Congenital rubella syndrome
|This article needs additional citations for verification. (December 2007)|
|Congenital rubella syndrome|
|Classification and external resources|
White pupils due to congenital cataract in a child with congenital rubella syndrome
Congenital rubella syndrome (CRS) can occur in a developing fetus of a pregnant woman who has contracted rubella during her first trimester. If infection occurs 0–28 days before conception, there is a 43% chance the infant will be affected. If the infection occurs 0–12 weeks after conception, there is a 51% chance the infant will be affected.
If the infection occurs 13–26 weeks after conception there is a 23% chance the infant will be affected by the disease. Infants are not generally affected if rubella is contracted during the third trimester, or 26–40 weeks after conception. Problems rarely occur when rubella is contracted by the mother after 20 weeks of gestation and continues to disseminate the virus after birth.
It was discovered in 1941 by Australian Norman McAllister Gregg.
The classic triad for congenital rubella syndrome is:
- Sensorineural deafness (58% of patients)
- Eye abnormalities—especially retinopathy, cataract and microphthalmia (43% of patients)
- Congenital heart disease—especially patent ductus arteriosus (50% of patients)
Other manifestations of CRS may include:
- Spleen, liver or bone marrow problems (some of which may disappear shortly after birth)
- Intellectual disability
- Small head size (microcephaly)
- Eye defects
- Low birth weight
- Thrombocytopenic purpura
- Extramedullary hematopoiesis (presents as a characteristic blueberry muffin rash)
Children who have been exposed to rubella in the womb should also be watched closely as they age for any indication of the following:
- Developmental delay
- Autism spectrum disorders
- Growth retardation
- Learning disabilities
Vaccination of females of childbearing age against rubella can prevent congenital rubella syndrome. Therapeutic abortion is an option if early exposure occurs or CRS is suspected antenatally.
- Muhle, R; Trentacoste, SV; Rapin, I (May 2004). "The genetics of autism.". Pediatrics 113 (5): e472–86. doi:10.1542/peds.113.5.e472. PMID 15121991.
- Brown, A. S (9 February 2006). "Prenatal Infection as a Risk Factor for Schizophrenia". Schizophrenia Bulletin 32 (2): 200–202. doi:10.1093/schbul/sbj052. PMC 2632220. PMID 16469941.