What does wui mean during pregnancy? Fetal immune system

TORCH syndrome is diagnosed when there is no exact etiological diagnosis, they do not know which intrauterine infection of the fetus is the diagnosis. Diagnosing IUI is very difficult. It is necessary to examine not only the child, but also the mother, as well as the placenta and umbilical cord. An indirect diagnostic method is a blood test using ELISA for infections. However, even if a child has antibodies to any infection, this is not always evidence of IUI. After all, they could have been introduced into the child’s body from the mother. Then the child’s blood is taken again after 3-4 months, and if the antibody titer has increased 4 times or more, this is considered a diagnostically significant sign.

The causes of intrauterine infections during pregnancy are, as a rule, infection of the mother with these diseases. Infection of the fetus occurs more often precisely in the case of the first encounter of the mother’s body with infectious pathogens.

In turn, diagnosing intrauterine infections during pregnancy is almost impossible. There are only signs by which one can suspect trouble in a child. They are also determined using ultrasound.

Some symptoms of intrauterine infection during pregnancy that doctors pay attention to:

• delayed fetal development (determined by measuring the length of the uterus - with delayed development it grows slowly, and according to ultrasound data on the size of the head, limbs, volume of the torso);
• polyhydramnios or oligohydramnios;
• pathologies of the placenta;
• polycystic lung disease;
• hydrocephalus, etc.

Many women who have lost their children shortly before giving birth or within a few days after birth know the dangers of intrauterine infection during pregnancy. IUI is the most common cause of early childhood mortality. Approximately 80% of children born with developmental defects are diagnosed with IUI.

The consequences of intrauterine infections during pregnancy in a newborn child can be expressed in respiratory dysfunction, cardiovascular pathology, jaundice, feverish conditions, damage to the eyes, mucous membranes, encephalitis, etc.

Infection can occur in the following ways:

• through the blood, placenta, thus very easily penetrates into the child’s body, for example, toxoplasma - the causative agent of toxoplasmosis;
• from the genital tract, this happens with infections such as herpes during pregnancy, mycoplasmosis, chlamydia, etc., that is, those that are sexually transmitted are manifested precisely by damage to the genital organs;
• from the fallopian tubes;
• at the birth of a child in a natural way.

Prevention

Every woman planning a pregnancy should undergo a general examination before pregnancy to detect possible infections (they can be asymptomatic) and treatment if necessary. During pregnancy, you need to follow all known preventive measures to reduce the risk of contracting various infections. We will present several such measures.

1. Clean the animal toilet only with gloved hands, wash your hands. Be sure to cook the meat thoroughly and boil it well. Otherwise, you can become infected with toxoplasmosis, a very dangerous infection for a child.

2. Do not visit children's groups if you do not have a rubella vaccination and have not had it previously. If a woman gets rubella in the first trimester of pregnancy, she is advised to have an abortion, since this disease almost always causes severe malformations in the fetus, whose organs have just begun to form.

3. Do not travel on public transport or walk without a mask during the flu period. Any acute respiratory viral infection or acute respiratory infection, if severe, can kill a child. Don’t go out “in public” unless absolutely necessary. And if you go out, be sure to lubricate your nose with oxolinic ointment and wear a medical mask. Do not touch your face with unwashed hands. Wash your hands thoroughly with antibacterial soap after visiting clinics, hospitals, shops, or public transport.

4. If herpes (cold) appears on the lips, the infection can easily be transferred to the genitals by the expectant mother herself. And genital herpes, and even at the first manifestations during pregnancy, almost always greatly affects the health of the unborn child.

This is part of the measures that are guaranteed to protect you and your child from some dangerous infectious diseases.

Intrauterine infections (IUI) (synonym: congenital infections) are a group of infectious and inflammatory diseases of the fetus and young children, which are caused by various pathogens, but are characterized by similar epidemiological parameters and often have the same clinical manifestations. Congenital infections develop as a result of intrauterine (ante- and/or intrapartum) infection of the fetus. In the vast majority of cases, the source of infection for the fetus is the mother. However, the use of invasive methods of monitoring women during pregnancy (amniocentesis, puncture of umbilical cord vessels, etc.) and intrauterine administration (through the umbilical cord vessels) of blood products to the fetus (erythrocyte mass, plasma, immunoglobulins) can lead to iatrogenic infection of the fetus. The true frequency of congenital infections has not yet been established, but, according to a number of authors, the prevalence of this pathology in the human population can reach 10%. IUIs are serious diseases and largely determine the level of infant mortality. At the same time, the relevance of the problem of IUI is due not only to significant peri- and postnatal losses, but also to the fact that children who have suffered severe forms of congenital infection very often develop serious health problems, often leading to disability and a decrease in the quality of life in general. Taking into account the wide distribution and seriousness of the prognosis, we can conclude that the development of highly accurate methods for early diagnosis, effective treatment and effective prevention of congenital infections is one of the primary tasks of modern pediatrics.

Epidemiology, etiology, pathogenesis. The main source of infection in IUI, as already noted, is the child’s mother, from whom the pathogen enters the fetus during the ante- and/or intranatal period (vertical transmission mechanism). In this case, vertical transmission of infection can be carried out by ascending, transplacental and transovarial routes in the antenatal period, as well as by contact and aspiration directly during childbirth. Antenatal infection is more typical for agents of a viral nature (cytomegaly viruses (CMV), rubella, Coxsackie, etc.) and intracellular pathogens (Toxoplasma, less often - representatives of the Mycoplasma family). Intranatal contamination is more typical for agents of a bacterial nature. At the same time, the range of potential pathogens is individual and depends on the characteristics of the microbial landscape of the mother’s birth canal mucosa. Most often during this period, the fetus is infected with microorganisms such as streptococci (group B), enterobacteria, as well as herpes simplex viruses (HSV) types 1 and 2, mycoplasma, ureaplasma, chlamydia, etc. Until recently, it was believed that the most common causative agents of IUI were CMV, HSV types 1 and 2, and Toxoplasma ( Toxoplasma gondii). However, the results of studies conducted in the last decade have largely changed our understanding of both the etiological structure of IUI and the frequency of intrauterine infection in general. Thus, it has been shown that the prevalence of intrauterine infection among newborns is much higher than previously thought, and in some cases can exceed 10%. It has been established that the etiology of intrauterine infection is represented by a wider range of microorganisms, among which, in addition to traditional pathogens, enteroviruses and chlamydia ( Chlamydia trachomatis), some members of the family Mycoplasmatacae (Ureaplasma urealyticum, Mycoplasma hominis), as well as influenza viruses and a number of other infectious agents. The results of our own studies indicate a high level of intrauterine infection (22.6%). At the same time, we most often noted intrauterine transmission Ureaplasma urealyticum, while vertical infection with CMV was detected only in isolated cases. In addition, in recent years, we, independently of C. B. Hall et al. (2004), have shown the possibility of intrauterine infection with herpes viruses type 4 ( Human Herpes Virus IV (Epstein-Barr virus)) and type 6 ( Human Herpes Virus VI) .

It should be especially noted that the potential threat of intrauterine transmission of infectious agents from a mother to her unborn child increases significantly in cases where a woman has a burdened somatic, obstetric-gynecological and infectious history. In this case, risk factors for intrauterine infection are: inflammatory diseases of the urogenital tract in the mother, unfavorable course of pregnancy (severe gestosis, threat of miscarriage, pathological condition of the uteroplacental barrier, infectious diseases).

However, intrauterine infection does not always lead to the development of manifest forms of the disease and largely depends on the characteristics of the condition of the fetus and newborn. Thus, the risk of congenital infection increases significantly:

• with prematurity;
• delayed prenatal development;
• perinatal damage to the central nervous system;
• pathological course of the intra- and/or early neonatal period.

In addition, the prognosis of intrauterine transmission depends on the gestational age in which the infection occurred, the characteristics of the pathogen (pathogenic and immunogenic properties), the type of maternal infection (primary or secondary), the functional state of the mother’s immune system, the integrity of the uteroplacental barrier, etc.

The nature of damage to the embryo and fetus, the severity of inflammatory changes, as well as the characteristics of clinical symptoms in congenital infections depend on a number of factors: the properties of the pathogen, the severity of infection, the maturity of the fetus, the state of its protective systems, the characteristics of the mother’s immunity, etc. In this case, the determining factors are considered the length of the gestational period in which the infection occurred, and the nature of the infectious process in the mother (primary infection or reactivation of a latent infection). An infection is called primary if the body is infected with a given pathogen for the first time, that is, the development of the infectious process occurs in a previously seronegative patient. If the infectious process develops as a result of activation of a pathogen that was previously in a latent state in the body (reactivation), or due to repeated infection (reinfection), then such an infection is classified as secondary.

It has been established that infection of the fetus and the development of severe variants of IUI are most often observed in cases where a woman suffers a primary infection during pregnancy.

In cases where infection occurs during the embryonic period, spontaneous miscarriages or severe developmental defects incompatible with life occur more often. Penetration of the pathogen into the fetal body in the early fetal period can lead to the development of an infectious-inflammatory process characterized by the predominance of the alterative component with the formation of fibrous-sclerotic deformations in the damaged organs. Infection of the fetus in the late fetal period can be accompanied by inflammatory damage to both individual organs and systems (hepatitis, carditis, meningitis or meningoencephalitis, chorioretinitis, damage to the hematopoietic organs with the development of thrombocytopenia, anemia, etc.), and generalized damage. In general, with antenatal infection, clinical symptoms of the disease usually appear at birth.

