Intrauterine infection of the fetus how to determine. Intrauterine infections in the newborn and during pregnancy. Diagnosis of intrauterine infection

Traditionally in Russian literature under the term "intrauterine infections"(IUI) refers to diseases in which infection occurs in the prenatal period or during childbirth and the source is the mother. It should be noted that intrauterine infection of a child from the mother occurs much more often than clinical signs of the disease develop. To denote the fact of intrauterine infection in practical medicine, the term is used "intrauterine infection". Term "intrauterine infection" usually used to refer to clinical manifestations infectious disease of the fetus and newborn, detected prenatally or shortly after birth.

The frequency of intrauterine infection. According to generalized literature data, at least 10% of newborns are infected in utero with various viruses and microorganisms. The risk of intrauterine infection depends on the type of pathogen, the initial health status of the pregnant woman and the fetus, as well as on the epidemiological situation in a particular geographic region. A higher frequency is observed in the primary infection of a pregnant woman than in a latent or secondary viral infection.

Intrauterine infections are a significant cause of reproductive losses. Thus, the frequency of early neonatal morbidity and mortality in IUI ranges from 5.3 to 27.4%, and the stillbirth rate reaches 16.8%. In the structure of perinatal mortality, infection accounts for 10.1%. An even more significant role of infectious inflammatory diseases play in the structure of perinatal morbidity, where they account for 20-38%.

At the same time, the true frequency of perinatal pathology caused by an infectious factor remains unspecified, which is due to the lack of screening studies, the discrepancy between the frequency of infection and direct morbidity, the frequent latent course of the pathological process, and the objective complexity of antenatal laboratory diagnosis. As a result

Thus, a significant part of infections remains unrecognized and is taken into account in statistical analysis as a consequence of complications of the birth act, intrauterine asphyxia, respiratory distress syndrome and other pathological conditions.

In 95.8%, the causes of death due to the infectious process are conditions that occur in the perinatal period. Of these, the most frequently noted: congenital pneumonia 47.5%, infections specific to the perinatal period 41.6%, and neonatal sepsis 6.7%.

Etiology. The list of unconditional pathogens is quite extensive and includes dozens of species of almost all classes of organisms from viruses to protozoa and fungi.

Percentage of children born with symptoms bacterial intrauterine infections is 20-36%. At present, the role of a wide range of aerobic and anaerobic bacterial agents, primarily representatives of opportunistic microflora: staphylococci, streptococci, Escherichia coli, Klebsiella, Proteus, enterobacteria, as well as non-spore-forming anaerobic microorganisms, has been proven. It should be noted that in this group of patients, significant disturbances in the composition of the vaginal microbiocenosis are usually detected (60-65% have vulvovaginal candidiasis or bacterial vaginosis).

The classic example of bacterial IUI is listeriosis, which is caused by Listeria monocytogenes- short gram-positive rods (coccobacilli). Among other bacterial pathogens of intrauterine infection, the role of group B streptococci has increased in recent years. Their significance in the pathology of the fetus, especially newborns, has increased markedly against the background of the widespread introduction of aminoglycoside antibiotics into practice, to which these microorganisms are naturally resistant. Currently, a close relationship has been established between the frequency of infections caused by group B streptococci in newborns and the frequency of carriage of these bacteria in the genital tract of mothers. The frequency of detection of carriage of group B streptococci in pregnant women varies widely - from 1.5 to 30%. The most dangerous is a massive focus (more than 10 5 CFU / ml) in the mother's cervical canal. In such cases, more than 60% of newborns are born infected. The clinical manifestations of infections caused by these bacteria in newborns are diverse - from local skin

to severe fulminant septic processes and meningitis, accompanied by high mortality (up to 80%) in premature newborns.

In recent years, in the structure of perinatal pathology, the importance of ssualno-transmissible intracellular infectious agents: mycoplasmas, ureaplasmas and chlamydia. The frequency of intrauterine infection with genital urea- and mycoplasmosis in a pregnant woman is 40-50%, and with chlamydia it reaches 70.8%.

A significant proportion of perinatal infections are caused by various viruses, among which the most important are cytomegaloviruses, herpes simplex, rubella, enteroviruses (ECHO, Coxsackie), hepatitis B, human immunodeficiency virus. In addition, influenza, measles, poliomyelitis, papilloma and parvoviruses influence the increase in reproductive losses and morbidity in newborns.

In recent years, there has been an increase in the number of patients with local forms of herpetic lesions, which determines the trend towards an increase in the frequency of herpes infection in newborns. The defeat of the virus of the genitals is detected in 7% of pregnant women. Herpes is an example of a classic chronic infection with a lifelong existence of the pathogen in the host organism. About 70 types of viruses of this group have been isolated, of which 4 affect people: herpes simplex virus I and II serotypes, varicella-zoster virus, Epstein-Barr virus and cytomegalovirus (all three isolated strains - Devis, Kerr and AD189) have clinical significance.

Enteroviral infections are also quite common in the population. As causative agents of intrauterine infections, echoviruses and Coxsackie viruses are of the greatest interest. The experiment proved the etiological significance of Coxsackie viruses types A 13 , A 3 , A 6 , A 7 , B 4 and B 3 , as well as echoviruses 9 and 11 types.

The retroviruses that cause AIDS deserve special attention. Up to 50% of children born to HIV-infected mothers become infected antenatal, intrapartum or in the early neonatal period. The incidence of disease in newborns from seropositive mothers varies widely - from 7.9 to 40%.

The highest value among fungal pathogens of IUI have widespread representatives of fungi of the genus Candida. Cryptococcosis, coccyoidosis, aspergillosis and histoplasmosis in pregnant women

nyh often occur against the background of immunodeficiency. Attention is drawn to the fact of a sharp increase in the frequency of clinical manifestations of vaginal candidiasis during pregnancy, which reaches 31-33% by the third trimester. This phenomenon is associated with a violation of the absorption of glycogen by the cells of the vaginal epithelium, as well as with an increase in the formation of mucin, which predetermines, due to the “dilution” effect, a decrease in the concentration of active factors of local immunity in the vaginal medium - lysozyme, cationic proteins, sretory antibodies, etc. Excess nutrients in the form of glycogen, combined with a weakening of local immunity, create favorable conditions for the implementation of the pathogenic effect of the fungal flora. According to DNA diagnostics, during vaginal delivery, the contamination of newborns from mothers of patients with candidiasis approaches 100%, and by the end of the neonatal period, spontaneous elimination of fungi is observed only in 35%, which suggests the formation of candidiasis in the rest. The frequency of clinically pronounced candidiasis in newborns in the first 35 days approaches 20-30%, and, despite treatment, after 1 month it is noted in every fifth observation. fungal infection not only causes oral, genital and cutaneous manifestations of candidiasis in newborns, but can also lead to intrauterine infection fetus with the formation of systemic mycosis with deep damage to the lungs, brain, as well as to spontaneous abortion (more often in the II trimester, in terms of 14-25 weeks).

Finally, perinatal infections are caused protozoa, treponemas and rickettsiae. In this group, the most important toxoplasmosis, the frequency of intrauterine infection in which is about 40%. In addition, in recent years there has been a trend towards an increase in the frequency of syphilis. Congenital syphilis occurs in more than 50% of newborns from sick mothers who have not received appropriate treatment.

It is important to note that in most cases, intrauterine infection is due to the association of several pathogens or is mixed (viral-bacterial, bacterial-fungal). In the structure of antenatal mortality due to intrauterine infection, 27.2% is due to a viral infection, 26.3% - to a mixed one, and 17.5% - to a bacterial one.

In 1971, a group of infections was identified that, despite pronounced differences in the structure and biological properties of pathogens, have similar clinical manifestations and cause persistent structural defects in various organ systems in the fetus, the most important of which are lesions of the central nervous system. To designate this infectious group, A.J. Nahmias (1971) suggested an abbreviation TORCH. This complex combines the following intrauterine infections: T- toxoplasmosis, R- rubella (rubella), C- cytomegalovirus infection, H- herpesvirus infection.

In the last 15 years, there has been a change in the etiological structure of perinatal infections. This is partly due to the expansion of the possibilities of specific diagnostics, primarily mycoplasmosis, chlamydia, cytomegaly, herpetic and streptococcal B infection and others. There is also a true change of pathogens, in particular, Listeria (Ailama-

Zyan E.K., 1995).

Despite the wide range of pathogens, it should be noted that all intrauterine infections have common features:

Latent, or erased, course, which significantly complicates diagnosis (especially with intracellular localization of the pathogen - chlamydia, mycoplasmas, viruses, etc.) and does not allow timely start of etiotropic therapy;

Activation of a latent persistent infection is possible with any violation of homeostasis in a pregnant woman (anemia, hypovitaminosis, overwork, stressful situations, decompensation extragenital disease non-infectious nature).

ROUTES OF INTRAUTERINE INFECTION AND THE MECHANISM OF INFECTION OF THE FETUS

Intrauterine infection occurs in the following ways: "ascending- in the presence of a specific lesion of the lower

sections of the genital tract (Fig. 34); "hematogenous(transplacental) - in most cases due to the ability of some microorganisms to persist for a long time in peripheral blood lymphocytes;

transdecidual(transmural) - in the presence of infection in the endometrium;

Rice. 34. The pathogenesis of ascending intrauterine infection

descending- with the localization of the inflammatory focus in the area of ​​​​the uterine appendages;

*contagious- direct contamination of the newborn when passing through the birth canal;

mixed.

Bacterial intrauterine infection with opportunistic pathogens develops mainly due to ascending infection from the birth canal. This pathway is also characteristic of mycoplasmas, chlamydia, fungi of the genus Candida and only certain viruses, in particular herpes simplex. Predisposing factors are urogenital infections, isthmic-cervical insufficiency, partial rupture of membranes, untimely outpouring water, chorion biopsy, amniocentesis.

Ascending infection occurs most rapidly when the membranes are damaged. The amniotic fluid of a woman in late pregnancy has antimicrobial activity, which, however, is weakly expressed and can only delay (but

do not inhibit) the growth of microorganisms. The bacteriostatic effect is very short-lived (from 3 to 12 hours). Inflammatory changes in the area of ​​​​the membranes adjacent to the cervical canal are always detected earlier than in the villi of the placenta. Due to the low virulence of most opportunistic microorganisms, the fetal membranes remain externally intact. At the same time, the membranes are permeable to many opportunistic microorganisms, so infection of the fetus can occur even with a whole fetal bladder. The causative agent penetrates into the amniotic fluid, its intensive reproduction and accumulation occurs. A focus of infection is formed, and the fetus is in an infected environment. The so-called amniotic fluid infection syndrome.

Infection of the fetus occurs by ingestion and aspiration of infected waters, which leads to the appearance in the newborn signs of intrauterine infection(pneumonia, enterocolitis, vesiculosis, omphalitis, conjunctivitis, etc.). At the same time, microorganisms, spreading through the membranes or between them, reach the basal plate of the placenta. (deciduitis). The chorionic plate and elements of the umbilical cord become infected upon contact with infected amniotic fluid. Further spread of the inflammatory reaction leads to the development of chorionitis (placentitis), which is manifested by leukocyte infiltration of the intervillous space and endovasculitis in the chorionic plate. Vasculitis in the decidua, stem and terminal villi lead to vascular obliteration, the appearance of heart attacks, calcifications, massive fibrinoid deposits, which can manifest as "premature maturation of the placenta".

The manifestations of the syndrome of "amniotic fluid infection", in addition to chorionamnionitis, include polyhydramnios, which can be detected in 5.5-63.6% of patients already at the end of the first trimester of pregnancy. The reason for its development is a change in the ratio of the processes of production and resorption of amniotic fluid by cells of the amniotic epithelium against the background of amnionitis. oligohydramnios with intrauterine infection, it is usually secondary and is a manifestation of damage to the kidneys (decreased diuresis in placental insufficiency) or the urinary tract of the fetus (obstructive hydronephrosis).

Formation placental insufficiency. In the genesis of the symptom complex of placental insufficiency in IUI, the main role belongs to vascular disorders (vasculitis and thrombosis of the vessels of the fetal part of the placenta against the background of chorionitis (placentitis). Changes in the morphofunctional state of cell membranes due to the activation of lipid peroxidation against the background of placentitis are also important. The main manifestations of placental insufficiency are chronic fetal hypoxia and intrauterine growth retardation, which, depending on the timing of infection, is symmetrical (infection before the completion of placentation) or asymmetric.

A typical manifestation of intrauterine infection is miscarriage pregnancy. In 70% of observations, spontaneous termination of pregnancy in the later stages and preterm labor begin with premature rupture of fetuses

shells and only in 30% - with an increase in the contractile activity of the uterus. Premature development of labor activity and untimely rupture of the membranes are due to the action of bacterial phospholipases that trigger the prostaglandin cascade and the damaging effect of inflammatory toxins on the membranes.

Due to the fact that phospholipases of gram-negative bacteria contribute to the destruction of surfactant in the lungs of the fetus, the newborn develops respiratory disorders. Thus, the following sequence of development of ascending infection is built: colpitis, cervicitis - infection of the amniotic fluid - damage to the epithelium of the amniotic space - membranitis - amnionitis of the chorionic plate - perivasculitis of the umbilical cord - damage to the respiratory tract, lungs, digestive tract and skin - antenatal fetal death.

The microbiological examination of women in groups at increased risk of developing IUI of bacterial etiology revealed the identity of the species composition of the microflora of the genitourinary tract of women and microorganisms isolated from their children. In newborns with clinical manifestations of IUI, massive seeding is observed mainly in internal cavities (gastric contents, nasopharyngeal swabs). Cultures of smears from the maternal surface of the placenta and cord blood most often remain

are sterile, and amniotic fluid and the fetal surface of the placenta have the highest rate of microbial colonization. This proves the predominantly ascending route of infection of the fetus and the leading role of amniotic fluid in infection of the fetus.

For hematogenous infection of the fetus is most characteristic of the presence of a focus in the mother's body, located extragenitally. The causative agent, breaking the placental barrier, penetrates into the bloodstream of the fetus. With hematogenous infection, a generalized lesion of the fetal body often occurs - intrauterine sepsis. All true congenital viral infections, mycoplasmosis, chlamydia, as well as such specific intrauterine infections as listeriosis, syphilis and toxoplasmosis, have a transplacental route of infection.

The hematogenous pathway is characterized by the predominance of vasculitis of the placental uterine bed, then - the development of intervillusitis, vasculitis of the chorionic plate, then - phlebitis and endarteritis of the umbilical cord, infection of the liver, brain, damage to other organs of the fetus - antenatal death.

For implementation transdecidual (transmural) the path of infection requires the presence of a focus of infection under the endometrium. A similar route of infection of the fetus most often occurs in patients who have had purulent-inflammatory diseases of the genital organs.

FROM descending by intrauterine infection, in which the penetration of the pathogen to the fetal egg occurs through the fallopian tubes, in clinical practice one has to deal with patients with acute surgical pathology of organs abdominal cavity, acute or chronic salpingo-oophoritis of gonorrheal, mycoplasmal or chlamydial etiology. The classic example is acute appendicitis, with the fetal mechanism similar to that of ascending infection.

IMMUNE SYSTEM OF THE FETUS

A mature immune response involves a complex sequence of interactions between several cell types. The process of maturation of individual cells involved in the immune response begins at early stages fetal life. The progenitor cells of the human immune system are produced in the bone marrow and liver of the fetus. Histocompatibility markers and antigens characteristic of T- and B-lymphocytes can be detected on lymphocytes as early as 8-10 weeks of gestation. As the cells of the immune system mature on macrophages, as well as on T- and B-lymphocytes, an increasing number of receptors and histocompatibility markers appear, however, full maturation is completed only approximately 2 years after birth.

In typical cases, one can observe responses to infectious agents that pass through the placenta already in the second half of pregnancy. This kind of immune response usually manifests itself in the form of the formation of antibodies of the IgM class, however, antibodies of the IgG class can also be formed. Identification of the fetal immune response in the form of IgG antibodies is more difficult due to the presence of passive maternal IgG antibodies.

Maternal IgG antibodies begin to cross the placenta around mid-pregnancy. During childbirth, the concentration of IgG in the blood of the child (mainly maternal immunoglobulins) is equal to the corresponding concentration in the mother's blood or even exceeds it. This means that the child has all the IgG antibodies formed in the mother's body. Maternal IgA and IgM antibodies do not pass through the placenta, and if antibodies of these classes are found in a child, this means that they were formed in the child's body.

The formation of IgA antibodies is often not fully established by the time of delivery. It has been shown that the full development of this system can continue during the first seven years of life. Thus, the main source of immunity in the fetus is the transfer of maternal IgG antibodies through the placenta, although already at a fairly early stage of development, its immune system is able to develop its own protection.

Difficulties in studying and interpreting the results of the study of humoral and cellular immunity in the mother and intrauterine fetus led to the search for new solutions for assessing immunoreactivity

against the background of an infectious process during pregnancy. Thus, we evaluated a number of pro- and anti-inflammatory cytokines (interferons, interleukins, tumor necrosis factor) in various terms gestation in the fetus, mother and newborn. Since cytokines and interferons are universal regulators of all immune reactions, both cellular and humoral, their study allows us to solve the most important problem. clinical problem- Is there an infection in the fetus and is it necessary to prescribe treatment? It has been proven that a decrease in the level of interleukin-4 in combination with an increase in the concentration of interferon gamma and tumor necrosis factor in the mother's blood indicates the presence of intrauterine infection in 86.4%. Such studies allow non-invasive assessment of the risk of infection in a newborn.

