Congenital rubella syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]

Overview

Pregnant women who are not vaccinated against rubella virus are at a risk of contracting the infection. It must be noted however, that not every pregnant woman's infection results in vertical transmission to her fetus. In addition, not every fetus infected with rubella virus has fetal abnormalities or CRS. The typical clinical course of CRS usually begins with a pregnant woman being exposed to the virus via the respiratory route. The virus then infects the placenta and spreads to the fetus. This results in systemic inflammation in the fetus and multiple fetal anomalies, due to disruption of organogenesis.
The timing of the maternal infection has important implications on the fetus. If the woman is infected just before conception or during the first 8-10 weeks of gestation, severe fetal anomalies are most likely to occur, including stillbirth. However, beyond 16 weeks of gestation, rarely any fetal defects are associated with maternal rubella infection.

Noninflammatory necrosis is seen in the epithelium of the chorion, as well as in the endothelial cells.^[1]
Cell mitosis is inhibited as a result of inhibition of actin assembly.^[1]

↑ ^1.0 ^1.1 Bouthry E, Picone O, Hamdi G, Grangeot-Keros L, Ayoubi JM, Vauloup-Fellous C (2014). "Rubella and pregnancy: diagnosis, management and outcomes". Prenat. Diagn. 34 (13): 1246–53. doi:10.1002/pd.4467. PMID 25066688.