At the same time, with intrapartum infection, the timing of the infectious-inflammatory process can be significantly delayed, as a result of which the clinical manifestation of IUI can debut not only in the first weeks of life, but even in the postneonatal period.

Infectious diseases specific to the perinatal period (P35 - P39)

It has been established that in the vast majority of cases of IUI of various etiologies in newborns have similar clinical manifestations. The most typical symptoms of IUI detected in the early neonatal period are intrauterine growth retardation, hepatosplenomegaly, jaundice, exanthema, respiratory disorders, cardiovascular failure and severe neurological disorders, thrombocytopenia. At the same time, attempts to verify the etiology of congenital infection only on the basis of clinical symptoms, as a rule, are rarely successful. Considering the low specificity of clinical manifestations of congenital infections, in the English literature the term “TORCH syndrome” is used to designate IUI of unknown etiology, which includes the first letters of the Latin names of the most frequently verified congenital infections: T stands for toxoplasmosis ( Тoxoplasmosis), R - rubella ( Rubella), C - cytomegaly ( Cytomegalia), H - herpes ( Herpes) and O - other infections ( Other), i.e. those that can also be transmitted vertically and lead to the development of intrauterine infectious and inflammatory processes (syphilis, listeriosis, viral hepatitis, chlamydia, HIV infection, mycoplasmosis, etc.).

Laboratory diagnostics. The absence of specific symptoms and the uniformity of clinical manifestations of congenital infections justify the need for the timely use of special laboratory methods aimed at reliable verification of the etiology of IUI. At the same time, examination of newborns and children of the first months must necessarily include methods aimed at both direct detection of the causative agent of the disease, its genome or antigens (“direct”), and at the detection of markers of a specific immune response (“indirect” diagnostic methods). Direct diagnostic methods include classical microbiological methods (virological, bacteriological), as well as modern molecular biological ones (polymerase chain reaction (PCR), DNA hybridization) and immunofluorescence. Using indirect diagnostic methods, specific antibodies to pathogen antigens are detected in the child’s blood serum. In recent years, enzyme-linked immunosorbent assay (ELISA) has been most widely used for this purpose. In order to obtain reliable results of serological examination of newborns and children in the first month of life and adequately interpret these data, it is necessary to follow certain rules.

• A serological examination should be carried out before the administration of blood products (plasma, immunoglobulins, etc.).
• Serological examination of newborns and children in the first months of life should be carried out with simultaneous serological examination of mothers (to clarify the origin: “maternal” or “own”).
• Serological examination should be carried out using the “paired sera” method with an interval of 2-3 weeks. In this case, the study must be performed using the same technique in the same laboratory. It should be especially noted that in cases where, after the initial serological examination, the child was administered blood products (immunoglobulin, plasma, etc.), the study of “paired sera” is not carried out.
• Evaluation of the results of serological studies should be carried out taking into account possible features of the nature and phase of the immune response.

It should be especially emphasized that seroconversion (the appearance of specific antibodies in a previously seronegative patient or an increase in antibody titers over time) appears later than the onset of clinical manifestations of the infection.

Thus, in the presence of clinical and anamnestic data indicating the likelihood of IUI in a newborn child, verification of the disease must be carried out using a complex of direct and indirect research methods. In this case, identification of the pathogen can be carried out by any of the available methods. In recent years, PCR has been increasingly used to detect pathogens. The material can be any biological environment of the body (umbilical cord blood, saliva, urine, tracheal, oropharyngeal washings, smears from the conjunctiva, urethra, etc.). However, in cases where the etiology of the disease is associated with viral agents, the criterion for the active period of IUI is the detection of the pathogen in the blood or cerebrospinal fluid (if there is damage to the central nervous system). In cases where the virus genome is found in cells of other biological environments, it is very difficult to unambiguously determine the period of the disease.

In this case, a parallel assessment of the nature of the specific immune response is necessary (see the figure in the “Under Glass” section).

At the same time, to clarify the activity of the infectious process, a serological study using the ELISA method is recommended with the quantitative determination of specific antibodies of the IgM, IgG classes and assessment of their avidity level. Avidity is a concept that characterizes the speed and strength of binding of an antigen to an antibody (AT + AGV). Avidity is an indirect sign of the functional activity of antibodies. During the acute period of infection, specific IgM antibodies are first formed, and a little later - specific low-avidity IgG antibodies. Thus, they can be considered a marker of the active period of the disease. As the severity of the process subsides, the avidity of IgG antibodies increases, and high-avidity immunoglobulins are formed, which almost completely replace the synthesis of IgM. Thus, serological markers of the acute phase of the infectious process are IgM and low-avidity IgG.

Detection of specific IgM in umbilical cord blood, as well as in the blood of a child in the first weeks of life, is one of the important criteria for diagnosing IUI. The active period of congenital infection is also confirmed by the detection of low-avidity specific IgG antibodies with an increase in their titers over time. It should be emphasized that repeated serological testing should be carried out after 2-3 weeks (“paired sera”). In this case, a comparison must be made with the results of a parallel serological examination of the mother.

It should be especially noted that the isolated detection of IgG class antibodies in the blood serum of a newborn without specifying the avidity index and without comparison with maternal titers does not allow an unambiguous interpretation of the data obtained, since the antibodies may be of maternal origin (entering the fetus through transplacental transfer). Only with a dynamic (with an interval of 14-21 days) comparison of the levels of specific IgG antibodies of the newborn child and mother can one judge their nature. If the titers of specific IgG antibodies in a child at birth are equal to the maternal ones, and upon repeated examination a decrease is noted, then there is a high probability that they are of maternal origin.

The totality of the results of direct and indirect research methods makes it possible to establish the etiology of the disease, as well as determine its severity and stage. The molecular biological method - PCR - is currently used as the main method for etiological verification of an infectious disease. Numerous studies have confirmed the reliability of PCR results in the search for pathogens of IUI. The capabilities inherent in the PCR method make it possible to achieve maximum specificity of the analysis. We are talking about the absence of cross-reactions with similar microorganisms, as well as the ability to detect typical nucleotide sequences of a particular infectious agent in the presence of other microorganisms. The advantages of the PCR method are the possibility of early detection of the pathogen in the patient’s body even before the formation of an immune response, as well as the possibility of detecting infectious agents in latent forms of the infectious process. These advantages of the PCR method over indirect methods of diagnosing an infectious process (ELISA) are especially obvious in newborns, which is associated with the specifics of their immune system. In this case, the most significant are the presence in the blood serum of newborns of maternal antibodies transferred transplacentally, immunological tolerance and transient immaturity of the immune system. The latter is especially typical for premature infants, in whom pronounced immaturity of the immune system causes an inadequate immune response. In addition, intrauterine infection of the fetus can create prerequisites for the development of immunological tolerance to this pathogen with the formation of its long-term persistence and reactivation in the postnatal period. Some authors also point to the ability of TORCH-group pathogens to suppress the immune response.

Among the most well-studied IUIs are diseases such as rubella, cytomegalovirus infection (CMVI), herpes infection and toxoplasmosis.

Congenital rubella syndrome

The rubella virus belongs to the family Togaviridae, family Rubivirus. The genome of the virus is represented by single-stranded plus-strand RNA. Rubella virus is a facultative pathogen of slow viral infections. Congenital rubella is a slow viral infection that develops as a result of transplacental infection of the fetus. A rubeolar infection suffered by a woman in the first months of pregnancy, especially before the 14-16th week of gestation, leads to miscarriages, severe fetal damage, stillbirth, prematurity and various health problems in the postnatal period. In children born alive, severe malformations and embryofetopathies are often detected, leading to an unfavorable outcome already in the neonatal period. Thus, L.L. Nisevich (2000) notes that rubella virus antigens are detected in 63% of fetuses and deceased newborns with signs of embryofetopathies. It has been established that the most common clinical signs of manifest forms of congenital rubella in newborns are: congenital heart disease (in 75%), prematurity and/or prenatal malnutrition (in 62-66%), hepatosplenomegaly (in 59-66%), thrombocytopenic purpura (in 58%) and damage to the organs of vision (in 50-59%). It should be especially noted that with manifest forms of the disease, a high level of unfavorable outcome remains in the postneonatal period. Thus, the overall mortality rate among these patients during the first 18 months of life reaches 13%.

The manifest course of congenital rubella in the neonatal period occurs only in 15-25% of children with intrauterine infection. At the same time, the presence in a child of congenital heart defects, abnormalities of the visual organs (cataracts, less often microphthalmia, glaucoma) and hearing impairments described as Gregg’s triad, suggest with a high degree of probability that the cause of these lesions is a congenital rubeolar infection. However, it should be noted that the classic Gregg triad is extremely rare. In most cases, other nonspecific clinical manifestations of TORCH syndrome develop (intrauterine growth and development retardation, hepatosplenomegaly, thrombocytopenia, jaundice, etc.). Verification of the etiology of congenital infection is possible only on the basis of the results of laboratory examination (virological, immunological, molecular biological methods).

An even more difficult task is the diagnosis of subclinical forms of congenital rubella. It should be noted that this variant of the course of congenital rubeolar infection is observed in the vast majority of children (75-85%).

In newborns, there are no symptoms of TORCH syndrome, and various health disorders appear only at further stages of postnatal development. Prospective observation of this group of children makes it possible to identify serious lesions of various organs and systems in 70-90% of cases in the subsequent months and years of life. Drugs for the specific treatment of rubella have not been developed.