Pathogenesis. In the pathogenesis of intrauterine infection of the fetus, a significant role is given to the direct interaction of the pathogen and the fetus. The range of damage detected during intrauterine infection is very wide and depends on the characteristics of morphogenesis and fetal responses in a given period. prenatal development, specific properties and duration of the damaging factor.

The relationship between the virulence of the pathogen and the severity of fetal damage is not always directly proportional. Often, an obliterated or mild infection in the mother caused by Toxoplasma, Listeria, Mycoplasma, Chlamydia, viruses, or fungi of the genus Candida can lead to fetal death or the birth of a seriously ill child. This fact due to the tropism of pathogens to certain embryonic tissues, as well as the fact that fetal cells with high metabolic activity represent a favorable environment for the reproduction of microbes.

The damaging effect of a bacterial infectious agent can be realized through the development of a destructive inflammatory process in various organs with the formation of a structural or functional defect and by direct teratogenic action with the formation of persistent structural changes in the form of malformations. Viral agents usually cause lethal disorders or developmental defects by suppressing mitotic cell division or by direct cytotoxic effects. Repair processes that develop after inflammation

I eat, often lead to sclerosis and calcification of tissues, which also disrupts the process of histogenesis.

The period of embryogenesis covers the first 3 months of pregnancy, and the most sensitive phase to the effects of damaging factors is the first 3-6 weeks of organogenesis ( critical period development). During implantation, sensitivity to the action of damaging factors increases significantly. Infectious embryopathies that occur at this time are characterized by the occurrence of deformities (teratogenic effect), embryotoxic effects are less often observed. First of all, tissues are affected that were in the process of active differentiation at the time of the agent's action. In different organs, the laying periods do not coincide in time, therefore, the multiplicity of lesions will depend on the duration of exposure to the damaging agent.

With the beginning of the early fetal period, the fetus develops a specific sensitivity to pathogens of intrauterine infections. Fetal lesions that occur after 13 weeks are called "fetopathies". With fetopathy of septic etiology, the formation of malformations is possible. The morphological basis for this is alterative and proliferative processes leading to obliteration or narrowing of natural channels and openings. Such changes lead to further development already established body. So, urinary tract infection can lead to hydronephrosis, transferred meningoencephalitis - to hydrocephalus against the background of narrowing or obliteration of the Sylvian aqueduct.

When infected after 27 weeks of gestation, the fetus acquires the ability to specifically respond to the introduction of the infectious agent with leukocyte infiltration, humoral and tissue changes. The damaging effect of an infectious agent is realized in this case in the form of functional defects.

It should also be noted that important links in the pathogenesis of IUI are intoxication with metabolic products of the infectious agent, hyperthermia and hypoxemia. The influence of the above factors on the intrauterine fetus is manifested by a delay in the growth and differentiation of the lungs, kidneys and brain, even in the absence of other manifestations of intrauterine infection.

Clinical signs intrauterine infectious disease in a newborn, or are already present at birth, or manifest

lyatsya during the first 3 days of life (most often on the 1st-2nd day). When infected in the postnatal period, the symptoms of the infectious process are detected at a later date. A longer incubation period is possible with intrauterine infection("late" meningitis, osteomyelitis, chlamydial lesions, etc.) or, on the contrary, early manifestations of a nosocomial infection (especially in premature babies).

The most common clinical manifestation of bacterial intrauterine infection in newborns in the first days of life is the so-called infection syndrome. Such a child has general clinical symptoms that reflect signs of intoxication and are expressed in general lethargy, decreased muscle tone and reflexes (in particular, the sucking reflex), regurgitation, and refusal of the breast. From the side of the cardiovascular system - deafness of heart sounds, changes in the ECG of a hypoxic nature. Pallor of the skin, violation of the rhythm and frequency of breathing, bouts of cyanosis are observed. Infection may result in the development of a septic process, in the implementation of which the state of the newborn in the first hours of life, and the dose of the pathogen, are important. Prematurity, impaired breathing and hemodynamics, intracranial injury, hypoxia contribute to a decrease in the resistance of the newborn's body and are the favorable background against which the infection becomes pronounced, acquiring the character of a septic process.

Specific manifestations of intrauterine infections in newborns are different - from mild local forms to severe septic ones.

Clinical manifestations of congenital bacterial or mycotic skin lesions in a newborn may be vesiculopustulosis. The percentage of positive results of the microbiological study of the contents of vesicles taken immediately after the birth of a child is low, so it is debatable whether to attribute "aseptic" vesicles to a congenital infection or to consider it as a manifestation of a bacterial allergy with the appearance of a skin rash. True (microbiologically confirmed) vesiculopustulosis manifests itself in prenatally infected children, usually by the end of the 1st and on the 2nd day of life, and the causative agents are most often streptococci

ki groups B and D, Escherichia, yeast-like fungi (Ankirskaya A.S. et al., 1989).

Conjunctivitis, rhinitis and otitis, appeared on the 1st-3rd day of life, can also be manifestations of intrauterine infection. In case of congenital conjunctivitis, in addition to microbiological examination of discharge from the eyes for opportunistic microorganisms, it is necessary to take smears for examination for gonococcus.

Intrauterine pneumonia- the most common form of congenital infections of the newborn. In children from the moment of birth, signs of respiratory failure are observed: shortness of breath, cyanosis, often dullness of percussion sound and small bubbling wet rales. X-ray examination, carried out in the first hours of life, confirms the presence of foci of pneumonia. Congenital aspiration pneumonia can also appear on the 2nd or 3rd day of life. In a microbiological study of aspirate from the tracheobronchial tract in newborns with aspiration pneumonia gram-negative bacteria are most often isolated, while in case of hospital-acquired neonatal pneumonia, Staphylococcus aureus is most often isolated. The course of congenital pneumonia is severe, because as a result of aspiration, large areas of the lung (lower and middle lobes) are turned off from breathing due to bronchial obstruction with aspiration masses - infected amniotic fluid containing an admixture of meconium, fetal skin scales.

Enterocolitis in newborns, it can also be in the nature of an intrauterine infection, when the pathogen penetrates along with the amniotic fluid into the gastrointestinal tract. The following clinical manifestations are characteristic of congenital enterocolitis: sluggish sucking, regurgitation, bloating, enlargement of the liver and spleen, expansion of the venous network of the anterior abdominal wall, frequent liquid stool. Dyspeptic symptoms usually develop on the 2-3rd day of life. Microbiological examination of the intestinal contents is important (signs of a violation of the formation of intestinal microcenosis - the quantitative predominance of Klebsiella, Proteus, Pseudomonas aeruginosa).

Damage to the central nervous system in IUI in newborns can be both primary (meningitis, encephalitis) and secondary, due to intoxication. Penetration excite-

la in the fetal brain most often occurs through the CSF pathways, so the infection develops in the membranes of the brain and spinal cord and proceeds in the form meningitis and meningoencephalitis. There are also changes in the choroid plexuses of the lateral ventricles of the brain, which may be accompanied by the development of congenital hydrocephalus.

Sepsis in a newborn it is difficult to diagnose due to the low reactivity of his body. At the onset of the disease, clinical manifestations may be mild, there may be only signs of general intoxication, without an obvious focus of infection (the "infection" syndrome). Attention should be paid to symptoms such as lethargy, poor suckling, regurgitation, delayed recovery or secondary weight loss, delayed healing umbilical wound, the development of omphalitis. Typical symptoms of infectious intoxication in a newborn are respiratory and tissue metabolism disorders. There is a pale cyanotic, with a grayish tint, the color of the skin with a pronounced vascular pattern (skin marbling). Intoxication is accompanied by a violation of the excretory function of the liver, the development of prolonged jaundice. The symptoms of sepsis also include enlargement of the spleen and peripheral lymph nodes. Informative signs are edema subcutaneous tissue, hypochromic anemia, dysfunction of the kidneys and liver, water-salt and protein metabolism (hypoproteinemia) (Ankirskaya A.S. and

et al., 1989).

You should also take into account nonspecific manifestations intrauterine infection. In newborns of this group, the adaptation reactions of such vital systems as the central nervous, respiratory, cardiovascular, endocrine and immune systems are disrupted. Often there is a low Apgar score in the first minute after birth. Often in the early neonatal period there are failures of adaptation in the form of hypoxic syndrome, a syndrome of respiratory and cardiovascular disorders, adrenal and cerebral pathology. It should be borne in mind the possibility of such manifestations as congenital malnutrition, edematous syndrome, hyperbilirubinemia, DIC blood syndrome.

PRENATAL DIAGNOSIS OF INTERNAL INFECTIONS

Given the nonspecificity of the clinical manifestations of this pathology, its prenatal diagnosis is the most difficult.

The most rational is the phased diagnosis of intrauterine infections.

On the first stage based on the collection of anamnestic data and a general clinical examination, a group is identified high risk on the development of intrauterine infections. This group includes patients:

Having extragenital foci of infection, especially with an exacerbation of the infectious process during pregnancy, as well as those who have experienced acute respiratory viral infections during pregnancy;

With early onset of sexual activity and frequent change sexual partners who have had episodes of urogenital infections;

Those who have had inflammatory diseases of the uterus and its appendages, colpitis, sexually transmitted diseases;

who had interruption pregnancy with a complicated course of the post-abortion period;

With spontaneous abortion at any time in history;

With a complicated course of the postpartum period after previous births;

With infectious and inflammatory diseases of the genital organs (colpitis, bacterial vaginosis) during pregnancy;

C isthmic-cervical insufficiency;

With clinical signs of polyhydramnios or fetoplacental insufficiency.

On the second stage using a comprehensive ultrasound examination, sonographic markers of intrauterine infections are detected, as well as signs of fetoplacental insufficiency and its severity is assessed.

Sonographic signs indicating IUI can be divided into the following groups.

1. Pathology of the amnion and chorion: - polyhydramnios or oligohydramnios (can be diagnosed starting from the end of the first trimester of pregnancy);

Hyperechoic suspension in the amniotic fluid;

Amniotic bands;

Pathology of the villous chorion - hypoplasia of the villi (can be diagnosed during pregnancy up to 8-9 weeks and is manifested by thinning of the chorion around the entire circumference up to 1-3 mm, a decrease in its echogenicity, discontinuity and smoothness of the outer contour);

Placentitis, the signs of which are edema/thickening (71.8%), heterogeneous echogenicity of the placenta parenchyma, thickening/doubling of the contour of the basal plate, blurring of the boundaries of the lobules, uneven expansion of the intervillous spaces and subchorionic space;

Premature maturation of the placenta.

2. Abdominal and subcutaneous edema:

Non-immune dropsy (subcutaneous edema and pleural and/or pericardial effusion or ascites);

Hydrothorax;

Bilateral pleural effusion.

3. Calcifications in the internal organs of the fetus:

Calcifications of the periventricular region;

intestinal calcifications;

Parenchymal hepatic/splenic calcifications.

4. Change in echogenicity internal organs fetus:

Hyperechoic bowel (a sign has diagnostic value after 16 weeks of pregnancy);

Intestinal pneumatosis (detected in 25% of cases with IUI);

Bubbles of gas in the gallbladder;

Hyperechoic large kidneys with normal bladder sizes;

Bilateral increase in lung echogenicity (in combination with a slight pleural effusion and polyhydramnios is a sign of intrauterine pneumonia).

5. Structural defects (malformations of the internal organs of the fetus).

6. Hepatomegaly and splenomegaly.

Detection of echographic markers of IUI cannot serve as a basis for a diagnosis. We noted that with a combination of three echographic signs and more, the likelihood of intrauterine infection for a newborn reaches 80%.

When evaluating fetometric parameters, the diagnosis of fetal growth retardation syndrome (FGR) is carried out and its form is determined. A Doppler study of blood flow in the vessels of the fetoplacental complex makes it possible to detect disorders that, in IUI, are primarily detected in the fetal-placental blood flow. Cardiotocographic examination allows diagnosing signs of developing fetal hypoxia.

Parallel to ultrasound diagnostics conduct a comprehensive examination using modern laboratory methods studies to identify pathogens infectious diseases in a woman's body.

1. Enzyme immunoassay based on the determination of IgM and IgG specific for a particular infection, or antigens of the corresponding pathogens.

2. Molecular hybridization method (identification of DNA or RNA fragments of pathogen cells).

3. ELISA method (determination of monoclonal antibodies in body fluids and media by a test system).

4. Bacterioscopic examination of native and Gram-stained smears from the urethra, cervical canal and vagina.

5. Bacteriological examination with inoculation of the contents of the cervical canal, urethra and vagina on liquid and solid media in order to quantify the representatives of aerobic and anaerobic infections and their sensitivity to antibacterial drugs.

6. Examination of scrapings from the cervical canal by polymerase chain reaction to identify pathogens of sexually transmitted diseases.

On the third stage after using indirect diagnostic methods and obtaining data indicating the presence of intrauterine infection, it is possible to use methods for direct diagnosis of IUI in the material obtained from chorionic villus biopsy, amniocentesis and cordocentesis.

For the diagnosis of intrauterine infections in I trimester pregnancy is most convenient aspiration transcervical chorionic villus biopsy. Produced in terms of 6 to 10 weeks of pregnancy under the control of ultrasound scanning. The resulting biopsy specimen is subjected to bacteriological and virological studies, and karyotyping is also carried out. At

detection of an intrauterine infection, the question of abortion should be raised, since infection in the early stages is characterized by the formation of fetal malformations.

From the 16th week of pregnancy and throughout II trimester used to diagnose intrauterine infection amniocentesis. The operation is performed under aseptic conditions by transvaginal (through the anterior or posterior fornix of the vagina or transcervically) or transabdominal access (used more often). Under the control of ultrasound scanning, a puncture of the amniotic cavity is performed in the pocket of amniotic fluid free from loops of the umbilical cord and small parts of the fetus. For the study, three samples of amniotic fluid are taken, with a total volume of 24 ml, which are subsequently subjected to microbiological, biochemical and genetic studies.

There are a number of tests designed to detect intrauterine infections in the amniotic fluid: gas-liquid chromatography amniotic fluid in order to determine organic acids (acetate, succinate, butyrate, oxaloacetate, etc.), which is specific for the presence of infectious agents in the amniotic fluid.

They also use bacterioscopy of native and Gram-stained smears of amniotic fluid, sowing them on liquid and solid media. Detection in the culture of etiologically significant microorganisms in an amount exceeding 5 × 10 2 CFU / ml is diagnostic criterion intrauterine infection.

In the diagnosis of viral intrauterine infections, the cultivation of viral agents on chicken embryos and the polymerase chain reaction are used.

An important role belongs to serological research methods, the most sensitive and specific of which is the determination of monoclonal antibodies by the ELISA test system.

The activity of alkaline phosphatase of cord blood leukocytes is determined, the number of platelets is counted (thrombocytopenia below 150-10 9 / l is considered a sign of infection), the ratio of young forms of leukocytes and neutrophils and the radioisotope determination of β-lactamase (typical for infection with β-lactamase-producing microorganisms). Blood is also subjected to bacteriological, virological and immunological studies.

Preclinical diagnosis of IUI is based mainly on targeted microbiological examination of newborns (immediately after birth) and histological examination of the placenta in pregnant women with an increased risk of infection in the fetus.

In contrast to microbiological and histological methods, immunological examination of newborns at the time of birth, in particular, the determination of the main classes of immunoglobulins in umbilical cord blood, is not sufficiently informative for the preclinical diagnosis of IUI. This is due to the fact that the same values ​​of immunoglobulins G, M, A are recorded in newborns with and without clinical manifestations of infection. An elevated level of IgM in the cord blood reflects the antigenic stimulation that took place in the antenatal period, but does not always indicate the presence of an infectious process.

FEATURES OF INDIVIDUAL NOSOLOGICAL FORMS OF INTRAuterine INFECTIONS

Cytomegalovirus

Cytomegalovirus (CMV) - a DNA-containing virus from the herpes family of viruses, is ubiquitous and can be transmitted with various body secretions (blood, urine), but most often through sexual contact. In adults, the infection, as a rule, proceeds without obvious clinical manifestations, but its mononucleosis-like course is also possible.

CMV infection occurs through close contact with an infected person or by ascending infection from mother to child. The virus is occasionally shed in saliva, urine, and genital secretions and is transmitted through kissing, sexual intercourse, or other contact.

Cytomegalovirus, having once entered the human body, after the primary infection is not eliminated into the external environment, but persists in it for life. The long-term latent course of infection is facilitated by the intracellular existence of the virus, where it is reliably protected from the action of specific antibodies. Serological studies conducted in Russia have shown that 90% of pregnant women have antibodies to CMV, which indicates an extremely high

com level of virus carrying. During pregnancy, real conditions are created for the reactivation of the infection, which is associated with the gestational features of the functioning of the immune system (the state of physiological immunosuppression).

The probability of intrauterine infection of the fetus with a latent course of infection is practically absent, with its reactivation it is 0.5-7%, and with primary infection it exceeds 40%. The overall incidence of prenatal CMV infection is 5-20 per 1000 live births. Prenatal infection with cytomegalovirus is 5% in seropositive women, up to 20% of infections occur during childbirth, and another 10% of children acquire infection in the early postnatal period - most often from the mother, through contaminated mother's milk.

