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VIII.32 - Cytomegalovirus Infection

from Part VIII - Major Human Diseases Past and Present

Published online by Cambridge University Press:  28 March 2008

Kenneth F. Kiple
Affiliation:
Bowling Green State University, Ohio
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Summary

Cytomegalic inclusion disease (CID) usually occurs as a subclinical infection followed by periodic reactivation revealed by shedding of the virus. It may be serious in the neonate when infection is transmitted to the fetus in utero.

Clinical Manifestations and Pathology

Cytomegalic infection is characterized histologically by the presence of large cells containing inclusion bodies in the midst of an infiltration of mononuclear cells that may be present in any of the body organs.

In prenatal infections most infants are born without clinical evidence of disease, although some 10 to 15 percent may show microcephaly, retardation of growth or mental development, hepatosplenomegaly, jaundice, and calcifications in the brain. There may be abnormalities in liver function tests and in hematopoiesis. Some 10 to 30 percent of infants with symptomatic disease die in early life. Evidence of involvement of the central nervous system can develop in the early years of life, even though the child may appear normal. The evidence is manifested as impaired intellect, neuromuscular abnormalities, chorioretinitis, optic atrophy, or hearing loss.

Neonatal infection acquired at birth from an infected cervix or later from the mother’s milk usually goes unnoticed but can be identified by the development of antibodies. In addition, respiratory symptoms including pneumonia, as well as petechial rash and enlargement of the liver and the spleen, may occur. In these cases, however, acute involvement of the central nervous system is rare. Infection in children is generally asymptomatic and is evidenced only by the development of antibodies and the shedding of virus. Occasionally hepatosplenomegaly and abnormal liver function are found. There is no proof that pharyngitis occurs at the presumed portal of entry.

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Publisher: Cambridge University Press
Print publication year: 1993

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References

Anon, . 1985. Epidemiologic Note. Prevalence of cytomegalovirus excretion from children in five day care centers – Alabama. Morbidity and Mortality Weekly Report. Centers for Disease Control. U.S. Public Health Service 34.Google Scholar
Diosi, P. L., et al. 1967. Cytomegalovirus infection associated with pregnancy. Lancet 2.Google ScholarPubMed
Goodpasture, E. W., and Talbot, F. B.. 1921. Concerning the nature of “protozoan-like cells” in certain lesions of infancy. American Journal Diseases of Children 21.Google Scholar
Hanshaw, J. A. 1971. Congenital cytomegalovirus infection: A fifteen year perspective. Journal of Infectious Disease 123.CrossRefGoogle ScholarPubMed
Harris, J. R. 1975. Cytomegalovirus infection. In Recent advances in sexually transmitted diseases, ed. Morton, R. S. and Harris, J. R. W., Chap. 42. London.Google Scholar
Jordan, M. Colin. 1983. Cytomegalovirus infections. In Infectious diseases, ed. Hoeprich, Paul D., Chap. 75, 3d edition. Philadelphia.Google Scholar
Lang, David J. 1924. Cytomegalovirus infections. In Sexually transmitted diseases, ed. Holmes, King K. et al., Chap. 44. New York.Google Scholar
Pass, R. F., et al. 1987. Young children as probable source of maternal and congenital cytomegalovirus infection. New England Journal of Medicine 316.CrossRefGoogle ScholarPubMed
Weller, Thomas H. 1971. The cytomegaloviruses: Ubiquitous agents with protean clinical manifestation. New England Journal of Medicine 185.Google Scholar
Weller, Thomas H. 1981. Clinical spectrum of cytomegalovirus infection. In The human herpesviruses: An interdisciplinary perspective, ed. Nahmias, Andrew J. et al. New York.Google Scholar

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