The primary goal of prevention is to protect women of childbearing age. However, rubella is one of the few perinatal infections that can be prevented through routine vaccination. Pregnant women, especially in the early stages of pregnancy, should avoid contact with patients with rubella, as well as with children in the first year of life who had signs of congenital rubeolar infection at birth.

Congenital cytomegalovirus infection

Pathogen Cytomegalovirus hominis— DNA-containing virus of the family Herpesviridae, subfamilies Betaherpesviridae. According to the classification proposed by the International Committee on Taxonomy of Viruses (1995), CMV belongs to the group “Human Herpesvirus-5”. The incidence of congenital CMV infection ranges from 0.21 to 3.0% depending on the type of population studied.

With intrauterine infection with CMV, which occurs in the early stages of pregnancy, teratogenic effects of the virus are possible with the development of dys- and hypoplasia of fetal organs. However, it should be noted that compared to other viruses (enteroviruses, rubella virus, etc.), CMV is characterized by a less pronounced teratogenic effect. Congenital CMV infection can occur in clinical and subclinical forms. Symptomatic forms of CMV are rare and do not exceed 10% of the total number of all cases of intrauterine CMV infection. Manifest forms of intrauterine CMV infection are characterized by severe symptoms and a severe course. In this case, jaundice, hepatosplenomegaly, damage to the nervous system, hemorrhagic syndrome, and thrombocytopenia are most often observed. Severe variants of manifest forms of congenital CMV are characterized by a high mortality rate (more than 30%). Surviving children often experience serious health problems in the form of severe mental retardation, sensorineural hearing loss, chorioretinitis, etc. Factors that determine an unfavorable neuropsychiatric prognosis are the presence of microcephaly, chorioretinitis, intracranial calcifications, and hydrocephalus. It has been established that severe forms of CMV develop, as a rule, in cases where the mother suffered a primary infection during pregnancy. Intrauterine infection occurs much less frequently if the mother suffers recurrent CMV infection during pregnancy. It has been noted that children with an asymptomatic form of intrauterine CMV infection may also have health problems. For example, K. W. Fowler et al (1999) detected sensorineural hearing loss in 15% of children with asymptomatic variants of intrauterine CMV infection.

Treatment of congenital CMV infection consists of etiotropic and syndromic therapy. The indication for etiotropic therapy for congenital CMV infection is the active period of the clinically manifest form of the disease. The criteria for the activity of the CMV infectious process are laboratory markers of active viral replication (viremia, DNAemia, AHemia). Serological markers of CMV activity (seroconversion, anti-CMV-IgM and/or an increase in the dynamics of the concentration of low-avidity anti-CMV-IgG) are less reliable. This is due to the fact that the results of a serological examination often turn out to be both false positive (for example, anti-CMV IgG detected in a child may be maternal, transmitted transplacentally, etc.) and false negative (for example, the absence of specific antibodies in the child’s blood serum to CMV due to immunological tolerance or due to a low concentration of antibodies to CMV (beyond the sensitivity limit of test systems) in the initial period of the immune response, etc.).

The drug of choice for the etiotropic treatment of congenital CMV infection is Cytotect. Cytotect is a specific hyperimmune anticytomegalovirus immunoglobulin for intravenous administration. The therapeutic effectiveness of Cytotect is due to the active neutralization of the cytomegaly virus by specific anti-CMV IgG antibodies contained in the drug, as well as the activation of antibody-dependent cytotoxicity processes.

Cytotect is available in the form of a 10% solution, ready for use. Cytotect is administered intravenously to newborns using a perfusion pump at a rate of no more than 5-7 ml/hour. For manifest forms of CMV infection, Cytotect is prescribed: 2 ml/kg/day with administration every 1 day, per course - 3-5 injections or 4 ml/kg/day - administration every 3 days - on the 1st day of therapy, on 5th and 9th days of therapy. Subsequently, the daily dose is reduced to 2 ml/kg/day, and depending on the clinical symptoms and activity of the infectious process, Cytotect is administered another 1-3 times at the same interval.

In addition, recombinant interferon alpha-2b (Viferon, etc.) is used as antiviral and immunomodulatory therapy. Viferon is available in the form of rectal suppositories containing 150,000 IU interferon alfa-2b (Viferon-1) or 500,000 IU interferon alfa-2b (Viferon-2). Directions for use: rectally. Dosage regimen: 1 suppository 2 times a day - daily, for 7-10 days, followed by 1 suppository 2 times a day every other day for 2-3 weeks.

Due to the high toxicity of anti-CMV drugs (ganciclovir, foscarnet sodium), they are not used for the treatment of neonatal CMV infection. The question of the need for etiotropic treatment of newborns with asymptomatic congenital CMV infection has not been completely resolved. The advisability of prescribing various immunomodulators is also not recognized by everyone.

Prevention of congenital CMV infection is based on identifying the seronegative layer among women of childbearing age. Preventive measures include limiting exposure of seronegative pregnant women to potential sources of CMV infection. Since the highest incidence of CMV infection is observed in children of early and preschool age, such women are not allowed to work with children (in kindergartens, schools, hospitals, etc.). Seronegative pregnant women should also not be allowed to care for children with congenital CMV infection due to the high risk of infection.

Effective methods for active specific immunoprophylaxis of CMV infection have not been developed to date.

Congenital and neonatal herpes infection

The terms “congenital” and “neonatal” herpes are used only in relation to diseases caused by HSV types 1 and 2, although the possibility of vertical transmission of other representatives of the Herpesviridae family (types 4 and 6) has now been proven. Intrauterine and neonatal herpes is most often caused by HSV type 2 (75% of all cases), although both types of pathogen can lead to the formation of similar pathologies in the fetus and newborn.

The incidence of neonatal herpes varies significantly in different regions and, depending on the population studied, ranges from 1.65 to 50 cases per 100,000 population. Despite the low prevalence of neonatal herpes, it poses a serious problem due to the increased risk of adverse outcomes. It has been established that serious neurological complications can arise in the future even when antiviral therapy is prescribed. As with CMV infection, neonatal HSV infection is more common in children whose mothers suffered a primary infection during pregnancy. In cases where a woman suffers a recurrent herpes infection during pregnancy, the risk of antenatal infection is much lower. The level of intrauterine infection with primary genital herpes in the mother during gestation ranges from 30 to 80%, while with recurrent herpes it is no more than 3-5%. At the same time, it has been established that in cases where a relapse of genital herpes is noted at the end of pregnancy and childbirth occurs naturally, the risk of intrapartum infection reaches 50%. It should be especially emphasized that even the presence of specific antibodies does not prevent the development of severe forms of the disease. Thus, 60-80% of infected newborns develop herpetic encephalitis. Among the risk factors for the development of herpetic infection in a newborn are: the first episode of maternal infection in the third trimester of pregnancy, invasive measures during pregnancy, childbirth before the 38th week of gestation, maternal age under 21 years.

There are three clinical forms of neonatal herpes: a localized form with damage to the skin, oral mucosa and eyes; generalized form with multiple organ damage and herpetic damage to the central nervous system in the form of encephalitis and meningoencephalitis (). In cases where prenatal transmission of the pathogen has occurred, clinical manifestations of herpetic infection can be detected already at birth. At the same time, with intrapartum infection, clinical manifestation does not occur immediately, but after 5-14 days. At the same time, localized and generalized forms of neonatal herpes, as a rule, debut at the end of the first, less often - at the beginning of the second week of life. The most severe neonatal herpes occurs in the form of generalized forms and is especially unfavorable in cases where herpetic lesions of the central nervous system are associated. It should be noted that, in contrast to localized forms, in which there are always typical skin or mucocutaneous manifestations of herpes infection, generalized forms are often hidden “under the guise” of a septic process that is resistant to traditional therapy. Isolated herpetic lesions of the central nervous system (meningitis, meningoencephalitis) most often develop in the 2-3rd weeks of life. In this case, the clinical picture is dominated by neurological changes (convulsive syndrome, impaired consciousness, etc.), and when examining the cerebrospinal fluid, a high level of protein and lymphomonocytic pleocytosis is revealed.

It should be noted that in a significant proportion of children with generalized forms of neonatal herpes, as well as with isolated herpetic lesions of the central nervous system, mucocutaneous manifestations are observed extremely rarely, and the maternal history of most of them does not indicate a previous herpetic infection. In light of the above, the role of modern diagnostic technologies becomes clear, allowing the etiology of the disease to be verified in the shortest possible time and with a high degree of reliability.

The herpetic etiology of the disease is confirmed by the detection of the virus (classical or accelerated virological methods), its genome (PCR) or antigens by ELISA in the blood, cerebrospinal fluid, urine, and nasopharyngeal contents. The detection of specific antibodies related to IgM indicates the presence of a herpes infection in a newborn, however, the timing of their appearance in the blood serum often “lags behind” the clinical manifestations of the disease.

Treatment. For all forms of neonatal herpetic infection, specific antiviral therapy with acyclovir is indicated, and the drug must be administered intravenously. Acyclovir in all cases, even with a localized form, is administered intravenously, since there is a high risk of generalization of herpetic infection.

For localized forms of the disease, acyclovir is used at a daily dose of 45 mg/kg/day, for generalized infection and meningoencephalitis - at a dose of 60 mg/kg/day. The drug is administered in three doses by intravenous infusion. The duration of treatment with acyclovir depends on the form of neonatal herpes: the localized form requires therapy for 10-14 days, the generalized form and meningoencephalitis - at least 21 days.

