Cytomegalovirus infection: pathogenesis
Last reviewed: 23.04.2024
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The decisive condition for the development of an antenatal cytomegalovirus infection is viremia in the mother. The presence of the virus in the blood leads to infection of the placenta, its damage and infection of the fetus with possible consequences in the form of vices and intrauterine growth retardation, a pathological process with the defeat of internal organs, primarily the CNS. If there is a virus in the cervical canal of a pregnant woman, an ascending (transcervical) route of infection of the fetus is possible without the exit of the pathogen into the blood. Reactivation of Tzitomegalovirus in the endometrium is one of the factors of early abortion. Intranatal infection with the virus occurs when the fetus passes through the infected birth canal due to aspiration of cytomegalovirus-containing amniotic fluid and or secrets of the birth canal or through damaged skin and can also lead to the development of a clinically pronounced disease. In postnatal cytomegalovirus infection, the entrance gates for the pathogen are mucous membranes of the oropharynx, respiratory system. Digestive and genital tracts. After overcoming the entrance gate virus and its local reproduction, short-term viremia occurs, monocytes and lymphocytes transfer the virus to various organs. Despite the cellular and humoral response, cytomegalovirus induces a chronic latent infection.
The reservoir of virus particles is monocytes, lymphocytes, endothelial cells and epithelial cells. In the future, with a slight immunosuppression, "local" activation of the cytomegalovirus is possible with the release of the virus from the nasopharynx or the urogenital tract. In the case of deep immunological disorders with a hereditary predisposition to this pathology, resumption of active viral replication, viremia, dissemination of the pathogen, development of a clinically pronounced disease occur. Viral replication activity. Risk of manifestation of cytomegalovirus infection, the severity of its course is largely determined by the depth of immunosuppression, primarily by the level of decrease in the number of CD4-lymphocytes in the blood. With cytomegalovirus infection associated a wide range of organ damage: lung, digestive tract, adrenal, kidney, brain and spinal cord, retina. Immunosuppressive patients with cytomegalovirus infection posthumously detect fibroelectasectasis of the lungs, sometimes with cysts and encapsulated abscesses; erosive-ulcerative with marked fibrosis of submucosal layer, lesion of esophagus, colon, less often of stomach and small intestine; massive, often bilateral necrosis of the adrenal glands; encephaloventriculitis, necrotic lesion of the spinal cord, retina with the development of necrotizing retinitis. Specificity of the morphological pattern in cytomegalovirus infection is determined by large cytomegaloklets, lymphohistiocyte infiltrates, as well as productive-infiltrative panvasculitis with cytomegal transformation of cells of all walls of small arteries and veins with an outcome in sclerosing. Such a vascular lesion serves as a basis for thrombosis, leads to chronic ischemia, against which destructive changes develop, segmental necrosis and ulcers, marked fibrosis. A common fibrosis is a characteristic feature of CMV organ damage. In most patients, the pathological process associated with cytomegalovirus is of a generalized nature.
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