Congenital rubella syndrome pathophysiology: Difference between revisions
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*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 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]]. | ||
*Infected cells of the [[placenta]] enter the [[fetal]] [[circulation]] and spread to to various [[organs]], such as the [[heart]], [[brain]], [[eyes]] and [[ears]], resulting in [[thrombosis]] or [[ischemic]] lesions in these [[organs]]. | *Infected cells of the [[placenta]] enter the [[fetal]] [[circulation]] and spread to to various [[organs]], such as the [[heart]], [[brain]], [[eyes]] and [[ears]], resulting in [[thrombosis]] or [[ischemic]] lesions in these [[organs]]. | ||
*In rubella-infected [[human]] [[fetal]] [[cells]], [[interferons]] and [[cytokines]] are up-regulated. Hence, the [[immune system]] is thought to play a role in disrupting the normal differentiation of [[cells]] and result in the various [[congenital defects]] | *In rubella-infected [[human]] [[fetal]] [[cells]], [[interferons]] and [[cytokines]] are up-regulated. Hence, the [[immune system]] is thought to play a role in disrupting the normal differentiation of [[cells]] and result in the various [[congenital defects]] observed in congenital rubella syndrome. | ||
*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. | *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. | ||
===Microscopic Pathology=== | ===Microscopic Pathology=== | ||
*Noninflammatory [[necrosis]] is | *Noninflammatory [[necrosis]] is observed in the [[epithelium]] of the [[chorion]], as well as in the [[endothelial cells]].<ref name="pmid25066688">{{cite journal |vauthors=Bouthry E, Picone O, Hamdi G, Grangeot-Keros L, Ayoubi JM, Vauloup-Fellous C |title=Rubella and pregnancy: diagnosis, management and outcomes |journal=Prenat. Diagn. |volume=34 |issue=13 |pages=1246–53 |year=2014 |pmid=25066688 |doi=10.1002/pd.4467 |url=}}</ref> | ||
*[[Cell]] [[mitosis]] is inhibited as a result of inhibition of [[actin]] assembly.<ref name="pmid25066688">{{cite journal |vauthors=Bouthry E, Picone O, Hamdi G, Grangeot-Keros L, Ayoubi JM, Vauloup-Fellous C |title=Rubella and pregnancy: diagnosis, management and outcomes |journal=Prenat. Diagn. |volume=34 |issue=13 |pages=1246–53 |year=2014 |pmid=25066688 |doi=10.1002/pd.4467 |url=}}</ref> | *[[Cell]] [[mitosis]] is inhibited as a result of inhibition of [[actin]] assembly.<ref name="pmid25066688">{{cite journal |vauthors=Bouthry E, Picone O, Hamdi G, Grangeot-Keros L, Ayoubi JM, Vauloup-Fellous C |title=Rubella and pregnancy: diagnosis, management and outcomes |journal=Prenat. Diagn. |volume=34 |issue=13 |pages=1246–53 |year=2014 |pmid=25066688 |doi=10.1002/pd.4467 |url=}}</ref> | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Revision as of 14:31, 11 April 2017
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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Overview
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]
Pathophysiology
Pathogenesis
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]
- Pregnant women who are not vaccinated against rubella virus are at 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.
- Infected cells of the placenta enter the fetal circulation and spread to to various organs, such as the heart, brain, eyes and ears, resulting in thrombosis or ischemic lesions in these organs.
- In rubella-infected human fetal cells, interferons and cytokines are up-regulated. Hence, the immune system is thought to play a role in disrupting the normal differentiation of cells and result in the various congenital defects observed in congenital rubella syndrome.
- 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.
Microscopic Pathology
- Noninflammatory necrosis is observed in the epithelium of the chorion, as well as in the endothelial cells.[3]
- Cell mitosis is inhibited as a result of inhibition of actin assembly.[3]
References
- ↑ 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.
- ↑ 2.0 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.
- ↑ 3.0 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.
- ↑ 4.0 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.
- ↑ 5.0 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.