In addition, for the treatment of a generalized form, standard intravenous immunoglobulins and immunoglobulins with a high titer of antibodies to HSV, as well as viferon in suppositories at a dose of 150,000 IU once a day for 5 days, can be included in the complex therapy of newborns.

Prevention. In the prevention of neonatal herpes, a significant role belongs to the early detection of high-risk pregnant women, their timely and adequate treatment, as well as delivery. In this case, you must adhere to the following recommendations:

• if a woman develops a primary herpes infection less than 6 weeks before the expected birth, she must be prepared for a planned cesarean section;
• if the primary herpes infection occurred more than 6 weeks before birth, then vaginal delivery is possible. At the same time, to reduce the risk of exacerbation of the disease at the time of birth, it is advisable to use acyclovir from the 36th week of pregnancy;
• disseminated and severe primary maternal infections require treatment with acyclovir, regardless of the stage of pregnancy;
• in cases where a woman gave birth naturally and genital herpes was discovered during this period, the newborn is prescribed preventive therapy with acyclovir and additional examination is carried out for herpetic infection. If a negative laboratory test result is obtained and there are no clinical manifestations of the disease, antiviral therapy is stopped.

Very severe variants of the disease (diffuse encephalopathy, encephalitis, pneumonia, myocarditis) occur only in adults with immunodeficiencies (AIDS) and in prenatally infected premature infants.

The fetus becomes infected only if the woman becomes infected during pregnancy. Typical signs of congenital infection are chorioretinitis, foci of calcification in the brain, severe psychomotor retardation, hydro- or microcephaly, and seizures. In this case, there is a relationship between the severity of the disease in the fetus and the stage of pregnancy in which the infection occurred. In severe forms of the disease, the fetus dies or is born prematurely. Signs of the disease may appear at birth or may not be noticeable for many days after birth. Clinical symptoms may include intrauterine growth retardation, generalized lymphadenopathy, hepatosplenomegaly, jaundice, hydrocephalus, microphthalmia, and seizures alone or in combination. Intracranial calcifications and chorioretinitis can be detected by the time of birth, but often appear later.

According to the results of studies by G. Desmonts and J. Couvreur, 63% of women who became ill with toxoplasmosis during pregnancy gave birth to healthy children. Clinical manifestations of the disease in most newborns were minimal or absent. Only 16% of infected newborns had severe disease, 20% had moderate disease, and 64% were asymptomatic. To confirm the diagnosis, the PCR method, determination of Toxoplasma gondii antigens in the blood using the immunofluorescence reaction method, as well as serological methods for determining the titer of antibodies to Toxoplasma and the avidity index of these antibodies are used.

The scheme of using drugs in cycles has proven itself to be effective: tindurine for 5 days, sulfanilamide - 2 days more (7 days); three such cycles are carried out with breaks between them of 7-14 days.

According to indications (chronic, relapsing form in immunodeficiency state, exacerbation of chorioretinitis), this course of therapy is repeated after 1-2 months.

The side effects of all antifolates are eliminated by the administration of folic acid; folic acid derivatives are also active; the drug replenishes the patient's folic acid deficiency and helps restore the biosynthesis of nucleic acids. The official drug leucovorin (calcium folinate) is prescribed in a dose of 1-5 mg every 3 days (0.005 tablets) throughout the course of therapy.

Spiramycin is prescribed in two doses for 10 days for a body weight of up to 10 kg, 2 packets of granules of 0.375 million IU; roxithromycin (rulid) - 5-8 mg/kg/day for 7-10 days.

There is evidence of the effectiveness of clindamycin (for chorioretinitis in its late manifestation); in children over 8 years of age, a tetracycline drug, doxycycline monohydrate (Unidox Solutab), can be used: in the first 2 days, 4 mg/kg per dose, then 2 mg/kg once a day for 7-8 days. There are recommendations regarding the use of anticoccidial drugs such as aminoquinol and chemical coccide, but the degree of their effectiveness and side effects have not been sufficiently tested.

Prevention of congenital toxoplasmosis is aimed at identifying high-risk groups - seronegative girls and young women, with their subsequent clinical and serological observation before and during pregnancy. In addition, issues of prevention are raised during routine sanitary education. In this case, special attention is paid to the need to observe hygienic rules (do not taste raw minced meat when preparing dishes, eat only thermally processed meat, well-washed fruits and vegetables, sanitize cat feces, etc.). Active specific immunoprophylaxis for toxoplasmosis has not been developed.

Thus, congenital infections continue to be one of the most serious diseases in newborns and young children. The diverse etiology and uniformity of symptoms complicate the clinical verification of IUI, which determines the need for timely special studies. In this case, a targeted examination for IUI should be carried out in children at risk for intrauterine infection and the development of congenital infection. The risk group for intrauterine infection includes newborns born to mothers with a burdened urological and gynecological history and a pathological course of pregnancy. In turn, the detection of such conditions in newborn children as prematurity, delayed prenatal development, severe course of the intra- and/or early neonatal period should be considered as risk factors for the implementation of IUI. In these cases, immediate examination of newborns for IUI is indicated for timely verification of the etiology of the disease. The choice of methods for examining newborns for IUI should be based on a comprehensive assessment of clinical and laboratory parameters. At the same time, for laboratory diagnosis of IUI, the combination of molecular (PCR) and immunological (ELISA) diagnostic methods is optimal. n

Literature

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2. Zaplatnikov A. L. Clinical and pathogenetic rationale for immunotherapy and immunoprophylaxis of infectious and inflammatory diseases in children: Abstract of thesis. dis. ...Dr. med. Sci. M., 2003.
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6. Korovina N. A., Zaplatnikov A. L., Cheburkin A. V., Zakharova I. N. Cytomegalovirus infection in young children (clinical presentation, diagnosis, modern treatment options): A manual for doctors. M.: Posad, 1999.
7. Lobzin Yu. V., Vasiliev V. V. Toxoplasmosis in pregnant women: clinical manifestations, therapy and drug prevention of congenital toxoplasmosis // Ros. honey. magazine 2001. No. 5. P. 40-41.
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12. Tsaregorodtsev A. D., Ryumina I. I. Morbidity of newborns with intrauterine infections and tasks to reduce it in the Russian Federation//Ros. Vestn. perinatol and pediatrics. 2001. T. 46. No. 2. P. 4-7.
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16. Fowler K. W., Stagno S., Pass R. F. et al. The outcome of congenital cytomegalic virus infection in relation to maternal antibody status//N Engl J Med; 1992; 326:663-667.
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A. L. Zaplatnikov,
N. A. Korovina, Doctor of Medical Sciences, Professor
M. Yu. Korneva
A. V. Cheburkin, Candidate of Medical Sciences, Associate Professor
RMAPO, Moscow

Infections acquired by a child during intrauterine life make a significant contribution to the statistics of morbidity, infant mortality and further disability. Today there are frequent cases when a seemingly healthy woman (does not smoke, does not drink, has no chronic diseases) gives birth to an unhealthy child.

What explains this? During pregnancy, a woman's immunity decreases, and some hidden (latent) infections, which do not manifest themselves in any way before pregnancy, become more active (this is especially dangerous in the 1st trimester).

Important facts about IUI

• Up to 10% of all pregnancies are accompanied by transmission of infection from mother to fetus
• 0.5% of children born have some symptoms of infection
• Infection of the mother does not necessarily lead to infection of the fetus
• Many infections that are dangerous to the fetus are mild in the mother or have no symptoms at all.
• Infection of the fetus most often occurs when the mother has a new infection
• Timely treatment of a pregnant woman can reduce or eliminate risks to the fetus.

How does a fetus become infected?

There are three main ways of transmitting intrauterine infection during pregnancy:

• Transplacental (hematogenous) - viruses (CMV, herpes, etc.), syphilis, toxoplasmosis, listeriosis

The pathogen enters from the mother's blood through the placenta. If this happens in the 1st trimester, then malformations and deformities often occur. If the fetus becomes infected in the 3rd trimester, the newborn will show signs of acute infection. Direct entry of the pathogen into the baby’s blood leads to generalized damage.

• Ascending - mycoplasma, chlamydia, herpes

The infection ascends from the genital tract of the mother to the child. This usually occurs after rupture of the membranes, at the time of birth, but sometimes it also happens during pregnancy. The main cause of intrauterine infection is its entry into the amniotic fluid, and as a result, damage to the skin, respiratory and digestive tract of the fetus.

• Descending

The infection descends to the fetus through the fallopian tubes (with adnexitis, oophoritis).

Frequent causative agents of intrauterine transplacental infection

Most viruses and bacteria known to man can penetrate the fetus and cause various damage. But some of them are particularly contagious or pose an increased danger to the child. Some viruses (almost all that cause ARVI) are not transmitted to the baby, but are dangerous only when the pregnant woman’s temperature rises greatly.

Consequences of intrauterine infection for a child

Congenital infection can develop in 2 scenarios: acute and chronic. Acute infection is dangerous with severe sepsis, pneumonia and shock. Signs of ill health in such babies are visible almost from birth: they eat poorly, sleep a lot, and become less and less active. But often the disease acquired in the womb is sluggish or has no obvious symptoms. Such children are also at risk for long-term consequences: hearing and vision impairment, delayed mental and motor development.

