Aetiology

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 haemagglutination inhibition and neutralising 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 un-immunised 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 time the virus replicates in the nasopharynx and local lymph nodes and then spreads haematogenously 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 immunological basis.

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