Primary postnatal rubella virus infection is typically a mild self-limiting disease characterized by a maculopapular rash, fever, malaise and lymphadenopathy.1 In contrast to postnatal infections, primary prenatal
infections may have devastating effects. In utero infections may severely damage the fetus, particularly if occurring during the first four months of gestation. The congenitally infected infant may exhibit one or more of a
variety of defects collectively known as the congenital rubella syndrome (CRS). Among these are low birth weight, cataracts, deafness, congenital heart disease, and mental retardation.
The World Health Organization (WHO) conducted a worldwide survey on rubella, CRS, and rubella vaccine in 1995 and 1996. They reported an incidence of CRS of 60 to 220 cases with 100000 live births during epidemics in developing countries, a rate similar to those of industrialized countries before vaccination.
Both naturally acquired and vaccine induced immunity to rubella virus associated with antibody persistence have been shown to provide protection from clinical rubella upon reinfection. The widespread use of highly effective and safe vaccines dramatically reduced the incidence of rubella and CRS in the United States. In spite of this reduction, rubella outbreaks continue to occur. The number of cases of rubella reported annually to the WHO Regional Office for Europe has remained fairly stable over the past decade, with 304320 cases reported during 2003.
These occurrences indicate a need for continued serological surveillance to identify susceptible individuals and reduce the potential risk to CRS. The presence of at least 10 International Units (IU) of antibody per mL of sample is indicative of past exposure to rubella virus. Antibody levels below 10 IU/mL may be insufficient to provide protection from clinical illness upon exposure to rubella virus.
Manufacturer’s Reagent package insert Architect Rubella IgG, December 2016, Abbott Laboratories, Max-Planck-Ring 2 65205 Wiesbaden, Germany