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Rubella (German measles) is no longer endemic in the United States. Because of its worldwide distribution, imported cases continue to occur, although these sporadic cases do not result in sustained transmission.1,2 Rubella is usually a minor illness in adults. Of major significance, however, is the high incidence of a constellation of congenital defects in children whose mothers are infected during early pregnancy. Typical anomalies caused by this congenital infection, known collectively as the congenital rubella syndrome (CRS), include hearing impairment, cardiac defects, cataracts, and developmental delay.


Rubella is a member of the Togaviridae family (a single serotype and the only member of the genus Rubivirus) with an approximately 10-kb (9762 nucleotides) single-stranded, positive-sense polyadenylated RNA genome and a lipid envelope (thus the Latin name of toga or cloak). The virus was first isolated in 1962 by Weller from the urine of his son.3 Currently, standardized nomenclature for wild-type and vaccine rubella viruses describes 2 clades, 9 recognized genotypes, and 4 provisional genotypes.4 Rubella shares physicochemical properties with group A arboviruses. The virion is roughly spherical, 60 to 70 nm in diameter, with an icosahedral nucleocapsid composed of multiple copies of a single virus-specified structural capsid protein (C) that is covered by a lipid envelope in which 2 virus-specified structural glycoproteins (E1 and E2) are embedded. E1 appears to function in attachment, fusion, hemagglutination, and neutralization. In addition, there are two virus-specified nonstructural proteins (p90 and p150). The virus is thermolabile; inactivation is rapid at 37°C (98.6°F) and at room temperature. However, it can be stored for short periods at 20°C (4°F) and is relatively stable for months at 60°C (76°F).


Humans are the only natural host. Direct person-to-person airborne spread by infected droplets appears to be the usual mode of transmission. The patient with subclinical infection is also a source of rubella virus. Patients are most contagious for a few days before and after the onset of rash, although virus may be present in pharyngeal secretions for as long as 1 week before and 2 weeks after the onset of rash (Fig. 320-1). Infection acquired postnatally does not produce a chronic carrier state. Prolonged shedding occurs only in patients with congenital rubella syndrome, not when acquired postnatally, which is characterized by chronic infection; infants may remain contagious for months after birth.

Figure 320-1.
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Rubella. The rash consists of erythematous macules and papules that appear initially on the face and spread inferiorly to the trunk and extremities, usually within the first 24 hours. (From Wolff K, Johnson RA. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology. 6th ed. New York: McGraw-Hill; 2009.)




Although rubella occurs in all areas of the world, epidemiologic patterns vary from country to country. Mathematic modeling predicts that elimination of transmission requires approximately 90% ...

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