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.
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:
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% immunity