Common symptoms of intrauterine infections

With intrauterine penetration of infectious agents, miscarriages, miscarriages, antenatal fetal death and stillbirths quite often occur. Surviving fetuses may exhibit the following symptoms:

• Intrauterine growth restriction
• Micro- and hydrocephalus
• Chorioretinitis, cataracts (eye damage)
• Pneumonia
• Jaundice and enlarged liver
• Anemia
• Hydrops fetalis (edema)
• Skin rash
• Fever

At what stage of pregnancy is infection dangerous?

Infecting a baby before birth can be dangerous at any stage of pregnancy. But some infections pose a great threat to life and health in the first trimester (rubella virus, for example), and some diseases are terrible if infected a couple of days before childbirth (chickenpox).

Early infection often leads to miscarriages and severe malformations. Late infection is usually associated with a rapidly progressing infectious disease in the newborn. More specific risks and the degree of danger are determined by the attending physician based on test results, ultrasound, gestational age and the characteristics of a particular infection.

Risk groups for diseases dangerous to the fetus

• Women with older children attending school and preschool institutions
• Workers of kindergartens, nurseries, schools
• Medical workers
• Pregnant women with chronic inflammatory diseases
• Indication of repeated medical abortions
• Women with a history of giving birth to infected children
• Malformations and antenatal fetal death in the past
• Untimely rupture of amniotic fluid

Signs of infection in a pregnant woman

• Temperature rise
• Enlarged and painful lymph nodes
• Cough, shortness of breath, chest pain
• Runny nose, lacrimation, conjunctivitis
• Pain and swelling of the joints

The above symptoms may be signs of allergies, non-infectious diseases, or infections that are not dangerous for the baby. But any signs of ill health should be noticed by the pregnant woman and are a reason to consult a doctor.

Frequent causative agents of intrauterine infection

Viruses

	Maternal infection	Consequences for the child
Rubella	Airborne path	Fetal rubella syndrome
Cytomegalovirus	Through biological fluids: blood, saliva, semen, urine	Congenital CMV infection (with or without symptoms)
Herpes simplex virus 2	Predominantly sexual route	Congenital herpetic infection
Parvovirus B19	Airborne path	Anemia, hydrops fetalis
Chicken pox	Airborne, contact and household route	Developmental defects during early infection, congenital chickenpox during infection before birth
	Airborne path	Spontaneous abortion, congenital measles
Hepatitis B, C	Sexual tract	Neonatal hepatitis, chronic carriage of the virus
	Sexual route, injection route	Congenital HIV infection

Bacteria

Protozoa

CMV

CMV, which belongs to the herpesovirus group, is transmitted sexually and through blood through transfusions and other interventions, as well as through close household contacts. It is believed that half of European women have encountered this virus at least once in their lives. It more often penetrates the placenta during primary infection of the mother.

But activation of a dormant infection can also harm a child (see). The likelihood of infection of the fetus is greatest in the 3rd trimester, and the consequences for the baby are more severe if infected at the beginning of pregnancy. It is believed that the risk of fetal infection is 30-40%. Of these, 90% of children will not have any symptoms or consequences. And 10% of newborns will be born with various signs of intrauterine infection.

Consequences for the child:

• miscarriage, stillbirth
• low birth weight
• (various degrees)
• (insufficient brain size)
• (accumulation of fluid in the brain cavities)
• hepatosplenomegaly (damage to the liver and spleen with an increase in their size)
• pneumonia
• optic nerve atrophy (various degrees of blindness)

With severe combined damage, a third of children die in the first months of life, and some patients develop long-term consequences (deafness, blindness, mental retardation). With mild infection, the prognosis is much more favorable.

There is currently no effective treatment for CMV symptoms in newborns. It is believed that the use of ganciclovir somewhat mitigates pneumonia and eye damage.

CMV is not an indication for termination of pregnancy, since the outcome for the newborn may be good. Therefore, it is recommended to treat pregnant women in order to reduce the risks of complications.

HSV

The herpes simplex virus, especially type 2 (genital), can cause congenital herpes infection in babies. It manifests itself during the first 28 days after birth (see).

Children from mothers who were diagnosed with herpes during pregnancy for the first time in their lives often become ill. In most cases, infection occurs when the child passes through the birth canal, but transplacental transmission is also possible.

Consequences of congenital herpes:

• miscarriage, stillbirth
• lethargy, poor appetite
• fever
• characteristic skin rashes (sometimes they do not appear immediately)
• jaundice
• bleeding disorder
• pneumonia
• eye damage (chorioretinitis)
• brain damage (with seizures, apnea, increased intracranial pressure)

Typically, the severity of the condition is maximum 4-7 days after birth, when many organs are affected and there is a risk of death from shock. If the virus attacks the brain, then encephalitis, meningitis and atrophy of the cerebral cortex are likely to develop. Therefore, severe congenital herpes makes a large contribution to the number of children with disabilities (cerebral palsy, mental retardation, vegetative state). Despite the danger of the disease, there are often cases when a child is born without symptoms of herpes, or has minor damage to the eyes and skin.

Treatment of pregnant women is most often carried out in the 3rd trimester with antiviral drugs (acyclovir, valacyclovir and others). Since with severe rashes on the woman’s genitals there is a risk of infection of the baby during childbirth, doctors may recommend a caesarean section. A child with signs of herpes should also be treated with acyclovir.

Rubella

One of the most dangerous viruses that causes deformities in the fetus is the rubella virus. The risk is especially high during pregnancy up to 16 weeks (more than 80%). Symptoms of the disease depend on the period at which the virus penetrated the fetus (see).

Congenital rubella syndrome:

• miscarriage, stillbirth
• low birth weight
• microcephaly
• cataract
• deafness (up to 50% of children)
• heart defects
• skin like “blueberry pie” - bluish foci of hematopoiesis in the skin
• meningitis and encephalitis
• hepatosplenomegaly
• pneumonia
• skin lesion

Signs of rubella in a pregnant woman are classic: fever, rash, swollen lymph nodes, joint pain and general malaise. Since the rubella virus is extremely contagious, all women are recommended to take an immunoglobulin test for it before planning a pregnancy. If it turns out that there is no immunity to the disease, then you must be vaccinated at least three months before pregnancy. There is no treatment for rubella during pregnancy or in newborns.

Parvovirus B19

The virus that causes erythema infectiosum usually goes undetected in adults. There are often no symptoms of infection. But during pregnancy, this disease can lead to miscarriages, stillbirths and intrauterine infection. The mortality rate for children is 2.5-10%. The virus is most dangerous from 13 to 28 weeks of pregnancy.

Consequences of intrauterine infection:

• anemia
• swelling
• myocarditis
• hepatitis
• peritonitis
• brain damage

In pregnant women, parvovirus infection manifests itself as pain in small joints, rash and fever. If such signs were noted, or the woman was in contact with a patient with parvovirus, then it is necessary to conduct laboratory diagnostics.

In cases of confirmed infection and fetal anemia, intrauterine administration of red blood cells is recommended. This technique often increases the level of red blood cells and saves the child's life.

Chicken pox

Chickenpox that occurs during pregnancy can cause severe damage to the fetus (congenital chickenpox syndrome). Infection of a child a few days before birth leads to classic, severe chickenpox with high mortality. The overall risk of infection to a fetus is 25%, although not all will develop symptoms.

Symptoms of congenital chickenpox:

• rash, zigzag scars
• underdevelopment of limbs (shortening and deformation)
• optic nerve atrophy, eye underdevelopment
• brain damage (underdevelopment)
• pneumonia

During pregnancy, if you come into contact with a patient with chickenpox, it is possible to administer immunoglobulin or antiviral treatment (acyclovir). Treatment of newborns is not advisable, since chickenpox symptoms do not progress after birth. Only if the mother is infected 5 days before birth or less does it make sense to administer immunoglobulin to the child, since the mother did not have time to transfer her antibodies to him.

Hepatitis B

The hepatitis B virus, spread primarily through sexual contact, can penetrate the placenta to the fetus at any stage of pregnancy. However, the maximum danger to the child occurs when the mother becomes infected with hepatitis in the 3rd trimester.

Consequences of intrauterine hepatitis infection:

• miscarriage, stillbirth
• light weight,
• psychomotor development delay
• acute form of hepatitis with liver failure and death
• carriage and chronic hepatitis B
• liver cancer
• hepatitis B with subsequent recovery

To diagnose hepatitis in the mother, the level of HBsAg is determined, which increases 1-2 months after infection. In case of chronic illness or carriage of the virus, this antigen does not disappear. Severe forms of hepatitis are treated with interferon-A. But even in the absence of symptoms, a pregnant woman can transmit the disease to her child, so special monitoring is required for such newborns.

HIV infection

The human immunodeficiency virus, which attacks special immune lymphocytes, has recently been capturing new territories. Most adult women become infected with it through sexual contact, while almost all children under 13 years of age acquired the disease during fetal life or at the time of birth.

Many children with HIV do not survive even two years without appropriate treatment, since their virus multiplication rate is very high. Subsequently, babies die from opportunistic infections, which are not scary for a healthy person.

Among the methods for diagnosing HIV in a newborn, it is better to use PCR. Determination of antibodies may be uninformative in the first 3-6 months of life. It is very important to detect HIV in pregnant women. Taking antiretroviral drugs throughout the entire period (zidovudine from 4 weeks of pregnancy) together with avoiding breastfeeding increases the chances of having a healthy baby by up to 90%. If the blood test results for HIV in a child are still positive, there is still a chance to slow down the disease for a long time. Recently, there has been more and more data on cases of complete recovery of children who regularly took medications from birth.

