Occasionally, the rash is scarlatiniform or purpuric. The rash typically lasts for 3 days and fades in the same directional pattern as it appears. Rubella infection during embryogenesis leads to the classic triad of cataracts, congenital heart defects, and sensorineural deafness; however, many other defects might be observed. During the neonatal period, CRS has been associated with low birth weight, thrombocytopenic purpura, hemolytic anemia, hepatosplenomegaly, and meningoencephalitis.
These manifestations are usually transient. Other clinical manifestations of CRS include ophthalmopathies retinopathy, glaucoma, chorioretinitis, iris hypoplasia, and microphthalmia , cardiac abnormalities patent ductus arteriosus, pulmonary artery hypoplasia , psychomotor retardation, and microcephaly.
Of all the manifestations, deafness is the most common finding and could be the only defect observed. Individuals that survive the neonatal period may face severe disabilities e. In addition, a variety of late-onset endocrine, cardiovascular and neurological abnormalities have been described.
The clinical diagnosis of rubella is difficult because the manifestations can be mild and non-specific. Therefore, physicians must rely on serological testing to confirm rubella. The most common diagnostic test for recent postnatal infection is the detection of rubella-specific IgM antibodies by using an enzyme immunoassay.
Rubella-specific IgM antibodies are usually detectable 4 days after the onset of rash. Recent primary rubella infections can also be confirmed by rubella-specific low avidity IgG. In those cases in which a pregnant woman has been exposed to a suspected rubella case, a specimen of blood should be tested as soon as possible for the measurement of rubella-specific IgG antibodies. If it is positive, then the woman was likely to be immune and could be reassured.
If it is negative, a determination rubella-specific IgG and rubella-specific IgM antibodies should be obtained in 3 weeks to exclude an asymptomatic primary rubella infection. Congenital rubella infection may be diagnosed prenatally either by a demonstration of specific IgM in fetal blood or by the detection rubella RNA in amniotic fluid, fetal blood, or chorionic villus biopsy using reverse transcription-polymerase chain reaction RT-PCR.
In the newborn period, the serologic diagnosis of congenital rubella is made by the detection of rubella-specific IgM within the first 6 months of life. Congenital rubella infection can also be confirmed by the increase or persistence of rubella-specific IgG in the infant after 6 to 12 months of age.
If the infection occurs after 18 weeks of gestation, the pregnancy could be continued with ultrasound monitoring and specific neonatal management. It usually involves a multidisciplinary approach and requires pediatric, ophthalmologic, cardiac, audiological, and neurodevelopmental evaluation. Long-term follow up is needed to monitor for delayed manifestations. Rubella needs to be distinguished from other infections with similar maculopapular rashes, including measles, human herpesvirus 6 and 7, infectious mononucleosis, cytomegalovirus, arboviruses Zika virus, West Nile fever, Ross River fever, and Chikungunya virus , enteroviruses, scarlet fever, and mycoplasma infection.
Other conditions to be considered in the differential diagnosis for rubella are non-infectious causes like Kawasaki disease, drug eruption, and contact dermatitis. Postnatal infection with rubella is generally mild, self-limited, and has an excellent prognosis. However, the prognosis of children with congenital rubella syndrome is less favorable and varies depending on the severity and number of organs affected.
The risk of mortality risk is high in infants with thrombocytopenia, interstitial pneumonia, hepatosplenomegaly, and pulmonary hypertension.
It is usually symmetric and involves the wrists, fingers, knees, and ankles. Rubella infection during pregnancy may lead to miscarriage, intrauterine fetal demise, premature labor, intrauterine growth retardation, and congenital rubella syndrome. Parents should be educated and counseled on the importance of routine immunization in infants and young children. It is also essential to identify and immunize all susceptible women of childbearing age prior to conception.
Universal immunization of all susceptible individuals with rubella vaccines is the cornerstone to the prevention of rubella and, more importantly, congenital rubella syndrome. The vaccine is usually administered in combination with measles and mumps MMR or measles, mumps, and varicella MMRV , with the first dose at ages months and the second dose at ages years. Contraindications for rubella vaccination include a history of an anaphylactic reaction to a previous dose or any of the vaccine's components e.
MMR vaccine is not contraindicated in individuals with an allergy to eggs. 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. Test Usage. Test Limitations. Days Set Up. Analytic Time. Soft Order Code. MiChart Code. Collection Instructions. Alternate Specimen. Rejection Criteria. Other Rejected Containers: Cadaver or other body fluids eg. Normal Volume. Up to half of all infections may be subclinical or unapparent. Many rubella infections are not recognized because the rash resembles many other rash illnesses.
Rubella virus is an enveloped, positive-stranded RNA virus classified as a Rubivirus in the Matonaviridae family. Before the rubella vaccine was licensed in the United States in , rubella was a common disease that occurred primarily among young children. Epidemics occurred every 6 to 9 years, with the highest number of cases during the spring. Rubella was declared eliminated the absence of endemic transmission for 12 months or more from the United States in However, it is still commonly transmitted in many parts of the world.
As a result, less than 10 cases primarily import-related have been reported annually in the United States since elimination was declared. Because rubella continues to circulate in other parts of the world, an estimated , infants are born with congenital rubella syndrome CRS annually worldwide. Rare complications include thrombocytopenic purpura and encephalitis. When rubella infection occurs during pregnancy, especially during the first trimester, serious consequences can result.
The most common congenital defects are cataracts, heart defects, and hearing impairment.
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