Etiology

Rubella is caused by rubella virus, which is a togavirus and the only member of the genus Rubivirus. Humans are the only natural host. The virus has a positive-stranded RNA genome and a glycolipid envelope. There is only 1 antigenic type. Rubella virus is readily inactivated by chemical agents, low pH, heat, and cold. It can be cultivated in a variety of cell lines. Cell-mediated immunity develops 2 to 4 weeks after infection and hemagglutination inhibition and neutralizing antibodies directed against the virus peak at approximately 4 weeks. Immunity following rubella usually persists for life, although recurrent infection has been reported. Rubella vaccines are reported to be approximately 97% effective in preventing disease after a single dose.[12] Most rubella infections in the US are imported from countries in which rubella is endemic and affects unimmunized people.

Pathophysiology

Rubella is transmitted from human to human only by direct or droplet contact with infected body fluids, most commonly nasopharyngeal secretions.[7] Patients may shed infectious virus from 7 to 30 days after infection (from 1 week before to 2 weeks after the onset of rash). However, infants with congenital rubella syndrome may be contagious for >1 year. The average incubation period is 17 days (range: 12 to 23 days), during which the virus replicates in the nasopharynx and local lymph nodes and then spreads hematogenously throughout the body (including, in pregnant women, to the placenta and fetus).[5]​ Systemic symptoms are due to viral infection, but some manifestations (rash, thrombocytopenia, arthritis) probably have an immunologic basis.

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