weeks of gestation, and continues to disseminate the virus after birth

• Discovered in 1941 by Australian apthomologist, Dr Norman McAlister Gregg
• Vaccinating the majority of the population is effective at preventing CRS