This article focuses on discussion of congenital rubella syndrome (CRS), also known as congenital German measles or prenatal rubella. The clinical presentation of late-onset rubella syndrome will also be discussed. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
Congenital rubella infection classically causes a severe syndrome with multi-organ manifestations encompassing visual, hearing, and neurologic disabilities; it may, however, also present with more subtle findings that can lead to significant diagnostic delays if the treating physician is not familiar with the consequences of maternal rubella infection. Although widespread vaccination programs have significantly reduced the global burden of rubella, rubella remains an important pathogen that remains endemic in many regions of the world, and its varied presentation requires vigilance on behalf of health providers.
• Rubella infection rates and risk of congenital rubella syndrome are highest during the first trimester of pregnancy and during primary infection of the pregnant mother.
• Because the virus may persist for up to 1 year of age, pregnant women should not handle or expose themselves to congenitally infected infants.
• Despite high vaccine coverage, rubella infection persists in unimmunized groups, those with low seroconversion status, or as a result of reinfection.
Historical note and terminology
In the mid-18th century, rubella (German measles) was termed "Rötheln" and was considered to be a lesser form of measles or scarlet fever, as symptoms and the associated exanthematous rash were less severe (Wesselhoeft 1947). By the 19th century, Rötheln was formally recognized as a distinct infection and renamed "rubella." An Australian ophthalmologist was the first to note cataracts and heart disease in newborn children of mothers infected during pregnancy (Gregg 1941). Subsequent studies confirmed rubella's teratogenic potential. The viral etiology of rubella was established in 1962 (Parkman et al 1962; Weller and Neva 1962). Diagnostic serologic tests soon followed, and by 1969 live attenuated vaccines were licensed for use.
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