The most common route of infection is transplacental, less often the fetus swallows infected amniotic fluid in the presence of placentitis and chorioamnionitis.

The virus can infect any organ of the fetus, including the central nervous system. Infection of epithelial cells is characterized by the development of large intranuclear inclusions (cytomegalic inclusions). In the affected tissues, cytolysis is observed with areas of focal necrosis and a predominantly mononuclear inflammatory reaction. Healing leads to fibrosis and calcification, especially in the subependymal membrane of the cerebral ventricles and in the liver. Severe cerebral complications, including microcephaly and calcification, are usually the result of intrauterine infection in the first 3–4 months of pregnancy, when the ventricular system is under development.

In connection with the defeat in the early stages of gestation, embryopathies are formed, severe trophic disorders develop gestational sac, the death of the embryo or fetus occurs, the pregnancy ends in a miscarriage. Stillborn fetuses are characterized by severe cerebral disorders, including microcephaly, hydrocephalus and calcification, porencephaly, pancreatic cystofibrosis, cirrhosis of the liver, atresia of the bile ducts, cortical dysplasia of the kidneys can also be noted.

In later periods, fetopathies with fetoplacental insufficiency, intrauterine growth retardation are formed, and dysembryogenesis stigmas occur. In newborns, there is damage to the epithelium of the salivary glands, convoluted tubules of the kidneys, bronchi, bile

ducts. According to a comprehensive (sonographic, Doppler and cardiotocographic) study (hormones - placental lactogen, progesterone, estriol, cortisol; AFP content) - signs of intrauterine fetal suffering are found in 33.9%.

Clinical manifestations. 90-95% of babies infected with CMV in utero have no symptoms at birth. Most of them develop normally, but close follow-up over a long period of time indicates that 10-30% of children subsequently develop symptoms of minor neurological damage - nervous deafness, delayed development, or mild mental retardation. In addition, a specific violation of the function of cellular immunity is possible - inhibition of the activity of T-helpers, an increase in the content of IgM and IgG.

In a small proportion of children with clinical signs of infection, the latter range from intrauterine growth retardation (found most often as an enlarged liver and spleen) or involvement of a single organ to a severe, generalized, life-threatening disease, which is rare.

Many of the extragenital manifestations of congenital cytomegalovirus infection (hepatitis, thrombocytopenia, hemolytic anemia and pneumonia) disappear within certain period without treatment. Neurological damage is irreversible, although the degree of disability varies. Most children with congenital cytomegalovirus infection children who are born with symptoms of nervous system damage suffer from serious irreversible neurological disorders, including cerebral palsy, epilepsy, and nervous deafness. Chorioretinopathy is quite common. It rarely causes any defect in vision and is a convenient diagnostic feature for suspected congenital infections, although it is indistinguishable from chorioretinopathy due to toxoplasmosis. Mortality in congenital cytomegaly is 20-30%.

Prevention and treatment. To date, effective safe vaccines or preparations of ready-made specific monoclonal antibodies have not been developed. Preventive measures are reduced to the isolation of infected newborns and the exclusion of contact of these newborns with seronegative pregnant women. The personnel caring for them work in gloves and a second

bathrobe. As a passive prophylaxis, you can use the introduction of preparations of ready-made antibodies with high content anticytomegalovirus IgG.

Despite recent advances in the treatment of infections caused by α-herpesviruses (herpes simplex virus and varicella-zoster virus), treatment for β-herpesvirus diseases has not been definitively developed. Valaciclovir and ganciclovir are used, but there is no sufficient experience of their use in pregnant women. The complex of treatment includes the use of plant adaptogens (eleutherococcus, ginseng, royal jelly), vitamins of group B (B 1, B 6, B 12) up to 14 weeks of gestation.

Starting from 15-16 weeks as a method of palliative treatment, a course of immunoglobulin therapy with normal human immunoglobulin or preparations of ready-made antibodies with a high content of anti-cytomegalovirus IgG - anti-cytomegalovirus immunoglobulins is carried out. With the introduction of immunoglobulin preparations, the mother's body receives ready-made antibodies (AT) against CMV. Abs of the IgG class actively pass through the placenta and create passive immunity in the fetus. In the body of a pregnant AT, they block extracellularly located viruses, create immune complexes with them, promote elimination from the body, and limit their spread in the lymphatic and blood circulation. Immunoglobulin therapy is carried out taking into account the risk of allergic, pyrogenic reactions, the production of anti-y-globulins, exacerbation of infection, i.e. in situations where the risk of adverse effects of infection is higher.

The obtained data on the reduced ability of leukocytes to produce α- and y-interferon in women with viral infections indicate the advisability of including immunomodulating and interferon-correcting components in the complex therapy of pregnant women with cytomegalovirus infection. A genetically engineered recombinant drug viferon is used, which is a2-interferon associated with antioxidants. It has interferon-stabilizing, immunomodulatory and antioxidant properties.

New in the treatment of herpes infections is the use of plasmapheresis and endovascular laser blood irradiation (ELOK). The therapeutic efficacy of plasmapheresis and ELOK is due to the detoxification effect, stimulating effect on

cellular and humoral immunity and nonspecific resistance reactions, normalization of coagulation and aggregation properties of blood.

herpetic infection

The most important role is played by viruses of the family herpesviridae. The herpes simplex virus (HSV) is DNA-containing and belongs to the same group as CMV, Epstein-Barr virus and varicella-zoster virus. Two of its serotypes HSV-1 (orolabial) and HSV-2 (genital) have been identified, but there is no complete correspondence between the serotype and the localization of the infection. In 20% of neonatal infections, it is associated with genital HSV-1 infection.

The herpes simplex virus is transmitted different ways, the most important is the sexual route. The defeat of the genital herpes virus is detected in 7% of pregnant women. Herpes in newborns is recorded with a frequency of 1:2000-1:5000, but, despite the relative rarity of neonatal herpes, the severity of its manifestations and the unfavorable prognosis for the newborn make it very important to develop rational approaches to the diagnosis, treatment and, in particular, prevention of this extremely serious disease. .

The frequency of detection of HSV-2 varies significantly depending on a number of factors (age, nature of sexual activity, socio-cultural level of the population, etc.). Thus, in adolescents under 15 years of age, seropositive results are less than 1%, while among patients of clinics specializing in sexually transmitted diseases, they range from 46-57%. In pregnant women, specific antibodies to HSV-2, for example in the USA, are detected on average in 20-30% of women.

Clinical manifestations of primary infection in the mother last 18-22 days, with an increase in symptoms during the 1st week. Asymptomatic desquamation of the epithelium damaged by the virus is observed over the next 2 weeks. The total duration of manifestations is almost 6 weeks. Non-primary genital infection is less pronounced: the duration of clinical manifestations is shorter (about 15 days), asymptomatic shedding of the virus is less common, and its duration decreases to 8 days. The severity and duration of clinical manifestations in relapses is even less pronounced, and the duration of desquamation of the damaged epithelium is only 4 days.

Primary genital herpes in the mother and exacerbation of the chronic process are the most dangerous for the fetus. If 0.5-1.0% of newborns are infected intranatally, then with an acute course or exacerbation, which is manifested by vesicular lesions of the skin and mucous membranes of the genitals, the risk of infection of the fetus during childbirth reaches 40%.

With intrauterine HSV-2 infection, in most cases, infection of the fetus occurs immediately before childbirth, ascending after rupture of the membranes (critical period 4-6 hours) or during childbirth when passing through an infected birth canal (85%). Transmission of infection occurs both in the presence of lesions in the cervix and vulva, and asymptomatic isolation of the virus. With the ascending path of infection, the pathogen multiplies and accumulates in the amniotic fluid, polyhydramnios is noted. Once infection has occurred, the virus can be spread by contact or hematogenous routes. In 5%, transplacental spread occurs during pregnancy.

The defeat of the placenta and fetus with herpes infection can occur at any stage of pregnancy and lead to the formation of congenital malformations in the fetus, antenatal death, miscarriage or premature birth. Infection in the first trimester leads to the formation of hydrocephalus, heart defects, anomalies of the gastrointestinal tract, spontaneous abortion often occurs, and intrauterine growth retardation develops. In the II and III trimesters, the infectious process leads to the development of hepatospelenomegaly, anemia, jaundice, pneumonia, meningoencephalitis, sepsis, malnutrition. Intrauterine infection in late pregnancy manifests itself early development clinical picture of neonatal infection (first day) in children born even as a result of caesarean section. Common manifestations of herpetic infection: damage to the skin, oral mucosa, chorioretinitis.

Neonatal herpesvirus infection manifests itself in three clinical forms.

Local form with lesions of the skin and mucous membranes- 45%. Skin and mucosal lesions are the most common but also the mildest form of neonatal herpes. Eyes: keratoconjunctivitis and chorioretinitis. Skin and oral mucosa: vesicles,

erythema, petechiae. If untreated, the disease may progress with the development severe complications. Mortality is about 18%.

Local form with CNS damage(encephalitis) - 35%. Characteristic: fever, lethargy, decreased appetite, depression or agitation syndrome, tremor, convulsions. Marked changes in the cerebrospinal fluid are found. Mortality in the absence of therapy is more than 50%.

Disseminated form- twenty%. With a disseminated form of neonatal herpes, several organs are usually involved in the process at once: the liver, lungs, skin, adrenal glands. Signs appear on the 1st-2nd week of life, include symptoms of a localized form in combination with anorexia, vomiting, lethargy, fever, jaundice, respiratory disorders, bleeding, shock (Fig. 35). The onset of bleeding and vascular collapse can be sudden and quickly leads to lethal outcome. Mortality in this form is extremely high - 90%. Modern antiherpetic chemotherapy can significantly improve the prognosis, but despite the ongoing treatment, the risk of long-term neurological disorders remains quite high.

Surviving children in the future have severe complications (neurological disorders, visual impairment, psychomotor retardation).

Rice. 35. Tissue tropism of herpes viruses

Prevention, treatment and management of pregnancy. The nature of preventive and medical measures, as well as obstetric tactics, depend on the type, form (typical, atypical, asymptomatic and duration of the course) and the presence of lesions of the genitals, the condition of the membranes.

With primary infection in the early stages of pregnancy, it is necessary to raise the question of its interruption. If the disease occurs late or the woman was infected before pregnancy, preventive measures include dynamic echographic monitoring of the development and condition of the fetus, prescribing courses of therapy, including the metabolic complex, cell membrane stabilizers, unitiol. The issue of termination of pregnancy is decided individually.

The advantage of complex treatment of herpetic lesions has been proven. The main chemotherapy is acyclovir or valaciclovir. Chemotherapy is possible starting from the first trimester of pregnancy. Despite the lack of evidence of teratogenic and embryotoxic effects, the appointment of acyclovir to pregnant women is limited due to the following indications: primary genital herpes, recurrent genital herpes (typical form), genital herpes in combination with a threatened miscarriage or symptoms of IUI. In pregnant women who have frequent recurrences of infection, permanent treatment with acyclovir (suppressive therapy) is carried out. In case of a complicated course of a herpes infection (pneumonia, encephalitis, hepatitis, coagulopathy), treatment is carried out together with an infectious disease specialist.

At the same time, it is advisable to prescribe immunoglobulin therapy, interferon preparations, "large" antioxidants (vitamins E and C). It should be noted the need to treat diseases associated with herpes (most often chlamydia, mycoplasmosis, trichomoniasis, candidiasis, bacterial vaginosis). As well as for the treatment of cytomegaly, plasmapheresis and endovascular laser blood irradiation have found their place in the treatment of herpes infection. After complex therapy, the frequency of complications for the mother and fetus is reduced by 2-3 times.

Obstetric management of women with genital herpes depends on its form and duration of pregnancy. In case of primary infection during pregnancy (1 month before delivery or less) or recurrence (a few days before delivery), chemotherapy is carried out,

delivery is carried out by caesarean section. In the presence of a history of genital herpes in one of the parents, a culture study or PCR is indicated before delivery. If the answer is negative - delivery through the birth canal.

Despite properly organized obstetric care, there are currently no conditions for the complete elimination of the transmission of HSV infection from mother to newborn. This is due to the impossibility of identifying all women with asymptomatic genital herpes infection. In this regard, in 70% of the transmission of herpes infection to newborns occurs precisely from mothers with asymptomatic herpes.

Rubella

The role of the rubella virus as a cause of congenital malformations was first recognized in 1941 by the Australian ophthalmologist Norman Gregg. He first described a syndrome of cataracts, deafness and congenital heart disease in children whose mothers had rubella during pregnancy during the Sydney epidemic of 1940. The virus was first isolated in tissue culture in 1962. By 1969, an effective live attenuated vaccine appeared

The rubella virus is an RNA-containing virus and belongs to the group of togaviruses (microviruses). Man is the only carrier. The rubella virus is unstable in the external environment, spreads by airborne droplets; long-term contact is required for infection, single contact is usually not enough, but since the disease is often asymptomatic, contact may not be known.

The vast majority of people who have had rubella develop stable immunity, however, 0.3-4.25% of people get rubella again, since it is possible to reactivate previously transferred rubella or re-infection as a result of the inferiority of the existing humoral immunity. At the same time, according to St. Petersburg researchers, in practice, such observations do not actually occur, and if acute rubella is excluded clinically and serologically, then the risk of intrauterine infection is excluded. If there is a high or increasing titer of antibodies to the rubella antigen, it is necessary to determine specific IgM antibodies in the mother, and if they are detected, in the fetal blood obtained by cordocentesis.

Infection of the fetus occurs only from a sick mother. Women who have been ill with rubella can be recommended pregnancy not earlier than 6 months after recovery. The defeat occurs as a result of viremia and transplacental penetration of the virus.

Clinical symptoms alone are not enough to make a diagnosis. For the same reason, a history of rubella is not indicative of immunity. Virus isolation or appropriate serological testing is required to prove rubella infection.

Criteria for the diagnosis of recent rubella are:

Isolation of the rubella virus (usually from the throat);

An increase in antibody titer by 4 times or more;

The presence of rubella-specific IgM, which is determined only within 4-6 weeks after the primary infection.

If the diagnosis remains in doubt, especially if contact occurred in the earliest stages of pregnancy, amniocentesis can be performed at 14-20 weeks and an attempt to isolate the rubella virus from the amniotic fluid, which, if successful, will indicate at least infection of the placenta. Negative results cultivation does not exclude infection of the placenta or fetus. The most accurate is the cordocentesis.

Rubella in a pregnant woman can have the following outcomes:

No effect on the fetus;

Infection of the placenta only;

Infection of the placenta and fetus (from asymptomatic to the defeat of many systems);

Fetal death (spontaneous premature termination of pregnancy or stillbirth).

Fetal infection may follow maternal infection at any stage of gestation, with rubella outcome highly dependent on gestational age.

The probability of infection of the fetus before 8 weeks of gestation is 54%, at 9-12 weeks - 34%, 13-24 weeks - 10-20% and no more than 12% - from the end of the II trimester. Viremia in a woman in the first 8 weeks of pregnancy leads to infection of the placenta and spontaneous miscarriage or stillbirth; when infected in the middle of pregnancy, rubeolar fetopathy is more often diagnosed in premature newborns; with rubella infection in the third trimester

proceeds without congenital malformations as chronic encephalitis and productive leptomeningitis in newborns.

Clinic of congenital rubella. The rubella virus exhibits an exceptional tropism for young embryonic tissue, which is associated with embryopathy in this disease. The fetus is affected by the rubella virus in many ways. Allocate "classic congenital rubella syndrome" which includes a triad of the most typical developmental anomalies: cataract with clouding of the cornea, heart defects(congenital defects of the ventricular septum - rubeolar embryopathy) and deafness(hemorrhages in soft tissues outer, middle and inner ear). Congenital rubella syndrome is often combined with productive interstitial pneumonia with giant cell metamorphosis of alveolocytes.

In addition to the classic, there is "Advanced Congenital Rubella Syndrome" which, in addition to the three named malformations, includes many other developmental anomalies: microcephaly, enlarged fontanelle, brain damage, glaucoma, cleft palate, interstitial pneumonia, hepatitis, damage to the vestibular apparatus, skeletal malformations, damage to tubular bones, hepatosplenomegaly, genitourinary malformations organs.

Up to 70% of surviving children with serologic evidence of infection at birth are healthy, but during the first 5 years of life, more than 2/3 of children develop any signs of infection. Most often, these are less obvious complications, which consist of mild to moderate deafness and brain damage with delayed psychomotor development. Late manifestations of rubella also include immunological dyscrasia (delay in the newborn's ability to synthesize its own immunoglobulins in response to a viral infection), hearing loss, psychomotor retardation, autism, cerebral syndromes (sclerosing panencephalitis), diabetes mellitus.

Among the neonatal manifestations of rubella, thrombocytopenic purpura is the most characteristic, which persists from 2 weeks to 3 months. Typical hepatitis with jaundice, hemolytic anemia with reticulocytosis and deformed erythrocytes, non-closure of the anterior fontanelle with cerebrospinal fluid pleocytosis, interstitial pneumonia, lesions of tubular bones (detected radiographically and consists in alternating areas of compaction and rarefaction of the bone). Of the heart defects, the most common

is the non-closure of the arterial (Botallov) duct, often in combination with stenosis of the pulmonary artery. There are also stenosis and coarctation of the aorta, VSD and ASD, transposition of large vessels; defects of the "blue" type are rare.