Listeriosis

Listeria is one of the few bacteria that can penetrate the placental barrier. Women become infected with listeriosis by eating meat, cheeses, vegetables and contact with animals. A pregnant woman may not notice any symptoms, but sometimes vomiting and diarrhea occur, the temperature rises, and a flu-like condition appears.

Manifestations of intrauterine infection:

• stillbirth, spontaneous abortion
• fever, refusal to eat
• meningitis
• sepsis
• multiple purulent foci, rash

If signs appear in a child in the first week, then the mortality rate is extremely high - about 60%. Therefore, all pregnant women with confirmed listeriosis are treated with ampicillin for 2 weeks. The same treatment for intrauterine infection is also necessary for sick newborns.

Syphilis

Primary syphilis (the formation of a hard chancre - an ulcer at the site of penetration of the bacterium), which occurs during pregnancy and is not treated, is transmitted to the child in almost 100% of cases, resulting in the death of 6 out of 10 children, the rest suffer from congenital syphilis.

After the primary ulcer, the mother’s disease enters a latent phase with periodic exacerbations. The fetus can become infected even in the absence of significant symptoms in the mother, starting from the 4th month of pregnancy.

Consequences of syphilis infection:

• stillbirth
• anemia, jaundice of a child
• cracks in the skin, rashes of various shapes
• damage to the eyes, ears, limbs, teeth (“Hutchinson’s teeth”)
• deafness
• impaired mental function

If the test results are positive for intrauterine infection, therapy with penicillin is carried out. Treatment for a pregnant woman is mandatory, as it helps prevent or treat syphilis in the fetus before birth. If a newborn has a positive reaction to syphilis, penicillin is also indicated. Due to effective diagnosis and simple therapy, the number of children with late congenital syphilis is currently insignificant.

Toxoplasmosis

Timely detection and treatment of toxoplasmosis in pregnant women reduces the risk of infection of the baby by 60%.

What are TORCH infections?

Toxoplasmosis, rubella, cytomegalovirus, herpes and some other diseases (syphilis, tuberculosis, etc.) are combined under the term TORCH for a reason. All of these infections are extremely dangerous when infected intrauterinely, some of them are asymptomatic or have few symptoms, and therefore require careful prevention and diagnosis.

When planning a pregnancy

Before conception, it is necessary to take tests for immunity to TORCH. The presence of IgG in the required titers indicates stable immunity to a previous infection. The absence of these is a sign of a woman’s vulnerability to infection. Therefore, vaccination against rubella is recommended, as well as careful care of cats (to avoid toxoplasmosis), and screening of the partner for herpes and cytomegalovirus. A high IgM titer indicates an acute infection. Such women are advised to postpone planning pregnancy.

During pregnancy the appearance

During pregnancy, IgM may indicate infection, which theoretically leads to intrauterine infection of the fetus. Such women will have to undergo additional tests to determine the condition of the child and further tactics.

Diagnosis of intrauterine infection

Blood tests for all pregnant women

• syphilis, hepatitis B and C, regular vaginal smears for microflora
• PCR to detect viruses in blood

Ultrasound

Ultrasound examination of the fetus is a simple, safe, although not absolutely accurate method for diagnosing infection. Based on its results, you can evaluate intrauterine growth retardation and see some defects that are a consequence of infection. In addition, cordocentesis is performed under ultrasound guidance. Signs of a possible infection on ultrasound:

• enlargement of the ventricles of the brain
• multiple calcium deposits in the brain, liver, intestines
• enlargement of the heart, liver and spleen
• enlargement of the abdomen and expansion of the renal collecting system
• intrauterine growth restriction syndrome
• swelling of the placenta, amniotic bands
• high or low water
• formed developmental defects

All of the above signs may be a consequence of non-infectious diseases or a variant of the norm (see).

Seroimmunological method

Determination of immunoglobulins is necessary for women at risk. The appearance of IgM indicates infection or reactivation of the infection. This may be an indication for invasive diagnostics: cordocentesis.

In domestic healthcare there is mandatory serological screening for rubella, syphilis, hepatitis, and in risk groups - for HIV. But often the doctor recommends taking additional tests for infections of the TORCH group and others. The results of some tests (for toxoplasmosis, for example) are easier to interpret if a similar study was carried out before pregnancy.

The essence of the definition of immunoglobulins:

• There is IgM, no IgG - most likely there is an acute infection
• There is IgG, no IgM – the infection was in the past, immunity is formed
• There is neither IgM nor IgG in sufficient titers - the woman has not encountered the infection, or has encountered it for a very long time, there is no immunity
• There are IgM and IgG – there is an infection to which immunity has already begun to form, or a reactivation of a previously existing infection has occurred. Most likely, the fetus is not in danger.

Serological testing of a newborn's blood is difficult, since it contains maternal antibodies, which distort the picture.

Cordocentesis and amniocentesis

Cordocentesis is a puncture of the skin and drawing blood from the umbilical cord, a fairly accurate method for determining infection. Umbilical cord blood may contain DNA of the pathogen, as well as immune complexes against it.
Amniocentesis is the study of amniotic fluid.

Tests of blood, saliva, urine, cerebrospinal fluid of the newborn

They make it possible to detect intrauterine infection in children with varying degrees of symptom severity.

Treatment and observation for intrauterine infection

Timely detection of a viral or bacterial disease is extremely important, since some infections respond well to treatment in the early stages, and the risk of severe consequences for the baby is reduced.

Drug treatment

Bacterial diseases in pregnant women can and should be treated with antibiotics. Penicillin drugs are used quite often - they are safe and effective for many diseases. A newborn baby with signs of bacterial infections is also given antimicrobial drugs, which often saves lives and prevents complications.

Viral infections are less easily treated in both pregnant women and newborns. Some drugs (acyclovir, valacyclovir and others) are used for herpetic rashes and some other diseases. If treated quickly, serious malformations and congenital infections can be prevented. Formed consequences in the form of heart defects, brain defects and other organs cannot be treated with antiviral drugs.

Choosing a method of delivery

Many diseases with rashes on the genitals require careful management of childbirth; acute herpes with blisters on the labia can be dangerous for the baby when passing through the birth canal. In such cases, a caesarean section is often recommended. But in most infectious lesions of the mother, childbirth can be carried out through natural means.

Monitoring infected children

Even in the absence of symptoms of CMV and rubella in the first months of life, infected children need to have their hearing checked before the age of 5-6 years.

Treatment of formed defects and damage due to intrauterine infections in newborns

Many congenital defects (CHD, cataracts) can be reduced or eliminated surgically. In such cases, the child gets a chance at life and independent activity. Children often require hearing aids many years after an infection, since hearing loss is quite common among those infected.

Prevention of fetal infection

• Vaccination of children and adult women before planning pregnancy
• Taking care of women's health
  • limiting contact with children, especially in educational institutions
  • restriction of visiting crowded places
  • careful contact with pets, avoiding cleaning cat litter
  • eating thermally processed foods, excluding soft cheeses and semi-finished products
  • an adequate way to protect against infection during sexual intercourse
• Determining the level of immunoglobulins for the main intrauterine infections TORCH before planning pregnancy

What to do if you come into contact with infected people?

If a woman during pregnancy communicated or spent a long time near an infected adult and child, she should consult her doctor. For example, when exposed to rubella, the presence of IgG is immediately checked. Their presence indicates strong immune protection for both the pregnant woman and the baby. The absence of such antibodies requires further tests 3-4 and 6 weeks after exposure. Negative results give reason to calm down. A positive test or the presence of clinical symptoms is a reason for additional examinations (ultrasound, cordocentesis, and others).

There are 3 main routes of infection of the placenta, membranes and fetus. One of them, the most likely if the mother has chronic sources of infection, is descending or transdecidual, from septic foci under the decidua. Penetrating through the membranes into the amniotic fluid, microorganisms simultaneously spread between the membranes, reaching the basal plate of the placenta, where leukocyte infiltration occurs in response. In the amniotic fluid, the pathogen also multiplies with the development of reactive amnionitis, which results in a disruption of the enzymatic and adsorption functions of the amniotic membranes, which is manifested by polyhydramnios and the accumulation of unlysed meconium. Infection of the fetus can occur through ingestion and aspiration of contaminated amniotic fluid.

In the ascending path, pathogens of vaginal infections predominate, causing significant disturbances in the microcenosis of the vagina. The pathogenesis of the lesion in this case is similar to that in the descending pathway.

The most dangerous is the third, hematogenous route of infection, which predominates when there is a purulent-inflammatory focus and a recurrent viral infection in the mother’s body. If the barrier function of the placenta is impaired and its fetal part is damaged, the pathogen may enter the fetal bloodstream. Transplacental infection can cause fetal abnormalities and intrauterine sepsis.

Thus, the route of infection is determined by the type of pathogen: bacterial infection spreads mainly through the ascending route; All true viral infections are characterized by a hematogenous route of infection; it is also typical of infectious diseases such as listeriosis, toxoplasmosis and syphilis.

The degree of structural and functional disorders in the mother-placenta-fetus system largely depends on the course of the infectious process during pregnancy - acute process, remission stage, exacerbation or carrier state. The acute infectious process is especially unfavorable. However, the degree of teratogenic effect of infection on the fetal-placental complex is not always clearly predictable: even an asymptomatic infection in the mother can have a fatal effect, and a specific acute infection can pass without a trace.

