Is Coxsackie virus dangerous for pregnant women? Effect on the fetus, treatment methods. Enterovirus infection: symptoms and treatment in pregnant women. Is enterovirus infection dangerous for pregnant women?

The route of transmission of Coxsackie enterovirus during pregnancy, as well as pathogens from the ECHO group, is from person to person. The following mechanisms of infection are distinguished:

• airborne;
• contact and household;
• fecal-oral.

The peak incidence of diseases occurs in the period August - October.

Enterovirus enters the body through the mucous membranes of the mouth, pharynx, and gastrointestinal tract. This is often accompanied by an inflammatory process localized in this location:

• enteroviral diarrhea;
• nasopharyngitis;
• herpangina.

After suffering from the disease, the patient develops a strong immunity to it. There are often crossovers immune reactions with other virus serotypes.

Symptoms and signs of enterovirus infection in pregnant women

The clinical course of the disease depends on the type of infection. The incubation period can last up to 10 days, but most often it is 2-3 days. The following signs are characteristic of all enteroviral infections:

• General intoxication syndrome - febrile state, weakness, aching joints, headache, chills, diarrhea, vomiting.
• Catarrhal syndrome - sore throat, conjunctivitis, pharyngitis, pain when swallowing.
• Relapses - after almost complete recovery, the disease again manifests itself in full force.

The following typical forms of enterovirus infection are present:

Much less common are the clinical types - serous meningitis, encephalitis, myelitis, enteroviral pericarditis, myocarditis.

For accurate diagnosis virological and serological studies are used.

Treatment of enterovirus infection during pregnancy

There is no etiotropic therapy, that is, there are no drugs aimed at combating a specific form of enterovirus infection.

For treatment, symptomatic and restorative medications are prescribed. This also applies to situations where it is recorded enterovirus infection at 14 weeks of pregnancy or in the last trimester.

If necessary, anticonvulsant therapy and nootropic drugs are prescribed. Antibiotics are prescribed to prevent bacterial infection.

Consequences of enterovirus infection for mother and fetus

It has been established that with proper treatment of enteroviruses during pregnancy in the 1st, 2nd, 3rd trimesters, there is no infection of the fetus. It is recorded in situations where the patient’s disease occurs in a latent form. This is what is associated with the manifestation of sudden infant death syndrome.

As tick-borne encephalitis enterovirus infection in the 2nd trimester of pregnancy has quite serious consequences. Therefore, it is necessary to take maximum measures aimed at preventing tick bites. It is better to avoid walking in the forest or on the grass in park areas.

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The data presented showed that the wide prevalence of viral infections, both acute and chronic, indicates the need for virological examination of newborns for a representative group of viruses, and not for a specific viral or specific taxonomic group of viruses. Chronic, predominantly enteroviral, infections occupy a leading place in the etiological structure of intrauterine viral infections and the associated pathology of the mother, fetus, and newborn. Failure of adaptation to viruses that persist in a woman’s body is the most common cause of antenatal fetal death, congenital and perinatal pathology, prematurity and perinatal mortality. A chronic form of congenital viral infection in newborns can be suspected already when collecting anamnesis in the presence of such high-risk factors for viral transmission as spontaneous miscarriages, premature birth, chronic diseases in the mother and their exacerbation during pregnancy, as well as a complicated course of the present pregnancy, which proceeded with a threat interruptions, gestosis, acute respiratory diseases, exacerbations of viral infections and contact with infectious patients.

placental insufficiency

enterovirus infections

pregnancy

1. Beznoshchenko G.B. Intrauterine infections (Diagnosis and medical tactics). – M.: Medical book, N. Novgorod: BSMA, 2003. – 87 p.

2. Glinskikh N.P., Patsuk N.B. Perinatal viral infections (etiopathogenesis, diagnosis, treatment and prevention). – Ekaterinburg: ENIZHI; AMB, 2001. – 128 p.

3. Kitsak V.Ya. Viral infections of pregnant women: pathology of the fetus and newborns - Koltsovo, 2004. - 70 p.

4. Samoilova A.V. Intrauterine infection in the structure of morbidity and mortality of newborns // Mother and Child: sat-ly II region, scientific forum. – Sochi, 2008. – pp. 252–253.

5. Giraldo P., Neuer A., ​​Korneeva I.L. Vaginal heat shock protein expression in symptom-free women with a history of recurrent enteroviruses an infection // Am.J.Obstet. Gynecol. – 2006. – Vol. 180, No. 3. – R. 524–529.

6. Kozovsky I. Cesarean section in modern obstetrics and methods of prophylaxis of prospective sepsis // Akush. Ginecol (Sofia). – 2007. – Vol. 39, No. 3. – R. 3–6.