The most typical eye disease - cataract - is the result of the direct action of the rubella virus, which can persist in the lens for several years. Cataracts may be absent at birth and appear in the neonatal period. Glaucoma is 10 times less common. In addition, with rubella, pigmentary retinopathy, corneal clouding, myopia, and underdevelopment of the eyelids can be detected.

The most common defect in congenital rubella is deafness, often combined with vestibulopathy - a defect in the organ of Corti.

The shorter the gestational age at which women get rubella, the more often the teratogenic effect of the virus is manifested. The teratogenic danger of rubella in the 1st month of pregnancy is 35-50% (according to some reports, approaches 100%), in the 2nd month -

25%, in the 3rd - 7-10%.

The adverse effect of rubella on the fetus is manifested not only by its teratogenic effect. Rubella infection in early pregnancy in 10-40% can lead to spontaneous abortion, 20% to stillbirth, 10-25% of children born alive die in the neonatal period.

Rubella disease in the first trimester of pregnancy, confirmed by clinical, epidemiological and laboratory data, is an indication for its termination. Upon contact of a pregnant woman with a patient with rubella, no later than 10-12 days, it is necessary to conduct a serological examination. If a seronegative reaction continues, close observation and re-serological examination after 2 weeks to detect asymptomatic infection.

Prevention is primarily through immunization. Vaccination of children is required. Pregnant women are not vaccinated, as a weakened live vaccine is used and a teratogenic effect is not excluded. Screening of women of childbearing age for the presence of antibodies to rubella virus antigens is recommended.

Toxoplasmosis

Toxoplasma gondii belongs to the protozoan that infects cells of almost any type in mammals. This infectious agent is widespread throughout the world, affecting humans and animals, but the final cycle of reproduction occurs only in the intestines of felines. Oocysts enter the body of a person who eats vegetables or other foods contaminated with oocysts from the soil. Following the absorption of oocysts in the intestine, trophozoites are released. They penetrate the epithelium, where they multiply and then through the lymphatic and circulatory system- distributed throughout the body. In the body of a healthy immunocompetent host, the reproduction of trophozoites is limited by the development of a cellular immune response and, to a lesser extent, by the production of specific antibodies. Some of these organisms prevent the formation of tissue pseudocysts, which are interstitial accumulations of organisms surrounded by a protective shell. In this form, they remain latent but viable throughout the life of the host, usually without causing any significant immune response. If normal immunity is reduced for some reason, the infection may reactivate.

Another important route of infection is eating raw or undercooked meat from an infected animal. In this way, a person most often gets an infection when eating lamb or pork. From one person to another, the infection is not transmitted, with the exception of transmission through the placenta from mother to fetus during the development of an acute infection during pregnancy. There is no convincing data on the association of chronic or latent infection with recurrent miscarriages.

Frequency of human infection T. gondii in any population depends on the climate, the method of food preparation and, in addition, contact with cats. The prevalence of detectable antibodies is steadily

The frequency of congenital toxoplasmosis is difficult to determine, since most infected children are practically healthy at birth, and infection in the mother is usually asymptomatic. There is evidence that the majority of infected children subsequently suffer from serious complications of this infection, which may require specialized long-term treatment. The theoretical estimated risk of congenital infection, based on annual seroconversion rates in women of childbearing age, ranges from 4 to 50 per 10,000 live births.

Clinical manifestations of infection. Clinical manifestations of infection in toxoplasmosis are as follows.

"Acquired toxoplasmosis. In most cases, human infection T. gondii is asymptomatic or unrecognized. The most common manifestation of infection is generalized lymphadenopathy, which, although not always, is associated with malaise, fever, sore throat, headache, and rash. Sometimes at the same time find atypical lymphocytosis without heterophile antibodies. The infection usually tends to be limited. In rare more serious cases, the brain, myocardium, liver, or lungs are involved in the infectious process, which requires specific treatment. Chorioretinitis is relatively rare and is usually unilateral. * Congenital toxoplasmosis. When a woman is infected with toxoplasmosis at the very beginning of pregnancy, the risk of transmission to her fetus is relatively small (about 20%), but infection during this period can have serious consequences, up to the death of the fetus. At birth, anomalies are detected in only 10-20% of children with congenital toxoplasmosis, most children with severe disorders become infected in early pregnancy. Severe intrauterine toxoplasmosis can lead to death or

serious anomalies in the development of the fetus, including hydrocephalus, the formation of cysts with calcifications or extreme thinning of the cerebral cortex with calcification, glial proliferates, productive endarteritis, the development of generalized edema with hydrothorax and ascites, widespread inflammation and destruction of tissues of various organs. In the afterbirth, chronic villusitis is detected, in the stroma of the villi - lymphoid infiltration with an admixture of plasmocytes. A specific sign is the detection of the pathogen in the form of cysts or free-lying forms when stained according to Romanovsky-Giemsa smears-prints from the maternal surface of the placenta or from the depth of the cut placental tissue; the final diagnosis is based on the detection of protozoa in interstitial pseudocysts in the fetus.

Severe congenital toxoplasmosis in newborns, it is often a generalized disease manifesting as anemia, enlargement of the liver and spleen, jaundice, fever, and lymphadenopathy. On careful examination of the fundus, most infected children show signs of bilateral chorioretinitis. CNS involvement may manifest as intracranial calcification, seizures, hydrocephalus, microcephaly, or changes in the cerebrospinal fluid (especially elevated protein levels). Approximately 80% of children with clinical signs of toxoplasmosis at birth have irreversible brain damage and 50% have visual impairment. When the mother becomes ill with toxoplasmosis later in pregnancy, the fetus is more likely to become infected, but at birth, clinical signs of infection are generally not manifested, and if they are, they are usually localized in the eyeball or central nervous system and often go unnoticed in the newborn.

Eye symptoms gradually appear in more than 80% of infected children, although they are sometimes recognized only in older children or adolescents. Approximately 4 children in this group suffer from significant visual loss and the same number from recurrent active chorioretinitis with at least temporary visual impairment.

Serious neurological disorders are less common (<10%), в отдаленном периоде прицельное изучение умственных способ-

The results show deterioration in outcomes in more children. Often there is partial hearing loss.

Prevention and management of pregnant women with toxoplasmosis. The risk of infection with toxoplasmosis can be reduced in the following ways.

1. Avoid eating undercooked or raw meat, especially pork or lamb, and wash your hands thoroughly after handling raw meat.

2. It is not necessary to avoid contact with a domestic cat during pregnancy, although it is better not to start a new animal at this time. Cat sand should be changed more frequently and preferably by someone else. It should be fed only boiled or canned meat.

3. It is necessary to wash fresh vegetables well before eating so that contaminated soil does not get into the food.

4. Wash your hands thoroughly after gardening, especially before eating.

Between acute toxoplasmosis in a pregnant woman and the onset of an infectious process in the fetus, a significant time passes. If the infection develops in the first half of pregnancy, the question of induced abortion can be raised, since the risk of its transmission to the fetus in the early stages approaches 20%, and the consequences are devastating. In the late stages of pregnancy, the pregnant woman is treated with pyrimethamine, sulfonamides, tindurin. The macrolide antibiotic spiromycin has been successfully used.

Chlamydia

Chlamydia are most often transmitted sexually and affect mainly the cells of the cylindrical epithelium. It has also been proven

the possibility of spreading chlamydia in the “domestic” way, mainly among young children.

Clinical manifestations of chlamydia. The introduction of chlamydia into the genitourinary tract is not always accompanied by noticeable clinical manifestations. The disease is often submanifest or asymptomatic. Half of the infected women have no clinical manifestations. Chlamydial urethritis has no specific manifestations, and patients rarely complain of dysuria. Sometimes chlamydia can cause exudative inflammation of the ducts and Bartholin glands. Cervicitis is observed as the primary and most frequent manifestation of chlamydial activity. Discharge from the cervical canal macerates the stratified squamous epithelium of the vaginal part of the cervix, causing its partial desquamation. The cervix becomes edematous, hyperemic, the so-called hypertrophic ectopia of the cervix is ​​​​formed. Chlamydial salpingitis is the most common manifestation of ascending chlamydial infection. A feature of chlamydial salpingitis and salpingo-oophoritis is their long, subacute, erased course without a tendency to "weight". Chronic infection can cause tubal obstruction, ectopic pregnancy, and infertility. Women with ascending chlamydial infection with pelvic inflammatory disease may develop perihepatitis, the Fitz-Hugh-Ciirtis syndrome. This syndrome is characterized by fever, pain in the liver and pelvic organs.

In addition to urogenital chlamydia, extragenital chlamydial infection (ophthalmochlamydia) is also possible, while 72% of patients with ophthalmochlamydia simultaneously have chlamydial infection of the urogenital tract.

Urogenital chlamydia is diagnosed in pregnant women in 3-12%, reaching 33-74% in chronic inflammatory diseases of the genital organs, chronic nonspecific lung diseases, aggravated obstetric history (stillbirth, intrauterine pneumonia in a newborn, premature birth, habitual miscarriage).

Pregnancy with chlamydia, as a rule, proceeds with complications. In the first trimester, the threat of termination of pregnancy, non-developing pregnancy, miscarriages are typical. The frequency of miscarriages is 25%, perinatal losses in preterm birth - up to 5.5%.

Chlamydia leads not only to habitual miscarriage, but also to intrauterine infection of the fetus and newborn. Chlamydia colonizes mainly the conjunctiva, nasopharynx, respiratory tract, intestines, but the most characteristic is the lesion of the meninges and brain substance, where cotton-like deposits are already macroscopically determined, mainly on the upper lateral surfaces of the hemispheres. Histologically, they look like granulomas. The result of chlamydial infection is an increase in antenatal mortality, the occurrence of trachoma-like conjunctivitis and pneumonia in newborns. When the amniotic membrane becomes infected, polyhydramnios develops, a specific lesion of the placenta leads to the development of fetoplacental insufficiency (27%), sdfd, and fetal hypoxia. Perinatal mortality in chlamydia reaches 15.5%, and the proportion of newborns who died in the postnatal period is more than half of all perinatal losses.

Clinical manifestations. In 17-30% of pregnant women, chlamydia occurs latently or with minor symptoms. In the presence of a mixed infection, it can be with a complete symptom complex, including cervicitis with cervical ectopia.

Chlamydia in pregnant women is usually combined with a bacterial and viral infection, so infection of the fetus often occurs due to the combined effect of these pathogens. This causes the polymorphism of the clinical manifestations of the infection in the newborn, therefore, along with the typical manifestations of chlamydial infection (conjunctivitis, vulvovaginitis, pneumonia), there are forms that are uncharacteristic of chlamydia (vesiculopustulosis, omphalitis, rhinitis, sepsis).

Clinical manifestations of intrauterine infectious diseases in newborns born to mothers with chlamydia are divided into three groups: minor forms, severe forms, and the so-called infection syndrome.

Small forms include:

conjunctivitis;

Vulvovaginitis;

Vesiculopustuloses, rhinitis, otitis media, omphalitis - with a mixed infection.

Severe forms of intrauterine infection in a newborn with chlamydial infection:

Chlamydial pneumonia;

A generalized inflammatory process with the development of sepsis and the presence of several foci of infection (pneumonia, phlebitis of the umbilical vein, meningitis, hepatitis) - with a mixed infection.

With infection syndrome, local and generalized manifestations of intrauterine infection are absent. There are violations of adaptation processes in newborns, skin discoloration, decreased muscle tone, instability of reflexes, prolonged jaundice, initial weight loss of 10% or more, its slow recovery with repeated falling.

Prevention and treatment of chlamydia during pregnancy. Treatment of chlamydia during pregnancy has certain difficulties, which is associated with the peculiarities of the course of the disease, concomitant dysfunction of the placental system, the possibility of adverse effects on the fetus of traditional treatment regimens.

Antibacterial therapy is carried out with drugs from the group of macrolides: josamycin, azithromycin. In case of individual intolerance to the above drugs, the use of III generation cephalosporins is acceptable.

local therapy. In 95% of patients with chlamydial infection, there are dysbiotic disorders of microbiocenosis of varying severity, accompanied by an increase in the pH of the vaginal contents to 5.9. In addition, patients with urogenital chlamydia often have significant contamination with yeast fungi of the genus Candida. These results indicate the need for combined use of antibiotics, eubiotics and antimycotic drugs. Local therapy includes sanitation of the vagina, followed by the appointment of eubiotics orally and locally.

Immunomodulators and interferon correctors. A characteristic feature of chlamydial infection is a change in the functional activity of the immune system, there are deviations in the level of circulating immune complexes, inhibition of cellular immunity, a decrease in the phagocytic activity of blood polynuclear cells and macrophages, and inhibition of the activity of nonspecific body defense factors. In order to prevent immune disorders associated with chlamydia, lactoflora preparations are prescribed (bifidobacteria bifidum, dried lactobacilli,

floradophilus), which not only correct the microbiocenosis of the gastrointestinal tract, but by stimulating the thymus-dependent zones of the mesenteric lymph nodes activate the immune response. Plant adaptogens have immunomodulatory properties, which increase the overall nonspecific resistance of the body to infection. The drug of recombinant interferon is used with high efficiency.

Prevention of dysfunctions of the fetoplacental complex. Vasoactive drugs and antiplatelet agents are used to improve uteroplacental blood flow. As a metabolic therapy, a diet with a high content of protein, fermented milk products is prescribed with the simultaneous use of enzyme preparations. Tocopherol acetate (vitamin E), hepatoprotective agents are used as drugs that activate metabolism.

Syphilis

Congenital syphilis develops as a result of transplacental spread Treponema pallidum from mother to fetus. With fresh forms of infection in the mother, the risk of infection of the fetus is relatively high compared with the risk of infection in the late stage of the disease. Almost all children whose mothers suffer early stages of untreated syphilis during pregnancy are infected, and the mortality rate is very high. Previously it was thought that T. pallidum begins to cross the placenta after 18-20 weeks of pregnancy, when the layer of Langerhans cells disappears. It has now been proven that transplacental infection of the fetus can occur earlier, but due to the immunological immaturity of the fetus, there is no typical reaction to infection. The use of appropriate staining methods detects spirochetes in embryos during abortion in the first trimester.

Infection in the early fetal period ends with stillbirth with maceration and dropsy of the fetus. Usually miscarriage has a characteristic appearance: collapsed skull, protruding abdomen, hepatosplenomegaly, vesicular skin lesions, sdfd. Histologically characteristic areactive necrosis in organs with accumulation of spirochetes in the form of nests or glomeruli in the centers of necrotic foci. Proliferative changes are not typical. In the placenta, focal villusitis prevails with characteristic endarteritis according to the type of appearance.

terational angiopathy, as well as various types of immaturity of the villous tree.

Clinical manifestations. Congenital syphilis is a multisystemic disease that varies greatly in severity and variety of forms. It develops in 50% of newborns born to mothers with primary or secondary untreated syphilis during pregnancy (the remaining 50% are stillborn, very premature and died in the early neonatal period). Its manifestations resemble secondary syphilis.

Manifestations of congenital syphilis

1. Miscarriage or stillbirth: macerated fetus, collapsed skull, protruding abdomen, hepatosplenomegaly, hydrops fetalis, vesicular skin manifestations.

2. Dropsy fetus.

3. Pathologically enlarged placenta (the child may be normal, obviously infected or stillborn).

4. Premature birth.

6. Mucocutaneous manifestations: persistent rhinitis, maculopapular, scaly or bullous rash, usually on the palms and feet.

7. Hepatosplenomegaly, lymphadenopathy.

8. Anemia, thrombocytopenia

9. Jaundice (hepatitis and/or hemolysis).

10. Bone lesions: symmetrical osteochondritis, periostitis, osteomyelitis of long bones, skull, spine and ribs. A typical x-ray picture, pseudo-paralysis may develop later.

11. Damage to the central nervous system, usually asymptomatic. Damage is indicated by changes in the cerebrospinal fluid.

Most live births appear healthy, some have vesicular bullous lesions on the palms and soles, but the following symptoms may appear 4 days after birth:

1) flu-like syndrome:

meningeal symptoms;

Tearing (inflammation of the iris);

Discharge from the nose; mucous membranes are hyperemic, edematous, eroded;

Angina (there are papules on the mucous membrane of the pharynx);

Generalized arthralgia (due to pain, there are no active movements in the limbs - Parro's pseudoparalysis; on the x-ray - the phenomenon of osteochondritis, periostitis is often noted, in particular the tibia (saber legs);

2) an increase in all groups of lymph nodes:

Cervical, elbow, inguinal, axillary, popliteal;

Hepatosplenomegaly (in severe cases - anemia, purpura, jaundice, edema, hypoalbuminemia);

3) rashes:

maculopapular;

Merging of papular lesions with the formation of wide condylomas.

Prevention. Prevention of congenital syphilis is reduced to a screening examination of pregnant women in order to timely identify patients. When a diagnosis is made in the first trimester of pregnancy, its interruption is indicated in view of the fact that infection in the early stages of pregnancy leads to the formation of severe lesions in the fetus. If syphilis is detected in late pregnancy, treatment is carried out according to the recommendations of the Ministry of Health of the Russian Federation, according to generally accepted schemes, depending on the stage of the course of the disease.

