Clinical Findings of Cytomegalovirus
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p491-492
2025-11-16
46
A. Normal Hosts
Primary CMV infection of older children and adults is usually asymptomatic but occasionally causes a spontaneous infectious mononucleosis syndrome. CMV is estimated to cause 20–50% of heterophil-negative (non-EBV) mononucleosis cases.
CMV mononucleosis is a mild disease, and complications are rare. Subclinical hepatitis is common. In children younger than 7 years old, hepatosplenomegaly is frequently observed.
B. Immunocompromised
Hosts Both morbidity and mortality rates are increased with primary and recurrent CMV infections in immunocompromised individuals. The virus may be restricted to a single organ, causing pneumonia, colitis, retinitis or hepatitis, or cause disseminated infection. Viral reactivation commonly occurs in bone marrow transplant recipients. Virus-associated leukopenia is common in solid organ transplant recipients; also seen are obliterative bronchiolitis in lung transplants, graft atherosclerosis after heart transplantation, and CMV-related rejection of renal allografts. CMV often causes disseminated disease in untreated AIDS patients; colitis and chorioretinitis are common problems, the latter often leading to progressive blindness.
C. Congenital and Perinatal Infections
Congenital infection may result in death of the fetus in utero (see Figure 1). Cytomegalic inclusion disease of newborns is characterized by involvement of the central nervous system and the reticuloendothelial system. Clinical features include intrauterine growth retardation, jaundice, hepatosplenomegaly, thrombocytopenia, microcephaly, and retinitis. Mortality rates are about 20%. The majority of survivors develop significant central nervous system defects within 2 years; severe hearing loss, ocular abnormalities, and mental retardation are common. About 10% of infants with subclinical congenital CMV infection develop deafness. It has been estimated that one in every 1000 infants born in the United States is seriously retarded as a result of congenital CMV infection.
Fig1. Congenital infections by cytomegalovirus and birth defects in symptomatic and asymptomatic children. Cytomegalovirus is the most common intrauterine infection associated with congenital defects. (Reproduced with permission from Pereira L, Maidji E, McDonagh S, Tabata T: Insights into viral transmission at the uterine-placental interface. Trends Microbiol 2005;13:164–174. Copyright Elsevier.)
Many women infected previously with CMV show reactivation and begin to excrete the virus from the cervix during pregnancy. At the time of delivery through the infected birth canal, infants may become infected, although they possess high titers of maternal antibody acquired transplacentally. These infants begin to shed virus at about 8–12 weeks of age. They continue to excrete the virus for several years but remain healthy.
Acquired infection with CMV is common and usually inapparent. The virus is shed in the saliva and urine of infected individuals for weeks or months. CMV may be a cause of isolated pneumonia or hepatitis in infants younger than 6 months of age.
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