This program helps families of eligible children who might not otherwise have access to vaccines. You can also contact your state VFC coordinator. Children may also get MMRV vaccine , which protects against measles, mumps, rubella, and varicella chickenpox. This vaccine is only licensed for use in children who are 12 months through 12 years of age.
Before the availability of rubella vaccines in the United States, rubella was a common disease that occurred primarily among young children.
The last major epidemic in the United States occurred during to , when there were an estimated Because of successful vaccination programs, rubella has been eliminated from the United States since However, rubella is still common in other countries. Unvaccinated people can get rubella while abroad and bring the disease to the United States and spread it to others.
Vaccine recommendations and contraindications; composition, dosage, and administration; handling and storage Skip directly to site content Skip directly to page options Skip directly to A-Z link. Section Navigation. Facebook Twitter LinkedIn Syndicate. International Travelers. Protect Against Rubella. Also, their babies can have birth defects, such as heart problems loss of hearing or eyesight intellectual disabilities liver or spleen damage.
Rubella Fact Sheet for Parents. Vaccine Shot for Rubella. Links with this icon indicate that you are leaving the CDC website. Linking to a non-federal website does not constitute an endorsement by CDC or any of its employees of the sponsors or the information and products presented on the website.
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The rubella virus is a member of the genus Rubivirus in the family Togaviridae. Postnatal rubella is often asymptomatic but may result in a generally mild, self-limited illness characterized by rash, lymphadenopathy, and low-grade fever. As is the case for many viral diseases, adults often experience more severe symptoms than do children. In addition, adolescents and adults may experience a typical mild prodrome that is not seen in infected children; this occurs 1 to 5 days before the rash and characterized by headache, malaise, and fever.
The typical picture of rubella Fig. It often fades on the face while progressing downwards. The lesions tend to be discrete at first, but rapidly coalesce to produce a flushed appearance. The onset of rash is often accompanied by low-grade fever. Clinical findings, virus shedding, and serologic response in postnatally acquired rubella.
The earliest and perhaps the most prominent and characteristic symptom of rubella infection is lymphadenopathy of the postauricular, occipital, and posterior cervical lymph nodes; this is usually most severe during the rash but may occur even in the absence of rash. Postnatal rubella usually resolves without complication.
Other complications of rubella, reported with much less frequency than arthritis, include encephalitis and thrombocytopenic purpura. Rubella infection acquired during pregnancy can result in stillbirth, spontaneous abortion, or several anomalies associated with the congenital rubella syndrome.
The clinical features of congenital rubella vary and depend on the organ system s involved and the gestational age at the time of maternal infection Table The classic triad of congenital rubella syndrome includes cataracts, heart defects, and deafness, although many other abnormalities, as noted in the Table, may be seen.
Defects may occur alone or in combination and may be temporary or permanent. The risk of rubella-associated congenital defects is greatest during the first trimester of pregnancy. Some defects have been reported after maternal infections in the second trimester.
Abnormalities Associated with Congenital Rubella Syndrome. Rubella virus is a spherical to nm, positive-sense, single-stranded RNA virus consisting of an electron-dense to nm core surrounded by a lipoprotein envelope. The virus particles are generally spherical with spiky hemagglutinin-containing surface projections. Rubella virus is the single member of the genus Rubivirus in the family Togaviridae.
It is serologically distinct from other members of the Togaviridae, and, unlike most other togaviruses, is not known to be transmitted by an arthropod. Only one genetically stable serotype of rubella virus has been identified. Phylogenetic tree analysis of nine virus strains indicate the existence of at least three distinct genetic lineages. Rubella virus contains three major structural polypeptides: two membrane glycoproteins, E1 and E2 and a single nonglycosylated RNA-associated capsid protein, C, within the virion.
One of the envelope proteins, E1, is responsible for viral hemagglutination and neutralization. E2 has been found in two forms, E2a and E2b due to differences in glycosylation. The differences among strains of rubella viruses have been correlated with differences in the antigenicity of E2. Humans are the only known reservoir of rubella virus, with postnatal person-to-person transmission occurring via direct or droplet contact with the respiratory secretions of infected persons.