If congenital syphilis is suspected or confirmed, the neonate must be isolated until specific therapy is initiated and for an additional 24 hours from its initiation.

Treatment. Specific therapy is carried out in newborns in the following clinical situations:

If the mother's treatment was inadequate;

If it was carried out in the last 4 weeks of pregnancy;

If nothing is known about him;

If drugs other than penicillin were used for treatment.

In addition, the results of reagin tests are taken into account. A higher antibody titer than that of the mother indicates an active infectious process. The antibody titer should be monitored over time, since it can only indicate a transplacental transfer of maternal antibodies to the fetus. If the antibody titer decreases in the first 8 months of life, then the newborn does not

infected. With a positive test result, treatment is carried out in those observations when it is not possible to control antibody titers over time.

The drug of choice for the treatment of congenital syphilis is penicillin G (procainepenicillin, benzathinepenicillin). The daily dose of the drug is calculated depending on the body weight of the newborn and his age.

Monitoring the effectiveness of treatment is carried out according to the results of quantitative non-treponemal tests, which are carried out at the age of 3, 6 and 12 months. A negative test result indicates the effectiveness of treatment. Preservation and increase in antibody titer requires further examination and re-treatment.

Viral hepatitis

Acute viral hepatitis can be caused by at least five different agents, but infections of the liver caused by Epstein-Barr virus, cytomegalovirus, and yellow fever virus are considered separate diseases and are not usually implied when using the term "acute viral hepatitis".

Allocate:

Viral hepatitis A;

Viral hepatitis B;

Viral hepatitis, neither A nor B (sporadic and epidemic), including hepatitis C (HCV);

Viral hepatitis D (simultaneous infection with hepatitis B - co-infection and sequential infection with hepatitis B - superinfection).

Hepatitis A virus (HAV) belongs to the genus Enteroviruses of the Picornovirus family. An RNA-containing virus consists of a non-enveloped virion.

Hepatitis B virus (HBV) is the most studied. Belongs to hepadnoviruses and has a more complex structure than the hepatitis A virus. The infectious particle consists of a core (cortex) and an outer shell (capsid). The composition of the virion includes circular double-stranded DNA and DNA polymerase; replication of viral particles occurs within the nuclei of infected hepatocytes.

At least four different antigen-antibody systems are associated with the hepatitis B virus.

1. Surface AG (HBsAg, Australian AG) is associated with the protein coat of the virus. Its detection in blood plasma makes it possible to diagnose acute hepatitis B and means that the patient's blood has become a potential source of infection. HBsAg is detected during the incubation period (1-6 weeks before the development of clinical and biochemical signs of the disease) and disappears upon recovery. Corresponding antibodies (anti-HBs) can be detected, which means that later, weeks or months after clinical recovery, their presence indicates past infection and relative protection in the future. In 10%, HBsAg continues to be detected after the acute phase, and the corresponding antibodies do not appear - such patients usually develop chronic hepatitis or become asymptomatic carriers of the virus.

2. Core AG (HBcAg) is associated with the core (core) of the virion. It can be found in infected liver cells, and in plasma it is detected only if viral particles are destroyed using special techniques. Corresponding antibodies (anti-HBc) are usually detected at the beginning of the manifestation period; subsequently, their titer gradually decreases. The presence of AT-HBc, along with AT-HBs, indicates a previous infection.

3. Antigen e (HBeAg), apparently, is a peptide that is part of the viral core. Found only in HBsAg-positive plasma. The presence indicates active replication of the virus and is combined with an increased infectious ability of the blood and the likelihood of developing chronic liver damage.

Hepatitis D virus (HDV, delta factor) is unique. Its RNA is defective, as a result of which this virus is able to replicate only in the presence of HBV. Hepatitis D occurs either as a co-infection in acute hepatitis B or as a superinfection in significantly chronic hepatitis B. Infected hepatocytes contain delta particles coated with HBsAg. Clinically, the infection presents with an unusually severe course of acute hepatitis B.

The term non-A non-B hepatitis (NANB) has been proposed to refer to infections not associated with A- and B-type viruses. Relatively recently, a specific single-stranded RNA virus similar to flaviviruses (hepatitis C virus) has been identified, which is

cause most post-transfusion and sporadic cases of NANB hepatitis. A feature of HCV is the extremely high heterogeneity of its genome. At least six major genotypes of the virus have been identified. Anti-HCV antibodies often appear in plasma several months after an acute infection. The titers then gradually decrease unless the infection becomes chronic (which is the case in 50%). The HCV virus is identified in plasma using a complex technique, the corresponding antigen is isolated from hepatocytes.

Virus hepatitis A spreads mainly by the fecal-oral route, infection through the blood and excretion products is also possible. The source of infection is only a patient in the early stage of the disease - virus carriers and chronic forms of infection are excluded. The prodromal (preicteric) stage is characterized by acute fever, chills, headache, and dyspeptic disorders. At this stage, itching is often noted, which is accompanied by an increase in the size of the liver, an increase in the level of transferases in the blood 5-7 days before the onset of jaundice. Often, the infection is asymptomatic.

Virus hepatitis B usually transmitted parenterally: through infected blood and its derivatives. Possible infection during tattooing. Transmission remains high among drug addicts, and the risk is increased for patients on hemodialysis and hospital staff who come into contact with blood. There is non-parenteral sexual spread. Chronic HBV carriers serve as a reservoir of infection.

HBV infection is accompanied by a wide range of liver lesions, from subclinical carriage to acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Following a long incubation period (6 weeks to 6 months), signs of acute infection appear. The preicteric period, in contrast to hepatitis A, lasts longer and is characterized by a gradual onset with arthralgia, urticarial rash, dyspeptic and asthenic disorders, and hepatolienal syndrome is growing. In severe forms of the disease, the temperature rises. In the blood - elevated levels of transaminases; HBsAg, HBeAg and

With the appearance of jaundice, intoxication, dyspeptic, asthenic manifestations increase, and even more - hepatolienal syndrome.

The course of jaundice is more pronounced. In severe cases, hemorrhagic syndrome, acute hepatic encephalopathy with a transition to a coma and even death can develop.

In pregnant patients with hepatitis B, there is a high incidence of preterm birth and preeclampsia. More than 50% of women have inflammatory changes in the afterbirth.

Hepatitis nor Ani B(NANB) has a variant similar to hepatitis A, predominantly spread by waterborne outbreaks. A variant close to hepatitis B, usually with a shorter incubation period, often leads to the formation of chronic hepatitis.

Finally, there are mixed variants of infection (A and B, B and D, B and CMV, B and HIV).

The average duration of the incubation period for infection with hepatitis A is 2-6 weeks, hepatitis B - 6-25 weeks, neither A nor B - 2-25 weeks. Children and young adults are more commonly affected, but the disease can occur at any age.

Viral hepatitis is the most common cause of jaundice during pregnancy. Usually it proceeds relatively easily, but with malnutrition, a severe epidemic form of hepatitis, neither A nor B, can occur. Maternal mortality is 0.64-1.79%, but can reach 15.6% (Farber N.A. et al., 1990 ). Hepatitis is more severe in the second half of pregnancy, which is associated with changes in hormonal levels, more pronounced symptoms of cholestasis

Congenital viral hepatitis occurs rarely, with acute or chronic hepatitis B of the mother during pregnancy; Also, a mother with an asymptomatic form of hepatitis (antigen carrier) can be a source of intrauterine infection. Fetal hepatitis is characterized by polymorphism of hepatocytes with the formation of multinuclear symplast cells, as well as cholestasis (intracellular and intratubular), the formation of adenomatous structures and biliary necrosis with poor lymphocytic infiltration of the portal tracts. Severe hepatitis in the mother can lead to antenatal fetal death. Macroscopically, in the afterbirth, a yellowish color of the membranes, the fetal surface of the placenta is noted, histologically - in miscarriages, numerous Kashchenko-Hofbauer cells are recorded in the stroma of the villi of the placenta and membranes that absorb bilirubin, with minimal inflammatory changes.

Convincing data on the teratogenicity of hepatitis in the first trimester of pregnancy is not available. The hepatitis B virus can be passed to the newborn at birth or, less commonly, through the placenta. In the I and II trimesters of pregnancy, acute hepatitis B is rarely transmitted to the fetus (5%). Placental transmission has not been definitively established and is most likely in e-antigen positive mothers who are chronic carriers of hepatitis B superficial hypertension (HBsAg) or who developed hepatitis in the third trimester. With a disease in the III trimester, the probability of infection of the fetus is 60-70%. Most often, infection occurs during childbirth due to microtransfusions of blood from mother to fetus or as a result of contact of the child with infected secretions of the mother when passing through the birth canal. A positive HBeAg test (reflecting a high degree of infection) is associated with an 80-90% chance of transmission to the fetus. More than 85% of newborns from such mothers become chronic carriers. If the mother has antibodies to HBeAg (their presence indicates resolution of the infection), the risk of infection is only 25%. Possible infection in the postnatal period (with milk, saliva)

Infected newborns often become carriers of HBV and have subclinical hepatic dysfunction. Observations of overt neonatal hepatitis are rare.

Forecast. Hepatitis A usually resolves spontaneously in 4 to 8 weeks - in most cases it does not require special treatment. Restriction of diet and physical activity is not required. The frequency of miscarriages does not exceed that in the population. The fetus is practically not at risk of infection and the newborn does not require prophylaxis.

With hepatitis B, the prognosis is less favorable than with A. Especially after blood transfusion, when mortality can reach 10-15%; in 5-10% a chronic form is formed. Mortality in pregnant women is 3 times higher than in non-pregnant women. The incidence of hepatitis in newborns is 45-62%.

The greatest danger for pregnant women is the epidemic variant of NANB hepatitis in the II and III trimesters of pregnancy. Complications: miscarriages, premature births, high maternal mortality, neonatal morbidity and perinatal mortality.

Infection prevention and treatment. Personal hygiene helps prevent hepatitis A. If a pregnant woman comes into contact with a sick person for 7-10 days, a standard γ -globulin 1.5-3.0 ml once intramuscularly. At a later date, the use of the drug is impractical.

To prevent hepatitis B, transfusion restrictions should be introduced, the use of HBsAg-tested blood should be introduced. Donor screening for HCVAg is required. Standard immunoglobulin provides protection against clinical HAV infection and is given to those who have household contacts with an established carrier.

Vaccination against HBV leads to the production of antibodies in healthy recipients and reduces the prevalence of hepatitis by 90%. Patients on dialysis, with cirrhosis of the liver and other immune disorders respond worse to vaccination. A small proportion of healthy people do not respond with the formation of AT-HBs.

Examination of pregnant women for HBsAg carriage should be carried out already in early pregnancy.

In hepatitis C, the role of perinatal infection in the spread of this infection has not been fully determined. Detection of hepatitis C virus RNA in the blood sera of children on the 1-5th day after birth makes it reasonable to assume that there is prenatal infection in this infection as well. The treatment of hepatitis C is based on interferon therapy (interferon, interferon inducers), as well as the use of antiviral drugs.

With mild and moderate hepatitis (any) in the first trimester of pregnancy, pregnancy may continue, since by the time of delivery the woman will be healthy and the likelihood of congenital anomalies in her child is not higher than in a healthy one. In severe hepatitis after recovery, depending on the characteristics of the course of infection and the duration of pregnancy, it is recommended to interrupt it: up to 12 weeks - medical abortion, after 12 weeks - intraamnial administration of hypertonic sodium chloride solution, prostaglandin F2a ; intramuscularly with the introduction of prostaglandin after a preliminary (12 hours) expansion of the cervix with medium-sized kelp.

In treatment, physical rest, balanced drinking, treatment of the threat of premature termination of pregnancy, and, if possible, a shift in the time of physiological childbirth, which in the midst of jaundice carry not only unwanted physical exertion, but also sudden hormonal changes that can bring the body out of compensated relative balance, are important. Shown cautious infusion detoxification therapy under the control of diuresis. With fluid retention, diuretics are used. A short course of glucocorticoids - as an integral part of a set of measures for dehydration in developing cerebral edema. The appointment of corticosteroid therapy is impractical and may even contribute to the growth of hepatocytodystrophy.

Children born to an HBsAg-positive mother, regardless of whether she has serum HBe antigen or antibodies, should receive prophylactic treatment immediately after birth with hepatitis B immunoglobulin (HBIg), after which they should receive three vaccinations with recombinant hepatitis virus vaccine C. Isolation of newborns from mothers and refusal of breastfeeding is not recommended, especially after the introduction of HBIg and antiviral vaccine. If HBsAg is excreted in breast milk to prevent infection during the neonatal period, breastfeeding is not indicated.

Treatment of newborns with acute hepatitis B is symptomatic with adequate nutrition; neither steroids nor HBIg are effective. It is necessary to isolate the infected newborn and exercise extreme caution when working with his blood and shit.

PREGNANCY PREPARATION AND MANAGEMENT OF PREGNANCY

Thus, intrauterine infections pose a serious threat to the life and health of the fetus and newborn, and often have adverse long-term consequences. Diagnosis and treatment of infectious diseases in pregnant women presents significant difficulties due to the blurring, variety and non-specificity of clinical manifestations, difficulties in obtaining material for laboratory tests, and the impossibility of widespread use of therapeutic drugs.

In connection with the foregoing, IUI prevention methods based on the prevention and treatment of infection in the mother are of particular importance. The most promising in this direction is the pre-gravid preparation of married couples, followed by the consistent implementation of therapeutic and diagnostic measures during pregnancy.

Pregravid preparation should include:

Identification of a risk group based on anamnesis data and results of a clinical examination, identification of concomitant extragenital diseases;

Comprehensive examination with the study of the immune, hormonal, microbiological status;

Etiotropic antibacterial or antiviral therapy;

Conducting an appropriate correction of the identified violations of the microcenosis of the genital tract, followed by the appointment of eubiotics;

Treatment of diseases with the use of immunostimulating and interferon-correcting therapy, as well as physiotherapy;

metabolic therapy;

Correction of menstrual irregularities and associated endocrinopathies;

Treatment of the sexual partner in the presence of sexually transmitted diseases.

During pregnancy at terms up to 12, as well as at 18-20, 28-30 and 37-38 weeks in pregnant women of this group, an assessment of the state of vaginal microcenosis is shown, up to 12 weeks (further according to indications at 18-20 and 37-38 weeks) - identification of pathogens of sexually transmitted diseases, and determination of the titer of specific Ig to viral and bacterial agents. If infections are detected, appropriate treatment is carried out, which is selected taking into account the duration of pregnancy and the possible effect of drugs on the development of the fetus.

Regular echographic, Doppler and cardiotocographic examination allows timely diagnosis of developing fetoplacental insufficiency, treatment and monitoring of its effectiveness.

Carrying out pre-gravid preparation and measures to identify endangered intrauterine infections

allows to reduce the frequency of intrauterine infections by 2.4 times. At the same time, the number of complications of pregnancy and childbirth (especially premature termination of pregnancy, as well as fetoplacental insufficiency) decreases, which helps to reduce the overall incidence of newborns by 1.5 times.

Intrauterine infection in a newborn is a special group of diseases that a baby becomes infected with even before birth. Cases of infection are also recorded directly during labor. Infections of this nature can lead to fetal death, miscarriage, or abnormal development.

Cases were recorded when pathologies led to early childbirth, defects, and severe damage to the central nervous system. That is why it is advisable to carry out diagnostics in a timely manner. It involves the implementation of research at the microscopic level. Additionally, functioning, immunity, enzymes, interaction of molecules and correctness in the work of biological processes are analyzed.

Treatment of infections of this nature is carried out with the help of immunoglobulins, modulators. A woman is prescribed regular intake of antiviral drugs, the action of which is aimed at destroying bacteria.

Intrauterine infection in newborns is observed in the presence of pathologies in certain processes. The situation is observed against the background of infection of the fetus. To date, it has not been possible to fully determine the route of infection. Today, about 10% of all children are born with this disease. This problem is especially acute in pediatrics, because of this a large number of deaths and the development of diseases immediately after birth are recorded. Parents are advised to pay attention to the prevention of infection. In this case, it will be possible to reduce the risk of developing dangerous diseases.

Diagnosis of infection is prescribed during pregnancy

Causes of diseases

The process of infection with these diseases begins even at the time the fetus is in the womb. The risk of infection also remains during labor. In this case, the carrier of the infection is the mother. The disease can be transmitted vertically or ascending. It all depends on the location of viruses and bacteria.

Only in rare cases, infection of a pregnant woman has been observed during diagnosis, which involved a biopsy or other specific procedures. The risk increases with the introduction of drugs to the baby through the blood, plasma.

Viral agents can be transmitted by the antenatal route. In this case, the fetus can be infected with rubella, herpes, hepatitis, HIV. Due to intracellular pathogens, toxoplasmosis or mycoplasmosis is diagnosed.

An important role is played by the state of the birth canal and the process of the birth of the baby. At this stage, there is a risk of microbes entering the baby's body in various ways. Among bacteria, the possibility of infection with streptococci, Proteus, Klebsiella and others is increased. The placenta is initially used as an effective barrier. However, even a slight damage to it can lead to the development of insufficiency. Through small holes, harmful bacteria can enter without any special obstacles. Among them, the syphilis virus is of particular danger.

