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Rubella Is an acute infectious anthropogenic disease caused by an RNA virus belonging to the Togaviridae (family Togaviridae, genus Rubivirus). Unlike other togaviruses, the rubella virus contains neuraminidase. The virus is unstable in the environment, dies rapidly on drying, changes in pH (below 6.8 and above 8.0), exposure to ultraviolet rays, ether, formalin and other disinfectants. The virus can remain viable for several hours at room temperature, easily tolerating freezing.
Epidemiology. The source of infection is humans. These are either patients with clinically severe rubella, or people with atypical rubella without a rash, as well as children with congenital rubella, in whose body the virus can persist for many months (up to 1,5 years or more). Infection is transmitted by airborne droplets.
The rubella virus is released into the environment one week before the onset of the rash and one week after the rash. People of all ages are susceptible to rubella, but preschool and school-age children get sick more often. Children under 6 months get sick very rarely because they are protected by the mother's hereditary immunity. But if the mother does not have rubella, the baby can get sick from the first days of life. 15-50% of women have a potential risk of getting rubella during pregnancy, the greatest risk to the offspring is the presence of deleted and latent forms of rubella in pregnant women, accompanied by pathogen resistance. In acute infection, the virus damages the placenta and can be transmitted to the fetus. Secondary exposure to the virus or re-infection is rarely associated with intrauterine transmission of the virus, indicating that maternal immunity (acquired naturally or through vaccination) provides protection against infection during fetal development. After rubella remains strong and long-lasting immunity. However, if immune individuals do not re-encounter this infection within 10 to 20 years, their immunity is weakened and re-infection may develop with or without clinical manifestations. Rubella is characterized by winter-spring seasonality.
Pathogenesis. When transmitted by airborne droplets, the virus damages the epithelial tissue of the upper respiratory tract, enters the bloodstream, and then into the lymph nodes, where it multiplies. Then develops viremia (persistence of the virus in the blood). Hematogenously the virus spreads throughout the body, has dermatotropic properties, causes changes in the lymph nodes that increase in size at the end of the incubation period. At this time it is possible to isolate the virus from the nasopharynx. When a rash appears, the virus is not detected in the blood or nasopharynx, but in some cases it lasts for 1-2 weeks after the rash. In pregnant women with viremia, the virus enters the fetal tissue through the placenta. This is evident when hormonal changes in the pregnant woman's body indicate a disorder of the immune system or a slow development of immunity (pregnant women produce increased amounts of cortisone, which has an immunosuppressive effect, which reduces the body's resistance and leads to the development of infection).
Clinical manifestations. The incubation period lasts 2-3 weeks. Rubella is asymptomatic in 30-50% of those infected. Symptoms of the clinical picture include fever, maculopapular rash (often barely noticeable) and a short period of rash, lymphadenopathy, possibly rash, and conjunctivitis. Adenopathy during rubella (usually in the occipital region, behind and below the mastoid process, on the side of the neck and under the lower jaw) is a permanent sign, often the only manifestation.
During transplantation, the virus infects first the endothelium of the placental capillaries, causing hypoxia of the fetus, and then the embryonic tissues, where it inhibits the mitotic activity of individual cell populations. The first infection with the rubella virus in the mother can be caused by: embryo infection, embryo resorption (only in the first week of pregnancy), spontaneous termination of pregnancy, intrauterine fetal death, infection without damage to the fetus, accompanying pathologies of the placenta and fetus. In the first 2 months of pregnancy, when the mother is infected, the fetus develops heart disease, infection in the 3-4th month of pregnancy causes central nervous system defects (microcephaly, mental retardation) and hearing organ damage (deafness, cortical defects). Congenital malformations are often combined. The outcome of fetal and neonatal pathology depends on the teratogenicity of the virus and the gestational age at which the infection developed.
Based on laboratory diagnostics of rubella Serological markers (Immunoglobulins IgM, IgG And avidity IgG) as well as virus isolation and identification. Since the isolation and identification of the rubella virus is usually a lengthy procedure (at least 2-3 days), in some cases it is conducted as a special study and this method of diagnostics has no clinical significance.
IgM antibodies. Immunological markers of primary or clinically asymptomatic rubella infection are specific IgM antibodies to the rubella virus. IgM antibodies can be detected in the first days of the disease, reach a maximum in 2-3 weeks and usually disappear completely after 1-2 months. In some cases, rubella virus IgM may persist for up to 1 year.
The absence of IgM antibodies at birth does not rule out the diagnostics of congenital rubella. Re-infection does not cause an increase in IgM antibodies (it is necessary to study the dynamics of IgG antibodies - a 4-fold increase in serum levels confirms the diagnostics). After vaccination IgM antibodies are detected in 15-25 days in 60-80% of cases. Low levels of IgM antibodies can be detected in infectious mononucleosis and other viral infections (cytomegalovirus, measles, herpes).
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