Although the early events surrounding infection are incompletely characterized, the virus almost certainly multiplies in cells of the respiratory tract, extends to local lymph nodes, and then undergoes viremic spread to target organs Fig. Subsequent additional replication in selected target organs, such as the spleen and lymph nodes, leads to a secondary viremia with wide distribution of rubella virus.
At this time approximately 7 days after infection and 7 to 10 days before the onset of rash the virus can be detected in the blood and respiratory secretions Fig. Viremia disappears shortly after the onset of rash; it is also associated with the appearance of circulating neutralizing antibodies.
However, virus shedding from the respiratory tract may continue for up to 28 days following the onset of rash. Rubella infection in the first 3 or 4 months of pregnancy provides opportunities during the period of maternal viremia for invasion of the placenta and subsequent fetal infection. Development of infection probably depends upon gestational age. It has been estimated that the fetus has a 40 to 60 percent chance of developing multiple rubella-associated defects if the mother is infected during the first 2 months of pregnancy, with the risk dropping to 30 to 35 percent during the third month of gestation and 10 percent during the fourth.
This difference in both risk for and severity of fetal infection seen with gestational age may be associated with immature host defenses during the first trimester of pregnancy. During fetal infection, the virus can multiply in and damage virtually any organ system.
Pathogenesis of the congenital defects is not fully understood; however, a number of mechanisms have been proposed. Cell culture studies show that the virus produces chromosomal abnormalities, slows cellular growth rates, and causes cell lysis and death in some cell types; these effects appear capable of producing the characteristic abnormalities of cell structure and function.
In the congenitally infected fetus and infant, virus persistence occurs in the presence of neutralizing antibodies; immunological tolerance does not develop. Postnatal infection rapidly induces a specific immune response which provides lifelong protection against the natural disease. Neutralizing and hemagglutination-inhibiting antibodies appear shortly after the onset of rash and reach maximum levels in 1 to 4 weeks. Specific antibodies persist after infection.
Cell-mediated immunity also develops in convalescence and can be detected for years following infection. When exposed to rubella virus, individuals with neutralizing or hemagglutination-inhibiting antibodies are most often protected. However, reinfection with rubella virus has been documented in individuals with demonstrated natural immunity and, more commonly, in vaccinees.
The vast majority of such reinfections are asymptomatic, detectable only by a boost in antibody titer; however, a few cases of reinfection-associated rash and arthritis have been reported. Rubella occurs worldwide. There have been no major epidemics in the United States since the licensure of the live attenuated rubella vaccine in However, limited sporadic outbreaks of rubella continue to occur each year, particularly in settings such as schools where susceptible individuals come into close contact.
The incidence of infection shows the same prominent seasonal pattern as for other respiratory diseases. The incidence increases in winter, peaks in spring, and then subsides to extremely low levels in summer and fall. Epidemiologic data suggest that maximum infectivity occurs from 3 days before the onset of rash until 3 days afterward. However, throat swabs from children with rubella have been reported to contain virus from as early as 10 days before the onset of rash to as late as 28 days afterward.
In addition, asymptomatic individuals have been reported to transmit rubella. In the prevaccine era, the disease usually affected children 5 to 9 years old. However, because rubella is less contagious than diseases such as measles and varicella, a significant proportion of the population 10 to 15 percent escaped rubella infection in childhood. Widespread vaccine use has reduced rubella incidence by more than 99 percent overall Fig. However, a greater percentage of cases that do occur are now reported in unvaccinated young adults.
In , 48 percent of reported rubella infections were in persons older than 15 years of age. In addition, about 6 to 11 percent of postpubertal women in the United States currently lack serologic evidence of immunity. These data continue to be of concern; such women continue to remain at risk for rubella during pregnancy.
An average of 39 cases per year of congenital rubella were reported to the Centers for Disease Control between and , falling rather dramatically to an average of only 7 cases per year between and A slight resurgence of rubella and congenital rubella was noted in to
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