The concept of “intrauterine infection” is conditional; it complements the clinical diagnosis suggesting the future birth of a child with the consequences of infectious exposure or an acute inflammatory disease. This is what should in a certain way influence the obstetric tactics of pregnancy and delivery.

It is not possible to reliably establish the prevalence of the infectious process during IUI without a special study of the fetal material. Therefore, the terms “placentitis, chorionitis, amnionitis, intrauterine fetal pneumonia” that appear in clinical diagnoses and conclusions of EI are not diagnostically reliable.

Detection of acute infectious processes with typical clinical manifestations in pregnant women does not cause serious problems. However, the specificity of IUI currently lies in the chronic persistent course of the disease with atypical manifestations and manifestation of associated pathogens in the third trimester of pregnancy. As a result, even the preventive measures taken during preconception preparation of the patient or in the first half of pregnancy do not always achieve the desired goal.

When managing pregnant women at high risk of IUI, it is important to follow the stages of examination and treatment and preventive measures. An algorithmic approach to solving this problem allows us to minimize the likelihood of giving birth to a child with an acute infectious process and avoid the unreasonable use of immunostimulating and antibacterial medications that increase the level of allergenicity in newborns.

Stages of examination of pregnant women at high risk of intrauterine infection

It is advisable to carry out an initial laboratory examination for carriage of BVI in the presence of an increased risk of IUI based on the results of anamnestic testing (prenatal counseling) in the first trimester of pregnancy using the following methods:

• Blood ELISA for IgM and IgG antibodies;
• polymerase chain reaction (PCR) of scrapings of the mucous membrane of the cervical canal, the surface of the cervix and vaginal walls;
• bacterial seeding of the discharge of the cervical canal and vagina;
• bacterial culture of urine;
• Viruria.

Search for prognostic echographic markers of IUI:

• premature maturation of the placenta (according to the classification of P. Grannum);
• contrasting the basal lamina of the placenta (up to 24 weeks);
• hyperechoic inclusions (foci) in the placenta;
• expansion of gaps and profit centers;
• thickening of the placenta, not corresponding to the gestational age, with normal area (size);
• bilateral pyeloectasia in the fetus with contrasting pattern of the pyelocaliceal system;
• increased hydrophilicity (or decreased echogenicity) of fetal brain tissue;
• hyperechoic inclusions in the structures of the fetal brain;
• choroid plexus cysts of the fetal brain;
• hyperechoic focus in the fetal heart;
• hyperechoic intestine.

To state in the EI conclusion the presence of echographic signs of IUI, it is sufficient to identify three markers relating to the fetus, placenta and amniotic fluid.

In conclusion, the use of the term “placentitis” and the establishment of a diagnosis of “intrauterine infection”, which implies certain clinical signs of the infectious process and morphological changes in the placenta, are categorically unfounded.

Based on EI data, conclusions should be drawn about identifying echographic signs of the influence of an infectious agent, which gives grounds for:

• extended laboratory examination of a pregnant woman in the absence of early detection of the fact of carriage of the infection;
• carrying out immunostimulating and specific antibacterial therapy in a pregnant woman with established carriage.

Rubella, prenatal tactics

Impact of rubella virus on the fetus

Maternal infection, either with obvious clinical symptoms or asymptomatic, can lead to infection of the fetus. If a woman contracts rubella in the first trimester of pregnancy, the fetus may become infected with the rubella virus or have an unobvious infection without clinical consequences; he may have damage to one organ (usually hearing loss) or multiple organ damage.

Variants of fetal development disorders

Most Frequent

• Developmental delay (prenatal malnutrition).
• Deafness.
• Cataract, retinopathy.
• Patent ductus arteriosus.
• Pulmonary artery hypoplasia (or valve stenosis).
• Hepatosplenomegaly.

Less frequent

• Thrombocytopenic purpura.
• Delayed psychomotor development.
• Meningoencephalitis.
• Osteoporosis of long bones.
• Coarctation of the aorta.
• Myocardial necrosis.

• Microcephaly.
• Brain calcification.
• Defects of the heart septum.
• Glaucoma.
• Hepatitis.

Late manifestations (after 3-12 months of life)

• Interstitial pneumonia.
• Chronic rash resembling rubella.
• Repeated infections.
• Hypogammaglobulinemia.
• Chronic diarrhea.
• Diabetes.

Frequency of occurrence of defects by trimester

Only primary infection poses an increased risk to the fetus. Rubella disease in the first weeks of pregnancy is accompanied by twice the frequency of spontaneous abortions. The highest risk of congenital rubella is observed in 4-8 weeks of pregnancy (according to prospective studies, 50-60%), in the remaining periods of the first trimester of pregnancy it is 25-30%. In all cases, congenital rubella disease after 9 weeks of pregnancy is accompanied by hearing loss, retinopathy and delayed psychomotor development. Deafness and retinopathy most often occur with rubella before the 120th day (up to 17-18 weeks). Cataracts and heart disease are almost always associated with disease that develops before the 60th day of development (before 9 weeks). Some risk may be associated with the occurrence of this infection before conception or after 20 weeks of pregnancy.

Pathogenesis

When infected with rubella, the virus begins to multiply in the mucous membrane of the upper respiratory tract and in the adjacent lymph nodes. After 7-10 days, it enters the blood and circulates in it until antibodies appear - usually another 7 days. The total incubation period (from the time of contact to the onset of symptoms) is 14-21 days (usually 16-18 days).

Diagnostic methods

The virus can be detected in the blood a week before the rash.

The titer of hemagglutinin-inhibiting antibodies begins to increase when symptoms of the disease appear, reaching a maximum level after 1-3 weeks, after which their level remains almost unchanged for several years. Complement-fixing antibodies increase more slowly (the maximum level is observed approximately 1-2 weeks after the peak of hemagglutinin-inhibiting antibodies), and disappear after several years.

Rubella-specific IgM antibodies are detected soon after the rash, reach a maximum by the 30th day and cease to be detected by the 80th day. IgG antibodies increase parallel to IgM antibodies, but remain at a high level indefinitely. The titer of rubella-specific IgM antibodies increases rapidly after a recent infection and is not detected 4-5 weeks after the onset of the disease; During these periods, only IgG is detected as residual antibodies. Positive IgM specific for rubella is the most accurate indicator of recent infection. A negative IgM result has little diagnostic value unless supported by other laboratory tests.

Obstetric tactics

Many contacts with rubella are actually contacts with patients who have a nonspecific skin rash due to the viral disease. Therefore, it is necessary to verify contact with rubella by serological examination of the suspected patient. To resolve the issue of the possibility of rubella infection in a pregnant woman, serological diagnosis of the disease is carried out.

When a diagnosis of rubella is made in a pregnant woman before 20 weeks, it is most advisable to terminate the pregnancy due to the high risk of developmental anomalies in the fetus that are not accessible to prenatal diagnosis.

Prenatal tactics

Determination of IgM and IgG in the blood of the fetus to diagnose acute rubella infection (T-lymphocytes of the fetus are able to recognize and inactivate Ig-mothers from 16-17 weeks of gestation). Disadvantage of the method: low production of immunoglobulins in the fetus.

Isolation of virus from fetal blood on culture media. Disadvantage of the method: low cultivation efficiency.

Sonographic signs of probable intrauterine infection

The issue of determining IUI is one of the most difficult in the field of prenatal diagnosis. Any deviation in echographic parameters that accompanies a pregnant woman’s infectious history is only one of the manifestations of disturbances in the fetal-placental complex. And each of the signs can only conditionally be interpreted as a consequence of the inflammatory process.

When considering the problem of IUI, it is necessary to correctly interpret this concept as a diagnostic position (diagnosis) both in prenatal diagnosis and in obstetric practice. A diagnosis of IUI may be the basis for a number of therapeutic measures, including antibacterial therapy.

However, the adopted abbreviation IUI should not be unambiguously interpreted as infection of the fetus - the impact of the infectious agent may be limited to the membranes and placenta, especially since the signs of the infectious state of the fetus itself are difficult to interpret.

In this regard, the conclusion of the EI signs of IUI must be treated as giving grounds for a special examination of the pregnant woman and carrying out preventive treatment measures.

It is advisable to replace the IUI with the influence of an infectious factor (IIF), as in the proposed publication.

The echographic marker VIF is never the only one isolated. By analogy with the syndrome complex of congenital diseases, there should be at least two echographic signs of VIF. At the same time, to establish a clinical diagnosis of “influence of an infectious factor”, it is necessary to comply with three correlating conditions:

• echographic signs of probable VIF are combined with the corresponding clinical picture of the course of pregnancy;
• in the long-term or immediate history there is confirmation of the likelihood of infection;
• in pregnancy periods of more than 26 weeks, when assessing the SP PC, signs of placental dysfunction or insufficiency are revealed.

Extraembryonic formations are subject to the predominant and most pronounced changes in VIF.

The earliest signs of infectious exposure in the first trimester of pregnancy are increased echogenicity and dispersion of the exocelomic contents, as well as thickening of the walls of the yolk sac.

A subsequent manifestation may be excessive thickening of the chorion with the presence of anechoic small cystic inclusions.

A rarely detected sign is a hyperechoic focus on the amniotic membrane. When identifying this echographic phenomenon, it is necessary to differentiate it from the zone of the former attachment of the yolk sac under the umbilical cord. Concomitant signs of possible exposure to BVI in this case may be nonspecific changes in the chorion, increased echogenicity of the exocoelomic contents, as well as increased myometrial tone as a sign of a threat of miscarriage.

