Rubella acquired in childhood or early adulthood is usually mild, however symptoms in adults tend to be more severe than in children. It is estimated that up to 50% of rubella infections are clinically inapparent. Symptomatic rubella encompasses combinations of maculopapular rash, lymphadenopathy, low-grade fever, conjunctivitis, sore throat and arthralgia. The rash is the most prominent and earliest feature and appears following an incubation period of 16-20 days. The rash begins as distinct pink maculopapules on the face that then spread over the trunk and distally onto the extremities. The maculopapules coalesce and the rash rapidly fades over several days. An associated posterior cervical and suboccipital lymphadenopathy is also characteristic. Fever is typically low grade. The entire clinical syndrome usually resolves in a few days. Infrequently occurring complications include thrombocytopenia and postinfectious encephalitis. Acute polyarthralgia and arthritis following natural rubella virus infections of adults are common and occur more frequently and with greater severity in women than in men. Joint involvement is usually transient, resolving within one to several weeks, however chronic arthritis persisting or recurring over several years has been reported. The most common symptoms of rubella, lymphadenopathy, erythematous rash, and low-grade fever, are nonspecific and easily confused with similar illnesses caused by other common viral and nonviral pathogens or drug-induced eruptions. Therefore, a definitive diagnosis of rubella requires confirmation by virus isolation or, more commonly, by serology.
Fetal infection with rubella virus has dire consequences for fetal development. The rate of CRS following maternal infection is highest early in pregnancy; 50%, 25% and 10% during the first, second, and third months, respectively. CRS is rare following maternal infection after week 16 of gestation. The clinical manifestations of CRS apparent at birth vary widely, most frequently including thrombocytopenia purpura ('blueberry muffin syndrome'), intrauterine growth retardation, congenital heart disease (patent ductus arteriosus or pulmonary artery or valvular stenosis), psychomotor retardation, eye defects (cataract, glaucoma, retinopathy), suspected or confirmed hearing loss and hepatomegaly and/or splenomegaly. Less frequent features include adenopathy, bony radiolucencies, hepatitis usually with jaundice, and hemolytic anemia. Nearly 80% of CRS
children show some type of neural involvement, particularly neurosensory hearing loss.
Most clinical manifestations of congenital rubella are evident at or shortly following birth and some are transient. However, recognition of retinopathy, hearing loss and mental retardation may be delayed for several years in some cases. Progressive consequences of congenital rubella have become increasingly appreciated as CRS children from the 1964 epidemic have been followed longitudinally. These predominantly involve endocrine dysfunction (diabetes melli-tus, which ultimately affects 40% of CRS patients, and thyroid dysfunction). A rare, fatal neurodegenerative disease, progressive rubella panencephalitis (PRP), was also described in CRS patients that bears superficial resemblance to subacute sclerosing panencephalitis associated with measles virus. Subsequently, PRP cases were also reported in individuals who were infected postnatally.
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