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I. DEFINITION

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Rubella is a viral infection capable of causing chronic intrauterine infection and damage to the developing fetus. Rubella is classified as a member of the togavirus family.

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II. INCIDENCE

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Rubella vaccination has virtually eliminated the majority of cases of congenital rubella syndrome (CRS) in the developed world. In the United States, between 2000 and 2005, only 4 cases of CRS have been reported, and only 1 was a child whose mother had been born in the United States. Rubella remains prevalent in developing countries and in nonvaccinated immigrant populations.

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III. PATHOPHYSIOLOGY

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Rubella virus is an RNA virus that typically has an epidemic seasonal pattern of increased frequency in the spring. In developing countries with no vaccination programs, epidemics have occurred at 4- to 7-year intervals, with major pandemics every 10–30 years. Humans are the only known hosts, with an incubation period of ∼18 days after contact. Virus is spread by respiratory secretions and also from stool, urine, and cervical secretions. A live virus vaccine has been available since 1969. In places with no vaccination, 15–20% of women of childbearing age are susceptible to rubella. Recent serologic surveys indicate that ∼10% of the U.S.-born population >5 years of age is susceptible to rubella. There is a high incidence of subclinical infections. Maternal viremia is a prerequisite for placental infection, which may or may not spread to the fetus. Most cases occur after primary disease, although a few cases have been described after reinfection.

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The fetal infection rate varies according to the timing of maternal infection during pregnancy. If infection occurs at 1–12 weeks and is associated with maternal rash, there is an 81% risk of fetal infection; at 13–16 weeks, 54%; at 17–22 weeks, 36%; at 23–30 weeks, 30%; there is a rise to 60% at 31–36 weeks; and 100% in the last month of pregnancy. No correlation exists between the severity of maternal rubella and teratogenicity. However, the incidence of fetal effects is greater the earlier in gestation that infection occurs, especially at 1–12 weeks, when 85% of infected fetuses will have congenital defects. Infection during weeks 13–16 results in 35% of fetuses having congenital defects; infection at later gestational ages rarely causes deafness or congenital malformations. The virus sets up chronic infection in the placenta and fetus. Placental or fetal infection may lead to resorption of the fetus, spontaneous abortion, stillbirth, fetal infection with multisystem disease, congenital anomalies, or unapparent infection. Spontaneous abortion may occur in up to 20% of cases when rubella occurs in the first 8 weeks of pregnancy.

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The disease involves angiopathy as well as cytolytic changes. Other viral effects include chromosome breakage, decreased cell multiplication time, induction of programmed cell death (apoptosis), and mitotic arrest in certain cell types. There is little inflammatory reaction.

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IV. RISK FACTORS

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Women of ...

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