The most common variant of blastopathies in IUI, which manifests itself at the beginning of the second trimester of pregnancy, is hypoplasia of the amniotic cavity with the presence of excess exocelomic space.

From the second trimester of pregnancy, the echographic manifestations of VIF become more pronounced and distinct.

An increase in the thickness of the placenta and expansion of the urinary tract, between which zones of increased echogenicity are identified, are associated with swelling of the terminal villi and slowing of blood flow in the lacunae.

Hemangiomas in the region of the marginal sinuses can take the form of multi-chamber formations and amniotic cords. At the same time, amniotic cords can create a picture of multi-chambered cavity fluid formations adjacent to the placenta.

This is due to the extremely low speed and non-directional movement of blood elements.

Slowing blood flow in the lacunae leads to the formation of hemangiomas of various sizes.

Differential diagnosis can be difficult and depends on the professional training of the doctor. But in both cases, the origin of these formations may be associated with VIF, and their presence can be interpreted as markers of a previous inflammatory process.

In an acute infectious process, the echographic picture may resemble placental cysts.

This is due to vasodilation, hemorrhages, heart attacks and degenerative changes.

It should be noted that placental cysts can have a varied appearance - more distinct contours and reduced echogenicity of the internal structure. Cysts with similar echographic characteristics may arise due to the influence of non-infectious factors.

A sign of completion of the inflammatory process is the appearance in the thickness of the placental tissue of diffusely scattered hyperechoic foci - calcifications or calcified foci of infarction measuring 3-5 mm.

From the point of view of pathomorphology, it is categorically incorrect to identify these echographic findings with fatty inclusions in the placenta, which often appears in the conclusions of echographic studies of first-level screening specialists.

The consequence of the inflammatory state of the placenta is always the accumulation and deposition of fibrin in the lacunae and urinary tract, which causes a picture of premature maturation of the placenta.

A coarse echo-positive suspension in the amniotic fluid - meconium, particles of compacted cheese-like lubricant occurs when the production of a proteolytic enzyme and the adsorption function of the amniotic membranes are impaired.

– a group of diseases of the fetus and newborn that develop as a result of infection in the prenatal period or during childbirth. Intrauterine infections can lead to fetal death, spontaneous abortion, intrauterine growth retardation, premature birth, the formation of congenital defects, damage to internal organs and the central nervous system. Methods for diagnosing intrauterine infections include microscopic, cultural, immunoenzyme, and molecular biological studies. Treatment of intrauterine infections is carried out using immunoglobulins, immunomodulators, antiviral and antibacterial drugs.

In the intranatal period, microbial contamination more often occurs, the nature and extent of which depends on the microbial landscape of the mother’s birth canal. Among the bacterial agents, the most common are enterobacteria, group B streptococci, gonococci, Pseudomonas aeruginosa, Proteus, Klebsiella, etc. The placental barrier is impenetrable to most bacteria and protozoa, however, if the placenta is damaged and fetoplacental insufficiency develops, antenatal microbial infection can occur (for example, with the causative agent of syphilis ). In addition, intrapartum viral infection cannot be ruled out.

Factors in the occurrence of intrauterine infections are a burdened obstetric and gynecological history of the mother (nonspecific colpitis, endocervicitis, STDs, salpingophoritis), unfavorable course of pregnancy (threat of miscarriage, gestosis, premature placental abruption) and infectious morbidity of the pregnant woman. The risk of developing a manifest form of intrauterine infection is significantly higher in premature infants and in cases where a woman is primarily infected during pregnancy.

The severity of clinical manifestations of intrauterine infection is influenced by the timing of infection and the type of pathogen. So, if infection occurs in the first 8-10 weeks of embryogenesis, pregnancy usually ends in spontaneous miscarriage. Intrauterine infections that occur in the early fetal period (before 12 weeks of gestation) can lead to stillbirth or the formation of gross malformations. Intrauterine infection of the fetus in the second and third trimester of pregnancy is manifested by damage to individual organs (myocarditis, hepatitis, meningitis, meningoencephalitis) or a generalized infection.

It is known that the severity of the manifestations of the infectious process in a pregnant woman and in the fetus may not coincide. An asymptomatic or minimally symptomatic course of infection in the mother can cause severe damage to the fetus, including its death. This is due to the increased tropism of viral and microbial pathogens towards embryonic tissues, mainly the central nervous system, heart, and organ of vision.

Classification

The etiological structure of intrauterine infections suggests their division into:

To designate the group of the most common intrauterine infections, the abbreviation TORCH syndrome is used, combining toxoplasmosis, rubella, cytomegalovirus, and herpes simplex. The letter O (other) denotes other infections, including viral hepatitis, HIV infection, chicken pox, listeriosis, mycoplasmosis, syphilis, chlamydia, etc.).

Symptoms of intrauterine infections

The presence of intrauterine infection in a newborn may be suspected already during childbirth. Intrauterine infection may be indicated by the outpouring of turbid amniotic fluid, contaminated with meconium and having an unpleasant odor, and the condition of the placenta (plethora, microthrobosis, micronecrosis). Children with intrauterine infection are often born in a state of asphyxia, with prenatal malnutrition, enlarged liver, malformations or stigmas of dysembryogenesis, microcephaly, hydrocephalus. From the first days of life, they experience jaundice, elements of pyoderma, roseolous or vesicular rashes on the skin, fever, convulsions, respiratory and cardiovascular disorders.

The early neonatal period for intrauterine infections is often burdened with interstitial pneumonia, omphalitis, myocarditis or cardiac, anemia, keratoconjunctivitis, chorioretinitis, hemorrhagic syndrome, etc. During instrumental examination, innate cataracts, and glaucoma, and glacity can be found in the newborn. Shadows and calcifiers of the brain.

In the perinatal period, the child experiences frequent and profuse regurgitation, muscle hypotension, central nervous system depression syndrome, and gray skin color. In the later stages, with a long incubation period of intrauterine infection, the development of late meningitis, encephalitis, and osteomyelitis is possible.

Let us consider the manifestations of the main intrauterine infections that make up the TORCH syndrome.

Congenital toxoplasmosis

After birth in the acute period, intrauterine infection manifests itself as fever, jaundice, edematous syndrome, exanthema, hemorrhages, diarrhea, convulsions, hepatosplenomegaly, myocarditis, nephritis, pneumonia. In the subacute course, signs of meningitis or encephalitis dominate. With chronic persistence, hydrocephalus with microcephaly, iridocyclitis, strabismus, and optic nerve atrophy develop. Sometimes monosymptomatic and latent forms of intrauterine infection occur.

Late complications of congenital toxoplasmosis include mental retardation, epilepsy, and blindness.

Congenital rubella

Intrauterine infection occurs due to rubella during pregnancy. The probability and consequences of fetal infection depend on the gestational age: in the first 8 weeks the risk reaches 80%; The consequences of intrauterine infection can include spontaneous abortion, embryo- and fetopathy. In the second trimester, the risk of intrauterine infection is 10-20%, in the third – 3-8%.

Babies with intrauterine infection are usually born premature or at low birth weight. The neonatal period is characterized by a hemorrhagic rash and prolonged jaundice.

Congenital herpetic infection

Intrauterine herpes infection can occur in a generalized (50%), neurological (20%), mucocutaneous form (20%).

Generalized intrauterine congenital herpetic infection occurs with severe toxicosis, respiratory distress syndrome, hepatomegaly, jaundice, pneumonia, thrombocytopenia, hemorrhagic syndrome. The neurological form of congenital herpes is clinically manifested by encephalitis and meningoencephalitis. Intrauterine herpes infection with the development of skin syndrome is accompanied by the appearance of a vesicular rash on the skin and mucous membranes, including internal organs. When a bacterial infection develops, neonatal sepsis develops.

Intrauterine herpes infection in a child can lead to the formation of developmental defects - microcephaly, retinopathy, limb hypoplasia (cortical dwarfism). Late complications of congenital herpes include encephalopathy, deafness, blindness, and delayed psychomotor development.

Diagnostics

Currently, prenatal diagnosis of intrauterine infections is an urgent task. For this purpose, in the early stages of pregnancy, smear microscopy, bacteriological culture of the vagina for flora, PCR examination of scrapings, and examination for the TORCH complex are performed. Invasive prenatal diagnostics (chorionic villus aspiration, amniocentesis with examination of amniotic fluid, cordocentesis with examination of umbilical cord blood) are indicated for pregnant women at high risk for the development of intrauterine infection. detects signs of otoacoustic emissions.

Treatment of intrauterine infections

General principles for the treatment of intrauterine infections involve immunotherapy, antiviral, antibacterial and syndromic therapy.

Immunotherapy includes the use of polyvalent and specific immunoglobulins, immunomodulators (interferons). Targeted antiviral therapy is carried out mainly with acyclovir. For antimicrobial therapy of bacterial intrauterine infections, broad-spectrum antibiotics (cephalosporins, aminoglycosides, carbapenems) are used; for mycoplasma and chlamydial infections, macrolides are used.

Syndromic therapy of intrauterine infections is aimed at relieving individual manifestations of perinatal damage to the central nervous system, hemorrhagic syndrome, hepatitis, myocarditis, pneumonia, etc.

Forecast and prevention, should be vaccinated no later than 3 months before the expected pregnancy. In some cases, intrauterine infections may be the basis for artificial termination of pregnancy.