The history of the mother and the presence of previously unfavorable pregnancies are also taken into account. The risk of intrauterine infections also increases if the baby was born prematurely. Additionally, the period in which the woman was infected (before and after the onset of pregnancy) is analyzed.

During childbirth, the doctor analyzes the main properties of amniotic fluid

The child is directly affected by the period of infection, as well as the virus that caused the development of pathology. For example, if the pathogen got inside during the first ten weeks of pregnancy, then it will end in an independent miscarriage. If the infection occurred at the twelfth week, then most likely the child will be born dead or he will have serious malformations in the development of internal organs and systems. Infection of the fetus from the second trimester is fraught with abnormal development of individual internal organs or the presence of a pronounced generalized infection after birth.

It should be noted that the symptoms are radically different in mother and child. Even if no negative manifestations were found in a woman, serious lesions can subsequently be detected in the fetus.

The possibility of a stillbirth cannot be completely ruled out. Viruses and bacteria tend to penetrate deep into the tissue and disrupt the central nervous system, heart and other important organs.

Symptoms of infections

The consequences of infection of the baby are visible even in the process of labor. The doctor pays attention to the condition of the amniotic fluid - they become cloudy, they contain a lot of meconium. The patient may feel unwell. If a child has an intrauterine infection, then the risk of having a baby with asphyxia, a large liver and other defects in general development increases. As a rule, rubella, pyoderma and various profuse skin rashes are additionally diagnosed. Some babies have fever, convulsions, various respiratory and cardiac disorders.

Antenatal intrauterine infection can lead to pneumonia, myocarditis, anemia and other diseases that appear within a few days after the baby is born. Next, the child is examined using special medical equipment. With its help, it is possible to identify diseases of the organs of vision, defects in the work of the heart, the presence of cysts and improper functioning of the brain.

With IUI, a child may develop pathologies

The neonatologist pays attention to the baby in the postpartum period. In the presence of diseases, he often burps, there is muscle weakness, an incorrect reaction of the central nervous system. The skin is examined regularly. It is not allowed that it be a pronounced gray color. Intrauterine infections have different incubation periods. Each disease is analyzed separately depending on the nature and specification of manifestation.

Each individual TORCH infection has different methods of diagnosis and treatment. It is recommended to consult in detail with a specialist in this field.

The main types of infections

Intrauterine infection is a broad concept. Its division is carried out depending on the source of the formation of the disease:

In medical practice, it is customary to combine the most common diseases with a special abbreviation - TORCH.

This syndrome includes toxoplasmosis, rubella, herpes and other lesions.

Including the study is carried out for the presence of HIV, hepatitis, smallpox, mycoplasmosis, syphilis.

Toxoplasmosis: features of infection

The disease is diagnosed if the fetus in the womb was infected with Toxoplasma Gondii cells. Pathology can lead to abnormal development, the presence of malformations of the brain, heart and other internal organs.

Diagnosis is made immediately after the birth of the baby. The infection manifests itself in the form of severe fever, jaundice, swelling, stool disorders, and periodic convulsions. Additionally, the baby may have symptoms of meningitis and encephalitis. If the disease becomes chronic, then the situation is aggravated by strabismus or complete atrophy of the optic nerve. Unfortunately, the infection can be fatal before delivery.

At a late stage in the development of the disease, the baby develops epilepsy and complete blindness.

Features of rubella in utero infection

Infection is carried out in the case of the transfer of the disease during the period of gestation. In the first eight weeks, the probability reaches eighty percent. In the second trimester, it drops to twenty, and in the third - to eight percent.

If the child has a disease, he will be born prematurely and will not gain weight well. Additionally, a rash and obvious manifestations of jaundice can be seen on the skin.

Rubella of a congenital nature is dangerous by the manifestation of the following symptoms:

• partial or complete damage to the eye muscle;
• wps();
• insufficient tone of the auditory nerve.

If the infection hit the baby in the second part of pregnancy, then he can be born with retinopathy or complete deafness.

Anomalies against the background of the transferred rubella are extensive. Defects can manifest themselves in the structure of the palate, hepatitis, abnormal structure of the skeleton or the genitourinary system. Infection is dangerous because the child may further lag behind in physical and mental development.

Diagnosis should be carried out during pregnancy and after the baby is born.

Cytomegaly: features of infection and the course of infection

This type of infection is dangerous because it leads to severe damage to the internal systems of a sick child. A complication can also lead to immunodeficiency or the appearance of purulent skin lesions. Defects can be either congenital or appear at a certain period of development. In the postpartum period, jaundice, hemorrhoids, pneumonia, anemia and other diseases may appear.

Subsequently, the organs of vision, liver, deafness and other diseases remain at risk.

Intrauterine infection with herpes

Herpes infection can manifest itself in several forms:

• the generalized form is characterized by toxicosis, the presence of respiratory diseases, jaundice, diseases of the upper respiratory tract and lungs, hemorrhoids;
• neurological;
• damage to the mucous membrane and skin.

If the bacterial infection becomes multiple, then the child is diagnosed with sepsis.

Herpes is a dangerous infection that can lead to a number of complications. Among the most dangerous are complete deafness, blindness, abnormal development or lag in it.

Features of the diagnosis

Today, the diagnosis of intrauterine infections is quite acute. It is necessary to find out about the presence of harmful bacteria, viruses and fungi as early as possible. To do this, a smear is taken in the gynecologist's office, sowing for the presence of bacteria and the state of the microflora. In some cases, PCR or a complex TORCH analysis is additionally prescribed. Invasive prenatal diagnosis should be carried out only for those women who are in.

The gynecologist will also be able to consider certain markers during an ultrasound examination. Attention should be paid to diagnosis in the event that low or polyhydramnios and other pathologies of pregnancy development were previously diagnosed. If there are deviations, the doctor additionally prescribes a study of the features of the functioning of the heart and blood flow.

The study must be additionally carried out even after the birth of the baby. For this, microbiological tests are carried out. DNA research should be done. For this, serological research methods are used. An important role is played by the result of the histology of the placenta, which can also be performed after childbirth.

If the baby is suspected of having any intrauterine infection, then during the first day of life he should be constantly under the supervision of a neurologist, cardiologist and other specialists in the field of childhood diseases. At their discretion, tests are prescribed to identify pathologies in the development of hearing, vision and other internal organs.

In order to prevent a woman should be regularly examined by a gynecologist

Basic principles of treatment of infections

At the first stage of eliminating pathologies, it is necessary to take drugs to increase immunity, against the development of viral, bacterial and other diseases.

To improve immunity, it is necessary to use special modulators and immunoglobulins. Acyclovir is most often used against viruses. Effective therapy against bacteria involves the use of broad-spectrum antibiotics.

Therapy must be carried out alternately to get rid of each individual symptom. Otherwise, the risk of pathologies in the work of the central nervous system increases. As a result, the child may experience problems in the work of the heart and lungs.

Infection prevention

If a patient is diagnosed with a generalized form of the infection, then the probability of passing it on to her child is eighty percent. With local manifestations, the risk of damage to only individual internal organs increases. Unfortunately, almost every infection can lead to problems in the central nervous system in the future.

The main methods of prevention involve a complete examination of the patient before pregnancy. During gestation, you should protect yourself from contact with sick people. If a woman has not previously had rubella and has not been vaccinated against it, then an injection must be made three months before the planned pregnancy. Additionally, it should be noted that some cases of infection involve termination of pregnancy at any time.

Intrauterine infection is a potential health hazard for the unborn child. In these cases, the fetus becomes infected from a sick mother with infections that can cause multiple congenital malformations of the brain or spinal cord, heart, as well as blindness, deafness, and even death of the fetus or newborn. All pathogens of intrauterine infection by foreign researchers are united under the term TORCH (according to the first letters of the English names of toxoplasmosis, rubella, cytomegalovirus, herpes). It should be noted that most of these infections are asymptomatic. Sometimes, after a short mild illness, the pathogen continues to be in the body of a woman for many years. In a latent state, it does not pose a danger to the fetus: the mother's immunity reliably protects it. Only primary infection with toxoplasmosis, cytomegalovirus infection, chlamydia, herpes in the first 3 months of pregnancy or exacerbation of a persistent (i.e. secretly ongoing infection) due to stress or drug-induced suppression of immunity are dangerous for the fetus.

IUI prevalence: 20-30% of women of childbearing age are infected with toxoplasmosis, 50-70% with cytomegaly virus, herpes simplex, etc.

Severe infections are the leading cause of neonatal deaths worldwide following preterm birth and asphyxia, accounting for up to half of all deaths in countries with very high mortality.

Causes of intrauterine infections in newborns

Etiology: viruses, mycoplasmas, chlamydia, protozoa, fungi, bacteria.

In the mother, the infectious process can proceed as acute, subclinical, latent. Of particular importance is the genitourinary infection in the mother as a source of pathogen in generalized IUI (pyelonephritis, inflammation of the appendages, vagina, etc.). Staphylococci, streptococci, intestinal flora, listeria, toxoplasma, Koch's bacilli, fungi can persist in the uterus for a long time in small quantities, causing chronic diseases of the urogenital area in a woman.

Pathways of penetration of the pathogen can be different. Antenatally, the infectious agent enters the fetus hematogenously or through infected amniotic fluid inside, on the skin, lungs, and eyes. The amniotic fluid of the mother can be infected ascending from the vagina and descending from the fallopian tubes, through the amniotic membranes with endometritis, placentitis, as well as by the fetus itself, infected hematogenously and excreting an infected agent with urine and feces.

Bacterial pathogens most often infect the fetus intranatally, causing severe bacterial infections in some children, up to sepsis (group B streptococcus, Escherichia coli, Pseudomonas aeruginosa, Citrobacter, Klebsiella, Proteus).

The pathogen, penetrating to the embryo or fetus, settles in the tissues and causes inflammation. Of great importance is the time of penetration of the infectious agent.

• Blastopathy: the penetration of the pathogen to the embryo in the first 14 days of pregnancy during blastogenesis leads to the death of the embryo, ectopic pregnancy, gross malformations with a violation of the formation of the axis of the embryo, which causes the occurrence of such gross malformations as cyclopia, rare twin malformations, gross malformations, incompatible with life, spontaneous abortions.
• When an embryo is infected during embryogenesis (from the 16th to the 75th day), embryopathies occur - malformations of individual organs and systems, teratoma, abortion. Gross malformations leading to miscarriages are especially often formed in the first 8 weeks of pregnancy. Rubella, cytomegaly, herpes, hepatitis B viruses play an important role in the formation of infectious embryopathies.
• When an infectious agent enters the fetus (from the 76th day to the 280th day of pregnancy), fetopathy occurs. The fetal period is divided into early (3 months - 7 months) and late (from 7 months to birth).

In the early fetal period, differentiation of tissues of already incorporated organs and systems occurs. If the fetus becomes infected during this period, then there is a violation of tissue differentiation with the development of sclerosis as a result of the growth of connective tissue. Examples of early fetopathy can be cirrhosis of the liver, hydrocephalus, microcephaly, hydronephrosis, fibroelastosis of the heart.

If the fetus is infected in the late fetal period, when the development of organs and systems occurs, then the birth of a child with IUGR is possible - intrauterine growth retardation, a clinic of the infectious process, premature birth, asphyxia in childbirth, impaired adaptation of the newborn.

Any microorganism that inhabits the urinary tract or lower digestive tract of the mother can cause early infections in newborns. These are gram-positive cocci - GBS, a-hemolytic streptococci (Streptococcus viridans), Staphylococcus aureus, enterococci (Enterococcus faecalis, Enterococcus faecium), rpa-negative rods (Escherichia coli, Proteus spp., Klebsiella spp., Pseudomonas spp., Haemophilus influenzae, salmonellae, shigella), gram-negative cocci (Neisseria gonorrhoeae, Neisseria meningitidis), gram-positive rods (Listeria monocytogenes), fungi (mainly Candida albicans), protozoa (Chlamydia trachomatis, Mycoplasma hominis, U. urealyticum), anaerobic bacteria. The etiological significance of microorganisms is different. Microorganisms with low virulence (such as lactobacilli, diphtheroids, and Staphylococcus epidermidis) rarely cause severe infections. Although U. urealyticum and M. hominis are sometimes isolated from the blood of fetuses weighing less than 1500 g at birth, their role in the development of early neonatal sepsis (RNS) remains unclear.

Also, the influence of some microorganisms on the development of RNS isolated from the amniotic fluid and even the blood of newborns is unknown. The role of Gardnerella vaginalis, most commonly isolated from amniotic fluid, has not been proven.

There is a statistically insignificant increase in infections of the mother and child when C. trachomatis is isolated from the amniotic fluid (in about 4% of cases, mothers of newborns are infected with C. trachomatis).

According to the National Institute of Child Health and Human Development, the most common causative agents of RNS are GBS (37.8%), E. coli (24.2%), S. viridans (17.9%), S. aureus (4.0 %) and H. influenzae (4.0-8.3%). GBS is the most common causative agent of infections in term infants, and E. coli in preterm infants. Mortality is higher in infants infected with E. coli compared with GBS (33% vs 9%; p<0,001). Также высока летальность недоношенных новорожденных при сепсисе, вызванном Н. influenzae (до 90%), который может иметь молниеносное течение, начинаясь как тяжелый РДС.

The detection of GBS in the amniotic fluid of women with intra-amniotic infection is accompanied by maternal or neonatal bacteremia in 25% of cases. When E. coli is detected, maternal or neonatal bacteremia is detected in 33% of cases.

In developing countries (Latin America, Caribbean, Asia and Africa) E. coli, Klebsiella spp. and S. aureus are more common and account for a quarter of all cases of RNS. The most common gram-positive pathogen in developing countries is Staphylococcus aureus.

anaerobic bacteria. Given that most anaerobic bacteria are part of the normal microflora of the gastrointestinal tract, genital tract and skin, they can be potential pathogens in newborns. Anaerobic infection develops mainly with a decrease in body resistance, impaired immunity, which is often observed in newborns, especially premature ones. Gram-positive anaerobic bacteria (Clostridium, Peptostreptococcus, Peptococcus) are of the greatest importance for RNS. Anaerobic infections caused by Clostridium may present as a systemic disease or localized infections such as cellulitis or omphalitis. Anaerobic bacteria were the cause of RNS for the period 1989-2003. in just 1% of cases.

Ways of infection of newborns

There are several main ways of spreading infection:

• Ascending path.
• Hematogenous (transplacental) route - as a result of bacteremia in the mother. In this case, a generalized infection usually occurs with frequent damage to the liver, lungs, kidneys, and brain.
• Contact way - contamination of the newborn when passing through the birth canal. In this case, colonization of the skin and mucous membranes of the newborn occurs first, including the nasopharynx, oropharynx, conjunctiva, umbilical cord, vulva and gastrointestinal tract (from aspiration of infected amniotic fluid or vaginal discharge). It should be noted that in most newborns, microorganisms multiply in these places without causing disease. The umbilical cord is the most common site for infection to enter. As a special case of the occurrence of RNS with a horizontal transmission mechanism, one can name an infection acquired in the absence of hygiene during childbirth, a violation of the method of processing the umbilical cord (for example, during childbirth at home), and poor hygiene skills when caring for a newborn.

Specific risk factors that increase the possibility of developing an infection have been identified:

• preterm birth is the most significant risk factor for acquiring infection in children immediately before or during childbirth;
• maternal colonization;
• rupture of the membranes of the membranes more than 18-24 hours before birth increases the likelihood of neonatal sepsis by 1%. If the baby is premature, the risk increases by 4-6%. The lower the gestational age of the newborn and the longer anhydrous period, the higher the likelihood of developing neonatal sepsis;
• maternal intra-amniotic infection (chorioamnionitis): according to the National Institute of Child Health and Human Development (USA), from 14 to 28% of women who gave birth to premature babies at 22-28 weeks. pregnancy, have signs characteristic of chorioamnionitis. According to various data, with chorioamnionitis of the mother, sepsis is observed from 1-4% to 3-20% of newborns. If chorioamnionitis is combined with a long anhydrous period, the risk of developing RNS increases by 4 times.

Other risk factors that increase the possibility of a generalized infection:

• low socio-economic status of women (there is a high frequency of infection of amniotic fluid, bacteriuria, reduced antimicrobial activity of amniotic fluid);
• the male sex of the child;
• low Apgar score (hypoxia and acidosis can impair immune defense function);
• complicated childbirth in premature newborns;
• the presence of signs of RDS;
• maternal diabetes;
• hypothermia in newborns, usually defined as rectal temperature<35°С, связана со значительным увеличением числа случаев сепсиса, менингита, пневмонии и других тяжелых bacterial infections;
• prolonged stay of the mother in the hospital;
• inadequate facilities for screening and antibiotic prophylaxis in labor;
• hereditary pathology of metabolism.

Symptoms and signs of intrauterine infections in newborns

History: miscarriage, stillbirth, miscarriage of previous pregnancies, birth of children with malformations and deaths at an early age, anomalies in the course of this pregnancy and childbirth, threatened miscarriage, polyhydramnios, short thick umbilical cord, premature discharge of amniotic fluid, their fetid odor, accretion or abruption of the placenta, diseases of the urogenital area in the mother, infections in a woman during pregnancy, including ARVI, the presence of chronic foci of infection in the urogenital area in a woman, chronic tonsillitis, chronic cholecystitis, fever in the mother during childbirth, severe infectious process in the mother before, during or immediately after childbirth, obstetric assistance in childbirth, the birth of a child in asphyxia, resuscitation of a child, deterioration in the state of intrauterine development, intrauterine malnutrition, prematurity, dysembryogenesis stigmas, malformations, hydrocephalus or microcephaly.

