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I. DEFINITION

Rubella virus is an enveloped, positive-stranded RNA virus classified as a Rubivirus in the Togaviridae family. It is capable of causing chronic intrauterine infection and damage to the developing fetus (congenital rubella syndrome [CRS]).

II. INCIDENCE

The incidence of rubella in the United States has decreased by >99% from the prevaccine era. In 2004, the United States was determined to no longer have endemic rubella, and from 2004 through 2014, 94 cases of rubella and 9 cases of CRS, including 3 cases in 2012, were reported; all of them were associated with individuals outside the United States or from unknown sources. Of childbearing women, 92% are estimated to be seropositive (rubella immune). Endemic transmission of rubella was declared eliminated from the Americas in 2015. However, rubella continues to be endemic in other parts of the world. It is estimated that >100,000 infants worldwide are born with CRS each year.

III. PATHOPHYSIOLOGY

Rubella 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 to 30 years. Humans are the only known hosts, with an incubation period of 14 to 21 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% to 20% of women of childbearing age are 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 few cases (2%) have been described after reinfection.

Rubella infection can have catastrophic effects on the developing fetus, resulting in spontaneous abortion, fetal infection, stillbirth, or intrauterine growth restriction. The fetal infection rate varies according to the timing of maternal infection during pregnancy. If infection occurs at 1 to 12 weeks and is associated with maternal rash, there is an 81% risk of fetal infection; at 13 to 16 weeks, 54%; at 17 to 22 weeks, 36%; at 23 to 30 weeks, 30%. There is a rise to 60% at 31 to 36 weeks and to 100% in the last month of pregnancy, but late infection is not associated with CRS. 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 to 12 weeks, when 85% of infected fetuses will have congenital defects. Infection during weeks 13 to 16 results in 35% of fetuses having congenital defects; infection at later gestational ages rarely causes deafness or congenital malformations. Spontaneous abortion may occur in up to 20% of cases when rubella occurs in the first 8 weeks of ...

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