Congenital rubella syndrome (CRS) can occur in a developing fetus of a pregnant woman who has contracted rubella, usually in the first trimester. If infection occurs 0–28 days before conception, the infant has a 43% risk of being affected. If the infection occurs 0–12 weeks after conception, the risk increases to 81%. If the infection occurs 13–26 weeks after conception, the risk is 54% of the infant being 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 McAlister Gregg. Signs and symptoms
The classic triad for congenital rubella syndrome is:
Sensorineural deafness (58% of patients)
Eye abnormalities—especially retinopathy, cataract, glaucoma, and microphthalmia (43% of patients)
Congenital heart disease—especially pulmonary artery stenosis and 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)
Low birth weight
Thrombocytopenic purpura
Extramedullary hematopoiesis (presents as a characteristic blueberry muffin rash)
Enlarged liver
Small jaw size
Skin lesions Children who have been exposed to rubella in the womb should also be watched closely as they age for any indication of:

Developmental delay
Autism
Schizophrenia
Growth retardation
Learning disabilities
Diabetes mellitus

Diagnosis
Prevention
Vaccinating the majority of the population is effective at preventing congenital rubella syndrome.
One of the highest incidences is in the isolated populations of the Lake Maracaibo region of Venezuela, where HD affects up to 700 per 100,000 persons. Other areas of high localization have been found in Tasmania and specific regions of Scotland, Wales and Sweden. Increased prevalence in some cases occurs due to a local founder effect, a historical migration of carriers into an area of geographic isolation. Some of these carriers have been traced back hundreds of years using genealogical studies. Genetic haplotypes can also give clues for the geographic variations of prevalence. Iceland, on the contrary, has a rather low prevalence of 1 per 100,000, despite the fact that Icelanders as a people are descended of the early Germanic tribes of Scandinavia which also gave rise to the Swedes; all cases with the exception of one going back nearly two centuries having derived from the offspring of a couple living early in the 19th century. Finland, as well, has a low incidence of only 2.2 per 100,000 people.Until the discovery of a genetic test, statistics could only include clinical diagnosis based on physical symptoms and a family history of HD, excluding those who died of other causes before diagnosis. These cases can now be included in statistics; and, as the test becomes more widely available, estimates of the prevalence and incidence of the disorder are likely to increase.