Measles: the war on childhood plague continues
Thanks to routine immunization, we managed to forget about the many incredibly contagious and dangerous diseases. Nevertheless, it’s too early to relax: if group immunity decreases due to refusal of…

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Measles: the war on childhood plague continues
Thanks to routine immunization, we managed to forget about the many incredibly contagious and dangerous diseases. Nevertheless, it’s too early to relax: if group immunity decreases due to refusal of…

Continue reading →

Modern approaches to pharmacotherapy of acute bronchitis. The benefits of herbal medicine
Bronchitis is an inflammatory disease of the lungs without the formation of infiltrative changes in their parenchyma. Bronchitis can be both a manifestation of ARVI and its complication due to…

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Is it possible to prevent the consequences of congenital cytomegalovirus infection?

Congenital CMVI is one of the most common intrauterine infections in the world and occurs on average in 0.2–2.5% of live births, and in developed countries, in 0.6–0.7% of newborns. In this case, the source of infection for the fetus is almost always the mother who undergoes CMVI during pregnancy. Exceptions are those extremely rare cases when transfusion transmission of cytomegalovirus (CMV) occurs during intrauterine administration of blood products infected with CMV to the fetus. Intrauterine CMVI develops as a result of pre- or intrapartum infection. With prenatal infection of the fetus, there is a transplacental transmission of CMV. With intranatal – the virus enters the body of the child by aspiration or ingestion of infected amniotic fluid and / or infected secrets of the birth canal of the mother.
The greatest risk of intrauterine CMV infection of the fetus and the development of severe forms of the disease is noted in cases when a pregnant woman suffers primary CMVI. CMVI is considered primary if CMV infection and the development of an infectious process occur in a previously seronegative woman. Laboratory markers of primary CMVI are:
viremia (detection of CMV in the blood);
antigenemia (detection of pp-65 antigen in the blood);
DNA -emia (detection of CMV DNA in the blood);
detection of anti-CMV-IgM in serum;
fourfold positive seroconversion in paired sera (fourfold increase in the titer of low avidity anti-CMV IgG).
The absence of intense specific humoral immunity in the initial stages of the disease and the low functional activity of cellular immune mechanisms cannot inhibit the active replication and viremia of the pathogen. Viremia, especially in conditions leading to a violation of the placental barrier, promotes transplacental transmission of CMV. The virus entering the body of the fetus is actively replicating and spreading in the body, because it does not meet the proper immune resistance. The degree of damage to the fetus in this case depends on the intensity of the reproduction of the virus and the gestation period in which the infection develops. In this case, both minimal manifestations of the disease (asymptomatic, subclinical forms) and severe lesions – embryo and fetopathies with generalized inflammatory changes are possible. Thus, the primary CMVI that developed in a woman during pregnancy is potentially dangerous to the fetus.
It was established that during primary CMVI during pregnancy, the level of intrauterine transmission of CMV reaches 30–55% (on average – 40%). Moreover, in 5–18% of live-born CMV-infected children, this leads to the development of severe forms of congenital CMVI with a high risk of adverse outcome, and in survivors to frequent (up to 80–90%) development of somatic and neuropsychiatric complications. Thus, our earlier analysis of the causes of hospital mortality among infants over a ten-year period in one of the largest multidisciplinary children’s hospitals in Moscow (Children’s Clinical Hospital named after Z.A. Bashlyaeva DZM, former Tushinskaya) showed that 5.3% are congenital CMVI . It was noted that the lethal outcome of congenital CMVI was most often observed (in 66.4%) at the age of 3–6 months. In the clinical picture, symptoms of damage to the central nervous system (76.5%), trophic disorders (70.2%), hepato- or hepatosplenomegaly (41.2%) predominated. Hematological changes (anemia, thrombocytopenia) occurred in 29.3% of children, and hyperbilirubinemia in 23.4%. Damage to the urinary system with the development of nephrotic syndrome was noted in 11.8% of children. It should be especially noted that the vast majority of patients (94.1%) developed combined lesions of various organs and systems. This was confirmed by a sectional study of children who died from congenital CMVI, the results of which testified to a long multi-organ infectious and inflammatory process with signs of embryo and fetopathy. It should be especially noted that even with primary CMVI during pregnancy, the asymptomatic course of congenital CMVI is much more common in children. The insidiousness of this form lies in the fact that in the absence of vivid symptoms of the disease, the course of the infectious-inflammatory process continues with the development of damage to neurons that are very sensitive to CMV. As a result of this, in 17–20% of children with asymptomatic congenital CMVI, sensorineural hearing loss, delayed psychomotor development, minor cerebral dysfunction, and other neurological disorders are subsequently detected.
It was established that in the case of secondary CMVI, i.e., reactivation of latent CMVI or reinfection with a new CMV strain, the mother during pregnancy has a significantly lower risk of fetal infection and does not exceed 2–8% (during reactivation) and 20% (during reinfection), and manifest forms of congenital CMVI are generally found in rare cases.

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