Congenital rubella syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2]

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Overview

Congenital rubella syndrome results from the spread of infection to the fetus by the mother during the viremic stage. Rubella virus enters the fetus through the placenta and causes damage to all the germ layers of the fetus. This results in rapid death of some cells.

Pathophysiology

Congenital rubella syndrome results from the infection of fetus by transmission of virus from the mother during the viremic stage of the infection. Virus travels through the blood stream of the fetus and damages the blood vessels. This results in ischemic injury to the cells in the germ layers. The risk of congenital infection and defects is highest during the first 12 weeks of gestation and decreases after the 12th week of gestation with defects rare after the 20th week of gestation. 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.

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