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Chapter 38 : Measles

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Measles, Page 1 of 2

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Abstract:

Measles is a highly contagious disease caused by infection with measles virus (MeV), and it has caused millions of deaths since its spread within human populations thousands of years ago. Disease begins with fever, cough, coryza, and conjunctivitis followed by the appearance of a characteristic maculopapular rash. Genetically, MeV is most closely related to rinderpest virus, a pathogen of cattle that was recently eradicated. MeV was originally a zoonotic infection that adapted to humans 5,000 to 10,000 years ago when populations achieved sufficient size in Middle Eastern river valley civilizations to maintain a continuous chain of transmission among susceptible individuals. Subsequent introduction of MeV into naive populations resulted in high mortality. Millions died as a result of European exploration of the New World, largely due to the introduction of diseases such as smallpox and measles into native Amerindian populations (1).

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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Image of FIGURE 1
FIGURE 1

Measles virus (MeV) in cell culture. An extracellular virion (large solid arrow) is coated with glycoprotein spikes (small open arrows) with the viral nucleocapsid (small solid arrows) positioned beneath the envelope. An infected cell has a region on the membrane (large open arrow) with viral glycoprotein spikes and subjacent viral nucleocapsids that is a site of MeV maturation and budding. Free paramyxovirus nucleocapsids (small solid arrows) from a disrupted virion are shown in the inset. (Courtesy of Cynthia Goldsmith, William Bellini, and Erskine Palmer of the Centers for Disease Control and Prevention, Atlanta, GA.) [Adapted from Oxman, 2nd edition of .]

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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Image of FIGURE 2
FIGURE 2

MeV structure, genome, and replication cycle. (a) MeV is a spherical, nonsegmented, single-stranded, negative-sense RNA virus. Of the six structural proteins, the phosphoprotein (P), large protein (L), and nucleoprotein (N) form the nucleocapsid that encloses the viral RNA. The hemagglutinin protein (H), fusion protein (F), and matrix protein (M), together with lipids from the host cell membrane, form the viral envelope. (b) The MeV RNA genome is comprised of approximately 16,000 nucleotides encoding eight proteins, two of which (V and C) are nonstructural proteins alternatively translated from the P gene. (c) The H protein interacts with F to mediate attachment and fusion of the viral envelope with the host cell membrane through specific receptors (CD46 and CD150) enabling viral entry into the cell. Remaining MeV proteins are involved in viral replication. The P protein regulates transcription, replication, and assembly of nucleocapsids. The M protein is critical for viral assembly. (From reference with permission of the publisher.) Source: Moss WJ, Griffin DE. Global measles elimination. 2006;4:900–908.

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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Image of FIGURE 3
FIGURE 3

Basic pathogenesis of MeV infection. Panels summarize features of the pathogenesis of MeV infection. (a) The spread of the virus from the initial site of infection in the respiratory tract to the skin. Sites of infection are overlaid with virus titer. (b) The appearance of clinical signs and symptoms in relation to viral replication and the immune responses. (c) The immune responses to measles virus. The clinical manifestations arise coincident with the onset of the immune response. (From reference with permission of the publisher.) Source: Moss WJ, Griffin DE. Global measles elimination. 2006;4:900–908.

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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Image of FIGURE 4
FIGURE 4

Histopathology of Koplik's spots (A) and the skin rash (B) of measles. The epidermal changes in both are characterized by multinucleated giant cells (arrows), focal parakeratosis, dyskeratosis and spongiosis, intracellular edema, and a sparse lymphocytic infiltrate. (Courtesy of D. W. R. Suringa, Tampa, FL). [adapted from Oxman, 2nd edition of .]

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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Image of FIGURE 5
FIGURE 5

Potential mechanisms of immune suppression following measles virus infection. (From reference with permission of the publisher.) Source: Moss WJ, Ota MO, Griffin DE. Measles: Immune suppression and immune responses. 2004;36:1380–1385.

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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Image of FIGURE 6
FIGURE 6

Schematic diagram of the clinical course of a typical case of measles. (Adapted from Oxman, 2nd edition of .)

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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Image of FIGURE 7
FIGURE 7

Measles rash. Note the characteristic blotchy appearance. (From reference with permission of the publisher.) Source: Moss WJ, Griffin DE. Global measles elimination. 2006;4:900–908.

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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Image of FIGURE 8
FIGURE 8

Measles giant cell pneumonia. Two multinucleated epithelial giant cells are visible in alveolar spaces in the lung of an immunosuppressed child who died of giant cell pneumonia. Eosinophilic Cowdry type A inclusion bodies are visible in many nuclei (arrows). (From reference with permission of the publisher.) [Adapted from Oxman, 2nd edition of .]

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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Image of FIGURE 9
FIGURE 9

Measles virus vaccines. Most attenuated measles vaccines were developed from the Edmonston strain of measles virus. The Edmonston B vaccine was the first licensed measles vaccine but was associated with a high frequency of fever and rash. The further attenuated Schwarz and Edmonston-Zagreb vaccines are widely used throughout the world. The Moraten vaccine is the only measles vaccine used in the United States. [: Markowitz LE. Measles control in the 1990s: immunization before 9 months of age. Document WHO/EPI/GEN/90.3. Geneva: World Health Organization, 1990. : Cutts FT. Measles. Module 7. The Immunological Basis for Immunization Series. Document WHO/EPI/GEN/93.17. Geneva: World Health Organization, 1993.] (From reference with permission of the publisher.) Source: Moss WJ, Griffin DE. Global measles elimination. 2006;4:900–908.

Citation: Moss W, Griffin D. 2017. Measles, p 903-928. In Richman D, Whitley R, Hayden F (ed), Clinical Virology, Fourth Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819439.ch38
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