Common clinical manifestations of intrauterine infection: intoxication, low birth weight, poor weight gain, poor appetite, regurgitation, vomiting, restless behavior or lethargy, skin dry, pale with a cyanotic, gray or icteric tint, jaundice may be pronounced, the skin collects in folds, there may be polymorphic rashes, thinning of the subcutaneous fat layer, enlarged lymph nodes, enlarged liver and spleen, the abdomen is enlarged, swollen, hemorrhagic syndrome - bleeding, hemorrhagic rash on the skin, intestinal syndrome.

Specific symptoms and syndromes characteristic of certain infections.

Rubella: meningoencephalitis, hepatitis with jaundice, pneumonia, congenital heart disease, rotation of the legs and feet, iridocyclitis, deafness in 50%, if the mother was ill in the first month of pregnancy - Gregg's triad - eye defects, heart defects, deafness.

Cytomegalovirus infection: any organ that has epithelial cells is affected. Jaundice, hepatitis, hemorrhagic manifestations (petechiae, melena), meningoencephalitis, pneumonia, calcifications in the brain, kidney damage, nephritis, eye damage. It often appears after the neonatal period. Possible microcephaly, polycystic kidney disease, heart failure, late complications - deafness, blindness, encephalopathy, microcephaly, pneumosclerosis, liver cirrhosis.

Herpes infection: vesicular rashes on the skin of mucous membranes, keratitis, severe hepatitis, jaundice, pneumonia, DIC. Defects: limb hypoplasia, microcephaly, microphthalmia, skin scars. Complications - blindness, deafness, lag in psychomotor development.

Viral hepatitis: hepatitis, jaundice, dark urine, discolored stools. Defects - atresia of the biliary tract, complications - cirrhosis of the liver, lag in psychomotor development.

Listeriosis: meningoencephalitis, papular-roseolous rash on the back, abdomen, legs, whitish-yellowish nodules with a diameter of 1-3 mm on the back of the pharynx, conjunctivitis, complications - hydrocephalus.

Tuberculosis: enlarged peripheral and abdominal lymph nodes, ascites, lung damage, meningitis, renal failure, defects of the skeletal system.

Syphilis: specific rashes on the skin, necessarily on the palms and soles, rhinitis, sniffling, periostitis, osteochondritis of tubular bones, cracks in the corners of the mouth. At preschool age: Hutchinson's triad (keratitis, deafness, dystrophy of teeth), saddle nose, saber legs.

Toxoplasmosis Key words: meningoencephalitis with kalydificates, hydrocephalus, eye damage, microcephaly, microphthalmia, hepatitis. Constantly scratching eyes at an older age.

Chlamydia: purulent conjunctivitis, rhinitis, otitis media, pneumonia, persistent paroxysmal cough.

Newborns from high-risk groups are subject to examination for the presence of IUI.

Diagnosis of intrauterine infections in newborns

Laboratory diagnosis of infections

There is no characteristic sign only for infection. To one degree or another, all parts of the immune system respond to any stressful situation, and not just to the introduction of an infectious agent. Therefore, it is very difficult to recognize an infection only by laboratory parameters. We decided to touch upon the main markers of infections, the laboratory determination of which can currently be afforded by most medical institutions. Many putative markers (cytokines, blood cell surface antigens, granulocyte colony stimulating factor) are being investigated but not yet used for routine diagnosis. Numerous publications show that taken separately, such indicators as the concentration of leukocytes, platelets, the ratio of mature and immature neutrophils and CRP have low sensitivity and specificity. In addition, they depend on:

• postnatal and gestational age;
• from the time of the onset of the infectious process.

The information content of these indicators can be increased by:

• their sharing;
• combination with clinical symptoms;
• the dynamics of changes (with non-infectious causes, such as birth stress, there is a rapid reverse development).

It should be remembered that no laboratory data can replace ongoing medical supervision, which may be more sensitive to the onset of symptoms of infection (eg, the onset or increase in the frequency of apnea) even before changes in laboratory parameters.

Leukocyte concentration. With infections, both leukocytosis and leukopenia can develop. At the same time, uninfected children may experience pathological changes in the concentration of leukocytes due to labor stress. Of the many definitions of leukocytosis/leukopenia in the neonatal period, the following are most common:

• leukopenia - the concentration of leukocytes is less than 6000 on the first day of life, then - less than 5000 in 1 mm3;
• leukocytosis - the concentration of leukocytes is more than 30,000 on the first day, then - more than 20,000 in 1 mm3.

Neutrophil concentration. A complete neutrophil count is slightly more sensitive for detecting infection than a leukocyte count, although abnormal neutrophil counts at the onset of septic symptoms are only seen in neonates. The total number of neutrophils increases after birth and reaches its peak by 6-8 hours of life. The lower limit of normal at this time is 7500, 3500 and 1500 / mm3, respectively, for newborns> 36 weeks, 28-36 weeks. and<28 нед. гестации.

A more sensitive indicator (sensitivity 60-90%) is the neutrophil index (NI), calculated as an increase in the ratio of immature forms of neutrophils (myelocytes, metamyelocytes, stab neutrophils) with the total number of neutrophils.

The reproducibility of this indicator depends on the quality of identification of the neutrophil species by laboratory assistants.

The normal value of the neutrophilic index at birth is 0.16; later, with an increase in postpartum age, it decreases to 0.12. Most authors use NI >0.2 to diagnose sepsis, but other values ​​are also used (0.25; 0.3).

Data obtained between 6 and 12 hours after birth are more likely to be altered than those obtained immediately after birth, because a change in the number and composition of leukocytes requires an inflammatory response.

Thrombocytopenia. Different authors consider thrombocytopenia a platelet concentration of less than 100 or 150,000x109/l. The number of platelets in a healthy newborn in the first 10 days of life is rarely less than 100x109/l. Values ​​below this may occur in early-onset sepsis, although this feature is commonly seen in nosocomial infection. Thrombocytopenia is not a specific sign of sepsis due to the large number of reasons leading to its development. In general, the presence of thrombocytopenia is a non-specific, insensitive indicator and is more characteristic of late sepsis.

Sedimentation rate of erythrocytes. The use of erythrocyte sedimentation rate during the neonatal period is of little value in either diagnosing or monitoring serious bacterial infection.

Analysis of urine for the diagnosis of RNS is uninformative.

SRP is an acute-phase protein of inflammation, an increase in its level is associated with tissue damage, and it is assumed that its main function is to neutralize bacterial or intrinsic toxic substances released from tissues in response to microbial aggression. CRP is elevated in 50-90% of newborns with systemic bacterial diseases.

6-8 hours after the onset of the infectious process, the concentration of CRP gradually increases and reaches maximum values ​​after 24 hours. Therefore, often in newborns with RNS, the first determination of CRP immediately after birth may not differ from normal values. Normal CRP ranges may change during the first 48 hours of life depending on age.

Gestational age probably does not affect the reliability of the results, however, some studies have noted that preterm infants may have lower baseline CRP values, and their role in the diagnosis of neonatal sepsis is less significant. Despite some age fluctuations, the cut-off value of 10 mg/l is most commonly used, regardless of gestational age and postpartum age of the newborn, since the sensitivity of CRP values ​​above 10 mg/l to detect neonatal sepsis is 90%. Normalization of CRP may be a good indicator of successful treatment of the infection. On the dynamics of CRP indicators, the determination of the duration of antibiotic therapy can be based. After the cessation of the inflammatory reaction, due to the relatively short half-life from the blood (about 19 hours), the level of CRP decreases rapidly and returns to normal values ​​in most children within 5-10 days.

The sensitivity of CRP at the onset of sepsis is 50-90%, the specificity is 85-95%. The sensitivity of the assay increases dramatically if the first assay is done 6-12 hours after birth. Two normal CRP values ​​(<10 мг/л) - первое через 8-24 ч после рождения, а второе спустя 24 ч - позволяют на 99,7% исключить сепсис.

Many other conditions (asphyxia, RDS, maternal fever, prolonged anhydrous period, IVH, meconium aspiration, viral infection) can also cause similar changes in CRP levels. In addition, approximately 9% of healthy newborns have CRP levels >10 mg/l.

Procalcitonin is a precursor of the hormone calcitonin, which has a hypocalcemic effect. Basically, procalcitonin is produced in the neuroendocrine C-cells of the thyroid gland. In severe systemic infection, procalcitonin is probably produced by tissues outside the thyroid gland (monocytes and hepatocytes). The sensitivity of procalcitonin in bacterial infections is the same as CRP or slightly higher, but more specific. For children under the age of 48 hours, the sensitivity of an increase in procalcitonin in relation to the diagnosis of early neonatal sepsis was 92.6%, and the specificity was 97.5%. It was also noted that the level of procalcitonin increases 3 hours after the administration of the bacterial agent, while CRP appears only after 12-18 hours.

Procalcitonin is a qualitative marker for distinguishing septic shock from shock of a different nature, although sometimes there are cases of an increase in the concentration of procalcitonin in RDS, trauma, hemodynamic disorders, perinatal asphyxia, intracranial hemorrhage, gestational diabetes, and also after resuscitation.

Methods not included in routine clinical practice:

• Pro-inflammatory cytokines IL-6 and IL-8.
• Iaip (Inter-alpha Inhibitor Protein).
• Serum amyloid (SAA).
• strem-1.
• Surface antigens of blood cells.

Other methods for diagnosing infectious diseases

Serological methods. The detection of antigens and antibodies by serological methods has not become widespread in the diagnosis of infections in newborns due to the insufficient accuracy of the results obtained or the difficulty of reproduction.

Molecular Diagnostics. Polymerase chain reaction and hybridization method for the detection of bacterial genomes make it possible to quickly identify any infectious agents based on the identification of a specific region of the genome that is present in bacteria but absent in humans. The sensitivity of molecular diagnostic methods for sepsis can be higher than culture methods, ranging from 41 to 100%, with most studies showing values ​​between 90 and 100%, and specificity in the range of 78-100%.

Heart rate variability monitoring. A number of studies have shown a high dependence of heart rate variability on the degree of maladaptation of the body, which is possible under various conditions, including sepsis. A change in heart rate was the first sign in newborns, recorded 24 hours before the first clinical signs of sepsis. Continuous monitoring of the heart rate may contribute to earlier detection of infection and early initiation of antibiotic therapy.

The advantage of this method may be the possibility of continuous and non-invasive monitoring and high information content in the early stages of diagnosis.

conclusions

So far, none of the current markers of the infectious process can unequivocally diagnose cases of infection by 100%. Many serious localized infections (such as pneumonia, deep abscess, ventriculitis) may require antibiotic therapy, but blood markers may be normal. For the early diagnosis of sepsis in clinical practice, sensitivity is more important than specificity, as the consequences of inappropriately treating an uninfected newborn are less harmful than not treating an infected child.

Diagnostic tests are more effective in follow-up than in a single study.

Microbiological diagnostics

The "gold standard" is the isolation of the pathogen from the usually sterile environments of the body, for example, from CSF, blood. Isolation of microorganisms from other places can only speak of contamination.

If sepsis is suspected, at least 1 blood culture should be taken. The minimum blood volume required for culture on the medium is 1.0 ml for all newborns with suspected sepsis.

Currently (in countries where mothers are given antibiotic therapy to prevent neonatal sepsis), the number of positive blood cultures in newborns with RNS has decreased to 2.7%. Other reasons for the rare isolation of cultures from biological fluids (blood, CSF) are the inconsistency of bacteremia in a newborn, the low density of the pathogen, and the small amount of material taken for sowing. Therefore, blood cultures are currently of little help in confirming neonatal sepsis.

Tracheal aspirate culture. Tracheal aspirate samples may be important if obtained immediately after tracheal intubation. The duration of intubation reduces the value of the study, so if the endotracheal tube is in the trachea for several days, the aspirate samples lose all value.

Isolation of bacteria from superficial areas of the body, from gastric contents and urine in the diagnosis of early sepsis is of no value.

Treatment of intrauterine infections in newborns

Treatment of severe infections can be divided into replacement and antimicrobial therapy.

General stabilization of the state

• Maintain normal body temperature.
• Correction of glucose and electrolyte levels.
• Correction of anemia: the optimal values ​​of red blood for severe infections in newborns are unknown, but it is recommended to maintain a hemoglobin level of 120-140 g / l, hematocrit - 35-45% (the minimum acceptable level of hemoglobin is 100 g / l, hematocrit - 30%).
• Respiratory support depending on the severity of DN: O 2 , nCPAP, mechanical ventilation, iNO, surfactant. It is recommended to maintain the following indicators of blood gases: pH 7.3-7.45, PaO 2 = 60-80 mm Hg. (SaO 2 \u003d 90-95%), PaSO 2 \u003d 35-50 mm Hg.
• Stabilization of hemodynamics (infusion, inotropes / vasopressors, corticosteroids) should be aimed at normalizing blood pressure, the appearance / maintenance of diuresis > 2 ml / kg / h, increasing BE and reducing serum lactate levels.
• DVS therapy.
• Nutritional support/infusion therapy: The enteral route should be used as much as possible. Even minimal enteral nutrition protects the intestinal mucosa and reduces bacterial translocation.

Interventions with questionable effectiveness/understudied

• Intravenous immunoglobulins (enriched with IgM).
• Myelopoietic cytokines (granulocyte colony-stimulating factor - G-CSF and factor stimulating the activity of granulocyte-macrophages - GM-CSF).
• Transfusion of granulocytes in newborns with neutropenia.
• The use of efferent methods of detoxification.
• Pentoxifylline.

Despite the fact that a large number of works of various designs (up to RCTs) performed by domestic authors show a positive effect of drugs such as roncoleukin (recombinant interleukin-2), betaleukin (recombinant interleukin-lb), licopid (glucosaminylmuramyl dipeptide), viferon (recombinant human interferon-α2β) on survival and reduction in hospital stay of newborns of different gestational ages with sepsis and pneumonia, we believe that serious multicenter studies are needed before these drugs can be recommended for routine use.

Activities that have not shown their effectiveness

• Intravenous immunoglobulins (enriched with IgG).
• Activated protein C (Drotekogin-alpha).

Postnatal prevention and etiotropic treatment

The main therapy for infections is the correct selection and timely administration of antibacterial drugs. Antibacterial therapy is prescribed for all children with clinical and laboratory signs of sepsis. The absence of bacteriological confirmation is not a decisive factor for not prescribing antibiotic therapy, especially since bacteriological data appear at best after 48-72 hours. Therefore, the decision to prescribe antibiotics is often made more on the basis of anamnesis data (mainly maternal). A Cochrane review of 2 randomized trials performed in the 1970s does not answer the question of whether asymptomatic newborns with one or more risk factors should receive prophylactic antibiotics. Many authors, based on their own experience, prefer to carry out antibacterial prophylaxis in the presence of risk factors for infection while monitoring the child. In most countries, the protocols used have much in common, differing more in developing countries (mainly in types of antibiotics and timing of therapy). Below is one of the protocols based on the latest recommendations from the Centers for Disease Control and Prevention.

Newborns requiring antibiotic therapy

I. Newborns with clinical signs of sepsis.

Every critically ill or deteriorating neonate should be evaluated to decide whether to initiate empiric antibiotic therapy (previously by blood culture, even in the absence of obvious risk factors for sepsis).

II. A healthy-looking newborn with a high probability of RNS.

GBS is not a risk factor if the mother received adequate antibiotic prophylaxis (penicillin, ampicillin, cefazolin) at least 4 hours before delivery or had a caesarean section with intact membranes in the absence of labor.

1. Newborns with gestational age<37 нед. без клинических признаков сепсиса, но с 1 фактором риска (длительный (>18 hours) anhydrous period, or chorioamnionitis, or inadequate antibacterial prophylaxis of the mother during childbirth):
   • antibiotic treatment;
   • • with a negative blood culture result, good condition child and normal laboratory parameters - stop antibiotic therapy.
2. Newborns with gestational age >37 weeks without clinical signs of sepsis, but with 1 risk factor (chorioamnionitis):
   • antibiotic treatment;
   • laboratory tests (leukocytes, CRP, blood culture at the age of 6-12 hours):
     • with a positive result of blood culture - lumbar puncture, continue antibiotic therapy;
     • with a negative result of blood culture, a good condition of the child, but pathological laboratory parameters - continue antibiotic therapy if the mother received antibiotics during childbirth;
     • with a negative result of blood culture, a good condition of the child and normal laboratory parameters - stop antibiotic therapy and observe for 48 hours.
3. Newborns with a gestational age > 37 weeks. without clinical signs of sepsis and with other risk factors (not chorioamnionitis): prolonged (>18 h) anhydrous period or inadequate maternal antibiotic prophylaxis in labor (use of antibiotics other than penicillin, ampicillin, or cefazolin, or if antibiotic administration was less than 4 h before birth):
   • antibiotic therapy is not carried out;
   • observation;
   • examination (leukocytes, CRP, blood culture at the age of 6-12 hours).

