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Chapter 3 : Cytomegalovirus

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Cytomegalovirus, Page 1 of 2

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Abstract:

Cytomegalovirus (CMV) has four fundamental structural elements: an outer lipid envelope, tegument, a nucleocapsid, and an internal nucleoprotein core that contains its genome. These components are essential for the biology of the virus and, as discussed in this chapter, are also major targets for diagnostic and therapeutic modalities. The clinical manifestations of CMV are also similar to those of solid organ transplants (SOT) patients and can be classified as CMV syndrome or tissue-invasive disease. Overall, there are important limitations to the clinical application of serology for the diagnosis of acute CMV infection in immunocompromised individuals. The major limitation of pp65 antigenemia assays is the lack of standardization across laboratories and the subjective and operator-dependent nature of the assay. Some experts argue that the presence of virus in a cell-free environment such as plasma is more indicative of active viral replication. One of the most common clinical applications of the antigenemia and molecular diagnostic tests is in the strategy of preemptive therapy, an approach of CMV prevention whereby an antiviral drug is administered upon the detection of CMV. The major toxicity of ganciclovir is myelosuppression, and this usually resolves upon the discontinuation of the drug. The major limiting toxicity of foscarnet and cidofovir is nephrotoxicity, and this has relegated them to use as alternative agents. CMV is an important pathogen that causes severe disease in immunocompromised hosts, including transplant patients, patients with AIDS, and immunologically immature newborns.

Citation: Sloma C, Grys T, Razonable R. 2009. Cytomegalovirus, p 69-89. In Hayden R, Carroll K, Tang Y, Wolk D (ed), Diagnostic Microbiology of the Immunocompromised Host. ASM Press, Washington, DC. doi: 10.1128/9781555815455.ch3

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Image of Figure 1.
Figure 1.

CMV-induced CPE. The image shows an unstained preparation. Original magnification, ×100. (Courtesy of Annette Ehrich.)

Citation: Sloma C, Grys T, Razonable R. 2009. Cytomegalovirus, p 69-89. In Hayden R, Carroll K, Tang Y, Wolk D (ed), Diagnostic Microbiology of the Immunocompromised Host. ASM Press, Washington, DC. doi: 10.1128/9781555815455.ch3
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Image of Figure 2.
Figure 2.

Diagnostic algorithm for transplant recipients and their donors with the use of CMV serology.

Citation: Sloma C, Grys T, Razonable R. 2009. Cytomegalovirus, p 69-89. In Hayden R, Carroll K, Tang Y, Wolk D (ed), Diagnostic Microbiology of the Immunocompromised Host. ASM Press, Washington, DC. doi: 10.1128/9781555815455.ch3
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Image of Figure 3.
Figure 3.

Illustrative algorithm utilizing various diagnostic assays for a transplant recipient prior to transplantation and during the period following transplantation.

Citation: Sloma C, Grys T, Razonable R. 2009. Cytomegalovirus, p 69-89. In Hayden R, Carroll K, Tang Y, Wolk D (ed), Diagnostic Microbiology of the Immunocompromised Host. ASM Press, Washington, DC. doi: 10.1128/9781555815455.ch3
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Image of Figure 4.
Figure 4.

Algorithm for the diagnosis of CMV disease in an immunocompromised patient.

Citation: Sloma C, Grys T, Razonable R. 2009. Cytomegalovirus, p 69-89. In Hayden R, Carroll K, Tang Y, Wolk D (ed), Diagnostic Microbiology of the Immunocompromised Host. ASM Press, Washington, DC. doi: 10.1128/9781555815455.ch3
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Tables

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Table 1.

Risk factors and clinical manifestations of CMV disease in immunocompromised patients

Citation: Sloma C, Grys T, Razonable R. 2009. Cytomegalovirus, p 69-89. In Hayden R, Carroll K, Tang Y, Wolk D (ed), Diagnostic Microbiology of the Immunocompromised Host. ASM Press, Washington, DC. doi: 10.1128/9781555815455.ch3
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Table 2.

Laboratory methods for diagnosis of CMV infection

Citation: Sloma C, Grys T, Razonable R. 2009. Cytomegalovirus, p 69-89. In Hayden R, Carroll K, Tang Y, Wolk D (ed), Diagnostic Microbiology of the Immunocompromised Host. ASM Press, Washington, DC. doi: 10.1128/9781555815455.ch3

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