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]

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The pathogenesis of congenital rubella syndrome is multifactorial. However, pregnant women who are not vaccinated against rubella are at high risk of contracting the infection. If they get infected during pregnancy, the virus can infect the placenta and spread to the fetus, leading to disruption of the normal process of organogenesis. The degree of severity of malformations depends on the gestational age of the onset of infection. The highest risk of fetal anomalies or poor pregnancy outcomes such as spontaneous abortion and stillbirth is highest if a woman becomes infected prior to conception or in the in the first 8-10 weeks of gestation.[1][2][3][4][5]



The pathogenesis of congenital rubella syndrome (CRS) is believed to be multifactorial. In an attempt to explain the pathogenesis, the following must be noted:[1][2][3][4][5]

Microscopic Pathology


  1. 1.0 1.1 De Santis M, Cavaliere AF, Straface G, Caruso A (2006). "Rubella infection in pregnancy". Reprod. Toxicol. 21 (4): 390–8. doi:10.1016/j.reprotox.2005.01.014. PMID 16580940.
  2. 2.0 2.1 Lambert N, Strebel P, Orenstein W, Icenogle J, Poland GA (2015). "Rubella". Lancet. 385 (9984): 2297–307. doi:10.1016/S0140-6736(14)60539-0. PMC 4514442. PMID 25576992.
  3. 3.0 3.1 3.2 3.3 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.
  4. 4.0 4.1 Lee JY, Bowden DS (2000). "Rubella virus replication and links to teratogenicity". Clin. Microbiol. Rev. 13 (4): 571–87. PMC 88950. PMID 11023958.
  5. 5.0 5.1 Adamo MP, Zapata M, Frey TK (2008). "Analysis of gene expression in fetal and adult cells infected with rubella virus". Virology. 370 (1): 1–11. doi:10.1016/j.virol.2007.08.003. PMC 2694049. PMID 17920097.