Each region should probably have its own protocol adapted to local conditions.

Etiotropic treatment of bacterial infections

Etiotropic therapy for RNS is almost always empirical. If there is no reason to assume an infectious history of the mother, the microflora is likely to be represented by the usual representatives of the urogenital tract. If the woman was in the hospital before giving birth, the presence of nosocomial flora is likely. Known data on maternal colonization should be taken into account when prescribing antibiotics.

Empiric antibiotic therapy for early infections in developed countries should target GBS, E. coli, and L. monocytogenes. Combination therapy is usually used, including the appointment of penicillins with an extended spectrum of activity (ampicillin or amoxicillin) and aminoglycosides (usually gentamicin or netromycin / tobramycin). In most cases, such treatment “covers” the entire possible spectrum of pathogenic maternal microflora and is inexpensive. At the same time, there are rare reports of the possible emergence of GBS resistance to penicillins. It should be remembered that aminoglycosides do not penetrate the blood-brain barrier well enough, therefore, in meningitis, a combination of ampicillin and third-generation cephalosporins is often preferred. III generation cephalosporins provide concentrations of drugs in most foci of infection, significantly exceeding the minimum inhibitory concentrations of susceptible pathogens (GBS, E. coli and other gram-negative intestinal bacteria) with low toxicity. However, none of the cephalosporins is active against Listeria and Enterococcus and has variable activity against Staphylococcus aureus.

III generation cephalosporins are not usually used as an alternative to aminoglycosides due to a number of features:

• rapid development of resistance to cephalosporins III and IV generations with their widespread use;
• with prolonged use, the risk of developing invasive candidiasis increases significantly;
• ceftriaxone is contraindicated in newborns due to the competitive displacement of bilirubin from protein binding, which can lead to the development of kernicterus.

Therefore, the use of cephalosporins (in the appointment of empirical therapy) is limited to the treatment of meningitis caused by gram-negative microorganisms. Cefotaxime is the safest of the cephalosporins, since it does not displace bilirubin from its association with albumin and does not pose a threat of toxic damage to the central nervous system.

In developing countries, where RNS pathogens differ from those in developed countries, the combination of penicillins and aminoglycosides may not be effective. Therefore, in such countries, empiric antibiotic therapy should be determined individually for each hospital or region.

A review of the literature on antibiotic susceptibility of community-acquired sepsis in Africa and Asia showed that the 2 most common pathogens, S. aureus and Klebsiella spp. - were highly resistant to almost all commonly used antibiotics (such as ampicillin, ceftriaxone, chloramphenicol, cotrimoxazole, macrolides and gentamicin). Good susceptibility to all these agents, except for cotrimoxazole, was demonstrated only by Str. pneumoniae.

Anaerobic microflora may require additional appointment metronidazole.

Once the pathogen is identified, antibiotic therapy should be narrowed down. There is considerable variation in recommendations for the duration of empiric antibiotic therapy for suspected RNS when blood cultures fail, but it is standard practice to discontinue antibiotic therapy when blood cultures are negative (usually 48–72 h) and there is no clinical or haematological evidence of infection.

Duration of treatment

The optimal duration of empirical antimicrobial therapy reduces the development of resistance, prevents unwanted changes in the flora in the NICU, and also minimizes unnecessary costs in negative blood cultures.

Bacteremia requires antibiotic therapy for 10-14 days (for GBS) or at least another 5-7 days after the clinical result is obtained.

Many authors recommend longer antibiotic therapy for negative blood cultures in newborns with suspected RNS and necrotizing enterocolitis. Limited data suggest that a 7-day course of treatment may be sufficient for uncomplicated bacteremia.

Many authors report that short courses of antibiotic therapy (5 days or less) in culture-proven sepsis (excluding meningitis and osteomyelitis) are as good as longer courses. Similar data were obtained with short (4-7 days) courses of therapy for pneumonia. The authors found that reducing the duration of antibiotic therapy did not increase the risk of recurrent infection in infants with early sepsis, while reducing the incidence of late-onset sepsis.

Long duration (>5 days) of initial empiric antibiotic therapy with broad-spectrum antibiotics is associated with an increased risk of necrotizing enterocolitis, late neonatal sepsis, and death in newborns with ELBMT. Other adverse effects of long-term empiric antibiotic therapy include an increased risk of neonatal candidiasis and altered intestinal microflora. The choice of cefotaxime (III generation cephalosporins) over gentamicin in the first 3 days of life is associated with higher mortality. Newborns (especially preterm infants) receiving long-term therapy with broad-spectrum antibiotics (especially cephalosporins) need fluconazole prophylaxis for candidiasis.

Control

The culture should be repeated 24-48 hours after completion of therapy to ensure that the bacteria have been killed. Persistent positive cultures suggest inadequate therapy and/or an existing site of infection (eg, infected infusion line). When determining the duration of antibiotic therapy, one should be guided by the clinical condition of the newborn and a combination of laboratory parameters: the neutrophil index, the total number of leukocytes and CRP, with successful therapy, should begin to normalize after 72 hours.

conclusions

In newborns immediately after birth, in most cases it is impossible to predict the development of infection in advance. Antibacterial therapy in the first days of life is almost always empirical. It is prescribed if there are reasonable assumptions of the development of an infectious process (this is especially true for preterm infants). The scope of "reasonableness" depends on many factors - they can narrow or expand depending on local conditions (qualifications, experience of staff, availability of resources, healthcare organization, etc.). In most cases, ampicillin and an aminoglycoside (gentamicin, netromycin) are sufficient. Subsequently, if data on a bacterial infection are not confirmed, antibiotic therapy is stopped. If the patient's condition does not improve, other causes must be ruled out. serious condition, infections of another etiology or resistance of the pathogen to the prescribed drugs.

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Infections received by a child during fetal life make a significant contribution to the statistics of morbidity, mortality of babies and further disability. Today, there are frequent cases when a seemingly healthy woman (does not smoke, does not drink, does not chronic diseases) an unhealthy baby is born.

What explains this? During pregnancy, a woman's immunity decreases, and some latent (latent) infections that do not manifest themselves before pregnancy are activated (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 babies born have some form 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 or asymptomatic in the mother.
• Infection of the fetus most often occurs with the first infection in the mother
• Timely treatment of a pregnant woman can reduce or eliminate the risks to the fetus.

How is the fetus infected?

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

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

The pathogen passes 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, then the newborn shows signs of acute infection. Direct entry of the pathogen into the baby's blood leads to a generalized lesion.

• Ascending - mycoplasma, chlamydia, herpes

The infection goes from the mother's genital tract to the child. This usually happens after the rupture of the membranes, at the time of childbirth, but sometimes it 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).

Common causative agents of intrauterine transplacental infection

Most viruses and bacteria known to man are able to penetrate the fetus and cause various damage to it. But some of them are particularly contagious or pose an increased danger to the child. Some viruses (almost all that cause SARS) are not transmitted to the baby, but are dangerous only with a strong increase in the temperature of the pregnant woman.

Consequences of intrauterine infection for a child

Congenital infection can develop according to 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 received in the womb is sluggish or has no obvious symptoms. Such children are also at risk for long-term consequences: hearing and vision impairments, delayed mental and motor development.

Common symptoms of intrauterine infections

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

• intrauterine growth retardation
• Micro- and hydrocephalus
• Chorioretinitis, cataract (eye damage)
• Pneumonia
• Jaundice and liver enlargement
• Anemia
• Dropsy fetus (edema)
• Rash on the skin
• Fever

At what stage of pregnancy is the 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 when 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 occurring infectious disease in the newborn. More specific risks and the degree of danger are determined by the attending physician based on the results of tests, 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
• Employees 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 an infection in a pregnant woman

• temperature rise
• Enlarged and sore 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-communicable diseases, or infections that are not dangerous for the baby. But any signs of ill health should be noticed by a pregnant woman and are a reason to see a doctor.

Common causative agents of intrauterine infection

Viruses

	Infection of the mother	Consequences for the child
Rubella	airborne way	fetal rubella syndrome
Cytomegalovirus	Through biological fluids: blood, saliva, semen, urine	Congenital CMV infection (with or without symptoms)
Herpes simplex virus 2	Predominantly sexual way	congenital herpes infection
Parvovirus B19	airborne way	Anemia, fetal dropsy
Chicken pox	Airborne, contact-household way	Malformations with early infection, congenital chickenpox with infection before childbirth
	airborne way	Spontaneous abortion, congenital measles
Hepatitis B, C	Sexual way	Neonatal hepatitis, chronic carriage of the virus
	Sexual route, injection route	Congenital HIV infection

bacteria

Protozoa

CMV

CMV, belonging to the group of herpes viruses, is transmitted sexually and through the blood during transfusion and other interventions, as well as through close household contacts. It is believed that half of the women in Europe have experienced this virus at least once in their lives. To the placenta, it often penetrates during the primary infection of the mother.

But the activation of a dormant infection can harm the child (see). The most likely infection of the fetus in the 3rd trimester, and the consequences for the baby are more severe when infected at the beginning of pregnancy. It is believed that the risk of infection of the fetus is 30-40%. Of these, 90% of children will have no symptoms and 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 their increase in size)
• pneumonia
• optic nerve atrophy (blindness of varying degrees)

With a severe combined lesion, 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 better.

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

CMV is not an indication for termination of pregnancy, as the outcome for the newborn may be good. Therefore, it is recommended to treat a pregnant woman in order to reduce the risk of complications.

HSV

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

Children from mothers who had herpes during pregnancy for the first time in their lives get sick more often. Infection in most cases occurs at the time of passage of the child through the birth canal, but transplacental transmission is also possible.

Consequences of congenital herpes:

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

Usually, 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 the development of encephalitis, meningitis and atrophy of the substance of the cerebral cortex is likely. Therefore, severe congenital herpes makes a large contribution to the number of children with disabilities (cerebral palsy, mental retardation, vegetative state). With all the danger of the disease, it is not uncommon for a child to be born without symptoms of herpes, or to have minor damage to the eyes and skin.

Treatment of pregnant women is carried out most often in the 3rd trimester with antiviral drugs (acyclovir, valaciclovir and others). Since with severe rashes on the genitals of a woman 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

The rubella virus is considered one of the most dangerous viruses that cause deformities in the fetus. The risk is especially high at gestational age up to 16 weeks (more than 80%). The symptoms of the disease depend on the period at which the virus entered 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, it is recommended that all women before planning a pregnancy be tested for immunoglobulins to it. If it turns out that there is no immunity to the disease, then at least three months before pregnancy, you must be vaccinated. There is no cure for rubella during pregnancy and in newborns.

Parvovirus B19

The virus that causes erythema infectiosum usually goes unnoticed in adults. Symptoms of infection are often absent. But during pregnancy, this disease can lead to miscarriages, stillbirths and intrauterine infection. Mortality in children is 2.5-10%. The maximum danger of the virus is from 13 to 28 weeks of pregnancy.

Consequences of intrauterine infection:

• anemia
• edema
• myocarditis
• hepatitis
• peritonitis
• brain damage

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

With confirmed infection and fetal anemia, intrauterine administration of red blood cells is recommended. This technique often allows you to increase the level of red blood cells and save the life of a child.

Chicken pox

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

Symptoms of congenital chickenpox:

• rash, zigzag scarring
• limb underdevelopment (shortening and deformation)
• optic nerve atrophy, underdevelopment of the eyes
• brain damage (underdevelopment)
• pneumonia

During pregnancy, upon contact with a patient with chickenpox, it is possible to administer immunoglobulin or antiviral treatment (acyclovir). Treatment of newborns is impractical, since the symptoms of chickenpox do not progress after birth. Only when 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, which is spread mainly through sexual contact, can cross the placenta to the fetus at any stage of pregnancy. Nevertheless, the maximum danger to the child occurs when the mother becomes infected with hepatitis in the 3rd trimester.

Consequences of intrauterine infection with hepatitis:

• miscarriage, stillbirth
• lightness,
• delayed psychomotor development
• acute form of hepatitis with liver failure and death
• carriage and chronic hepatitis B
• liver cancer
• hepatitis B followed by recovery

To diagnose hepatitis in the mother, the level of HBsAg is determined, which rises 1-2 months after infection. When chronic disease or carriage of the virus, this antigen does not disappear. Treatment of severe forms of hepatitis is carried out with the help of interferon-A. But even in the absence of symptoms, a pregnant woman can pass the disease on to her child, so special monitoring is required for such newborns.

HIV infection

The human immunodeficiency virus, which infects special immune lymphocytes, has recently captured more and more new territories. Most adult women become infected with it through sexual contact, while almost all children under 13 years of age got the disease during fetal life or at the time of childbirth.

Many children with HIV do not survive more than two years without appropriate treatment, as the rate of reproduction of the virus is very high. Subsequently, babies die from opportunistic infections that are not terrible 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 the refusal of breastfeeding, increases the chances of having a healthy baby up to 90%. If the results of the blood test for HIV in the child are still positive, there is still a chance to slow down the disease for a long time. Recently, there is more and more data on cases of complete recovery of children who regularly took medication from birth.

Listeriosis

Listeria is one of the few bacteria that can cross the placental barrier. A woman becomes infected with listeriosis by eating meat, cheeses, vegetables and contact with animals. A pregnant woman may not notice any symptoms, and 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 the 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 for 2 weeks with ampicillin. The same treatment of intrauterine infection is necessary for sick newborns.

Syphilis

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

The disease of the mother after the primary ulcer passes into a latent phase with periodic exacerbations. The fetus can become infected even in the absence of bright symptoms in the mother, starting from the 4th month of pregnancy.

Consequences of infection with syphilis:

• stillbirth
• anemia, jaundice
• skin cracks, rashes of various shapes
• lesions of the eyes, ears, limbs, teeth ("Hutchinson's teeth")
• deafness
• impaired mental function

With positive test results for intrauterine infection, penicillin therapy is performed. Treatment of a pregnant woman is mandatory, as it helps to prevent or cure syphilis in the fetus before delivery. With a positive reaction to syphilis in a newborn, he is also shown penicillin preparations. In connection with effective diagnostics and simple therapy, the number of children with late congenital syphilis is currently negligible.

Toxoplasmosis

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

What is TORCH infection?

Toxoplasmosis, rubella, cytomegalovirus, herpes and some other diseases (syphilis, tuberculosis, etc.) are united under the term TORCH not by chance. All these infections are extremely dangerous during intrauterine infection, 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 pass tests for immunity to TORCH. The presence of IgG in the required titers indicates a stable immunity to a previous infection. The absence of such 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 testing of a partner for herpes and cytomegalovirus. A high IgM titer indicates an acute infection. Such women are advised to postpone pregnancy planning.

During pregnancy, the appearance

During pregnancy, IgM can indicate infection, which theoretically leads to intrauterine infection of the fetus. Such women will have to pass 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 smears from the vagina for microflora
• PCR to detect viruses in blood

ultrasound

Fetal ultrasound is a simple, safe, although not completely accurate method for diagnosing infection. According to its results, it is possible to assess intrauterine growth retardation, to 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 pyelocaliceal system of the kidneys
• intrauterine growth retardation syndrome
• placental edema, amniotic bands
• much or little water
• formed malformations

All of the above signs can be the result of non-communicable 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 a 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 are no IgM or IgG in sufficient titers - the woman has not experienced an infection, or has experienced 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 examination of the blood of a newborn is difficult, since it contains maternal antibodies that distort the picture.

Cordocentesis and amniocentesis

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

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

They allow to detect intrauterine infection in children with varying degrees the severity of symptoms.

Treatment and monitoring for intrauterine infection

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

Medical treatment

Bacterial diseases in a woman in position can and should be treated with antibiotics. Quite often they use penicillin series They are safe and effective in many diseases. A newborn baby with signs of bacterial infections is also injected with antimicrobials, which often saves a life and prevents complications.

Viral invasions are treated worse both in pregnant women and in newborns. Some drugs (acyclovir, valaciclovir and others) are used for herpes sores and some other diseases. If treatment helps quickly, then serious malformations and congenital infections can be prevented. Formed consequences in the form of defects of the heart, brain and other organs of treatment antiviral agents are not subject.

Choice of 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 routes.

Surveillance of 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 up to 5-6 years.

Treatment of formed defects and injuries in intrauterine infections in newborns

Many birth defects(CHD, cataract) can be reduced or eliminated by surgery. In such cases, the child gets a chance for life and independent activity. Often children require hearing aids many years after infection, as hearing loss is quite common among those infected.

Prevention of fetal infection

• Vaccination of children and adult women before pregnancy planning
• Caring for women's health
  • limiting contact with children, especially in educational institutions
  • restriction of visits to crowded places
  • careful contact with pets, avoiding cleaning the cat litter box
  • nutrition with thermally processed foods, the exclusion of soft cheeses and semi-finished products
  • an adequate method of protection against infection during sexual intercourse
• Determination of the level of immunoglobulins for the main intrauterine TORCH infections before pregnancy planning

What to do when in contact with infected people?

If a woman during pregnancy communicated or was close to an infected adult and child for a long time, then you should contact your doctor. For example, upon contact with rubella, the presence of IgG is immediately checked. Their presence speaks of persistent immune protection for both the pregnant woman and the baby. The absence of such antibodies warrants further testing 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 surveys(ultrasound, cordocentesis and others).