Chapter 56 : Rubella Virus

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Rubella is a benign disease when acquired by a child or adult, but causes significant sequelae to a developing fetus when intrauterine transmission occurs. Following the devastating worldwide pandemic in 1962–1965, a safe and effective rubella vaccine was developed and widely utilized. As a consequence, the occurrence of congenital rubella syndrome has decreased dramatically in those regions of the world with rubella vaccination programs. In 2015 the Americas region became the first World Health Organization (WHO) region in the world to be declared free of endemic transmission of rubella. Despite this, rubella continues to circulate in other parts of the world, including a large outbreak in Japan occurring since 2012, and approximately 100,000 cases of congenital rubella syndrome still occur worldwide. Given the ease and frequency of global travel, however, clinicians need to remain aware of rubella even in the United States, so that imported cases can be identified and managed accordingly. This chapter reviews the current knowledge of the natural history, pathogenesis, diagnosis, treatment, and prevention of rubella.

Citation: Kimberlin D. 2017. Rubella Virus, p 1381-1393. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch56
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Image of FIGURE 1

Number of rubella and congenital rubella syndrome (CRS) cases—United States, 1966–2011. Source: Rubella and CRS data provided were reported voluntarily to CDC from state health departments. * By year of birth. (Reprinted from reference with permission.)

Citation: Kimberlin D. 2017. Rubella Virus, p 1381-1393. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch56
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Image of FIGURE 2

Likelihood and outcome of congenital rubella syndrome as a function of time of acquisition of maternal rubella virus infection. Hatched bars, rate of fetal infection; striped bars, rate of defects in infected persons; diamonds, overall risk of defects after maternal infection. (Adapted from reference with permission.)

Citation: Kimberlin D. 2017. Rubella Virus, p 1381-1393. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch56
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Image of FIGURE 3

Schematic of the immune response in acute rubella virus infection. Values on the axis indicate number of days. RIA, radioimmunoassay; EIA, enzyme immunoassay; HI, hemagglutination inhibition; LA, latex agglutination; FIA/FIAX and IFA, immunofluorescence; Nt, neutralization; PHA, passive agglutination. (Reprinted from reference with permission.)

Citation: Kimberlin D. 2017. Rubella Virus, p 1381-1393. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch56
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Image of FIGURE 4

Schematic of the immune response in the mother, fetus, and infant after maternal and fetal rubella virus infections in the first trimester of pregnancy. (Reprinted from reference with permission.)

Citation: Kimberlin D. 2017. Rubella Virus, p 1381-1393. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch56
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Image of FIGURE 5

(Left) Provisional zones of calcification are poorly defined and irregular. Radiolucent defects are present in metaphyses of femora and tibiae and the parallel long axis of the bone. (Right) Lower extremities 2 months later show nearly complete disappearance of osseous abnormalities. (Reprinted from reference with permission.)

Citation: Kimberlin D. 2017. Rubella Virus, p 1381-1393. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch56
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