Congenital rubella syndrome pathophysiology: Difference between revisions

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==Pathophysiology==
==Pathophysiology==
===Pathogenesis===
===Pathogenesis===
*[[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.
===Gross Pathology ===
===Gross Pathology ===
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Revision as of 19:13, 16 January 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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