Rubella (German Measles)

Andreea C. Cazacu

Gail J. Demmler

Rubella is an acute infectious disease characterized by low-grade fever, erythematous maculopapular rash, and adenopathy. Rubella infection in early pregnancy may result in fetal infection with severe congenital anomalies. Rubella was described in the 1700s by German physicians, and in 1866, Veale, a Royal Artillery surgeon, described an outbreak of illness that he named “rubella.” In 1941, Gregg, an Australian physician, described congenital defects in infants of mothers who had rubella during pregnancy. Rubella virus was isolated in tissue culture in 1962. Rubella and congenital rubella syndrome (CRS) became reportable in 1966 and 1969, respectively. Development of the hemagglutination inhibition (HAI) test in 1967 rendered possible the performance of large-scale surveillance studies and diagnostic testing. Attenuated rubella virus vaccine was developed in the late 1960s and was licensed in the United States in 1969. Vaccine use in children and in women of childbearing age dramatically reduced the number of cases of postnatally acquired rubella and congenital rubella.

ETIOLOGY

Rubella virus is a non-arthropod-borne, RNA-containing, heat-labile togavirus of the genus Rubivirus. It has no antigenic relationship with other togaviruses. Only a single type of rubella virus has been described. Several antigens have been defined, including an envelope antigen, a hemagglutinin, the inhibition of which by rubella specific antisera is the basis for the HAI test for rubella. Isolation of rubella virus in tissue culture from clinical specimens is achieved by viral interference. When African green monkey kidney cells are infected with rubella virus, they show no cytopathic effect, and when the same rubella-infected cells then are challenged with an appropriate enterovirus, they resist infection with the enterovirus and again demonstrate no cytopathic effect, or interference.

POSTNATALLY ACQUIRED RUBELLA

Pathogenesis and Epidemiology

Natural infection with rubella virus occurs only in humans, although several different animals have been infected experimentally with the virus. Transmission occurs by oral droplet in acquired rubella, compared with transplacentally in congenital rubella. In human volunteers, infection occurs easily after droplet presentation to the nasopharyngeal mucosa. The sequence of events includes replication of the virus in the nasopharyngeal mucosa, involvement of regional lymphatics, and subsequent viremia. The maximum titer of the virus in the nasopharynx is present several days before the rash appears, and an infected person is most contagious during this period. Periods of maximum communicability include the week before and the week after the appearance of the rash, and patients with known cases of acquired rubella should be isolated during this period. Viremia clears quickly after appearance of the rash, but the virus may be shed from the nasopharynx after the resolution of the rash.

Rubella virus has been isolated from the nasopharynx, blood, skin, synovial fluid, cerebrospinal fluid (CSF), placenta, and other specimens. Infected hosts develop both humoral and cell-mediated immunity. After infection, antibodies in both immunoglobulin M (IgM) and G (IgG) classes develop rapidly after appearance of the rash. Rubella-specific IgM antibody usually persists approximately 12 weeks and may aid in diagnosis of an acute infection. Antibodies of IgG class persist for life and are markers for immunity.

In the prevaccine era, major rubella outbreaks occurred every 6 to 9 years, with the highest attack rates in school-aged children (5 to 10 years) and lesser attack rates in preschool-aged children. Rubella occurs worldwide, and outbreaks are seen in the winter and spring months in temperate climates. After widespread immunization with rubella vaccine was achieved, incidence rates or reported rubella decreased steadily and reached an all-time low in 1988. Since 1989, however, the number of reported cases has increased steadily each year, marking a moderate resurgence of postnatal rubella and subsequent concern for an increase in CRS.

Whereas increases in incidence of acquired rubella have occurred in all age groups, the most dramatic increase has occurred in persons older than 15 years of age. In 1990, 26 rubella outbreaks were reported, and they appeared to fall into two categories. One type of outbreak was associated with settings in which unvaccinated adolescents and adults congregated, such as prisons, colleges, workplaces (especially hospitals), and recreational settings. Another form of outbreak occurred among children and adults in religious communities with low levels of rubella vaccination. Information from both these types of outbreaks suggests that failure to vaccinate, not primary or secondary vaccine failure, was responsible for this increase incidence of rubella. In 1996, 196 provisional cases of indigenous rubella were reported; most cases occurred in adults 20 years of age or older. In 1998, more than 90% of infants with CRS were born to foreign-born mothers, 81% of whom were of Hispanic ethnicity.

Clinical Manifestations

Incubation periods for postnatal rubella range from 14 to 21 days, usually 15 to 18 days. Inapparent infection may occur in 25% or more of infected individuals. Prodromal symptoms, usually appearing 1 to 5 days before the rash, are seen more commonly among older children and adults; they consist of low-grade fever, coryza, conjunctivitis, cough, and lymphadenopathy (Table 201.1). An enanthem of rubella, Forchheimer spots, consists of discrete, erythematous pinpoint or larger lesions found on the soft palate in the prodromal phase or on the first day of the rash. These lesions are not pathognomonic for rubella, however. The lymphadenopathy associated with rubella may appear as early as 7 days before appearance of the rash. The suboccipital, posterior auricular, and cervical lymph nodes are involved most commonly, but
generalized lymphadenopathy may occur. Maximum swelling of the lymph nodes and tenderness usually coincide with the first day of the appearance of the rash.

TABLE 201.1. COMPARISON OF COMMON CLINICAL MANIFESTATIONS OF CONGENITAL AND POSTNATAL RUBELLA

Congenital Rubella	Postnatal Rubella
Intrauterine growth retardation	Fever
Skin lesions	Maculopapular rash
Petechiae	Lymphadenopathy
Purpura	Polyarthralgia
Hepatosplenomegaly	Polyarthritis
Jaundice	Encephalitis
Ophthalmologic abnormalities	Thrombocytopenia
Cataracts
Retinopathy
Glaucoma
Cardiac abnormalities
Patent ductus arteriosus
Pulmonary artery stenosis
Meningoencephalitis
Thrombocytopenia
Hemolytic anemia
Sequelae long-term
Sensory neural hearing loss
Neurodevelopmental disabilities
Endocrinopathies
Hypogammaglobulinemia

The exanthem of rubella may be the first indication of this infection in young children. It begins on the face and moves rapidly downward to the trunk and lower extremities. The exanthem lasts approximately 3 days; it may persist for 5 days or disappear within the first day. The rash of rubella is erythematous, discrete, and maculopapular, and it generally does not coalesce or darken as in rubeola. Fever in rubella is more often of low grade (less than 38.8°C) and does not persist for the length of the exanthem.

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