Viral infections are considered probable cause development of about 80% of congenital malformations. Central nervous system defects account for 26-30% of all defects found in children. May be associated with various intrauterine viral infections birth defects hearts, which are included in the triad of defects in rubella. The results of a virological and clinical-epidemiological examination of 62 children with congenital heart defects indicated that congenital heart defects are etiologically associated with transplacental transmission of Coxsackie group enteroviruses from mothers with a persistent form of the corresponding infection. According to Kitsak V.Ya. , enteroviruses are found in 75% of children with congenital heart defects. It should be noted that the mothers of these patients had a history of chronic diseases in which the persistence of enteroviruses of the Coxsackie group was established.

A comprehensive study of the species composition of microorganisms in the birth canal, amniotic fluid, placenta, newborn, determination of antigens and antibodies to the putative pathogen in umbilical cord blood and amniotic fluid, histological examination of the placenta allows us to determine the route of infection of the child, the nature of the pathogen and clarify the scope of additional diagnostic procedures and treatment. preventive measures in the early neonatal period.

The purpose of the study is to give comparative assessment the condition of newborns born from mothers with mixed viral infection in modern conditions of Baku.

Materials and research methods

A comprehensive virological examination was carried out for the representation of the most common viruses using the enzyme immunoassay method (ELISA) and the method of indirect immunofluorescence of 54 newborns (main group) from mothers with a mixed viral infection and who had congenital and perinatal pathology: congenital anomalies of the development of internal organs (heart, kidneys, brain, liver), perinatal encephalopathies (hypertensive-hydrocephalic and convulsive syndromes), and 40 practically healthy newborns (control group).

The work was carried out on the basis of the Central Research Laboratory of the Azerbaijan Medical University. The entire procedure for diagnosing viral infections was carried out by laboratory specialists, which used ELISA and indirect immunofluorescence methods. Diagnosis of viral infections was carried out by determining class M and G antibodies to the corresponding viruses using the enzyme immunoassay method using standard test systems of Vector-Best JSC (Novosibirsk) on a Stat-Fax 2100 spectrophotometer (USA).

Grade functional state The “mother-placenta-fetus” system was carried out using ultrasound, Doppler studies and cardiotocography. All patients underwent ultrasound fetometry, placentography, assessment of the quality and quantity of amniotic fluid according to the generally accepted method, Doppler study of uteroplacental, fetal placental and fetal blood flow.

Statistical processing of the research results was carried out using generally accepted methods of variation statistics. The Student's reliability criterion, the reliability of differences, and the calculation of the arithmetic mean were determined. The significance of the differences (p) was determined by the parametric reliability criterion.

Research results and discussion

According to a retrospective analysis of medical records for the period from 2007 to 2011, 83 pregnant women were diagnosed with EVI of varying severity. It was found that most often the symptom complex of enterovirus infection (EVI) was determined in pregnant women in the first trimester - 41 (50.0%) sick women (subgroup IA), in the second trimester - 30 (37.0%) pregnant women fell ill (subgroup IB) and in the third trimester - 12 (13.0%) pregnant women (subgroup IC). 52.6% of pregnant women resorted to treatment at home, and only 47.4% of pregnant women were under the supervision of doctors in a antenatal clinic (general practitioner and obstetrician-gynecologist), clinic, or were treated in a hospital (Fig. 1).

Rice. 1. Frequency of detection of the EVI symptom complex in examined women by trimester of pregnancy

During pregnancy, in addition to non-specific manifestations of EVI, there was a symptom complex with fever and acute pain in the lower abdomen, which was often interpreted as premature placental abruption or acute appendicitis, but in fact it was a symptom of acute viral mesadenitis. Of 83 pregnant women with EVI with a temperature of more than 37.1 to 39 °C, the disease progressed in 79 (65.0%) patients. In the first trimester, in 45 (37.0%) pregnant women, the disease occurred with fever and acute pain in the lower abdomen.

Analysis of medical documentation for 2007-2011. showed that the threat of miscarriage developed in 54 (65.0%) pregnant women with EVI: in the first trimester, the threat of miscarriage developed in 34 (41.0%) pregnant women with EVI, in the second trimester in 28 (22.0%) pregnant women with EVI, and in the third trimester in 4 (4.0%) pregnant women with EVI. 31.0% of pregnant women required inpatient treatment. According to ultrasound data, intrauterine infection of the fetus was suspected in 22 (27.0%) pregnant women. This complication was suspected in the first trimester in 14 (35.0%) pregnant women of subgroup IA, in the second trimester in 6 (17.0%) pregnant women of subgroup IB, and in the third trimester in 2 (17.0%) pregnant women of subgroup IC.

It is known that an indicator of a high risk of vertical transmission of viruses is intrauterine fetal hypoxia, in which the reproduction in its tissues of almost all viruses that enter the fetal body during pregnancy increases. All newborns were diagnosed with enterovirus infection, which was represented by Coxsackie A and B, Polio 1-3 and Entero 68-71 viruses. In 97.5% of patients, a mixed enteroviral infection was registered, and from 2 to 6 viral antigens were detected simultaneously. Cytomegaly viruses (87.5%), herpes simplex 1 and 2 (70.0%), influenza (62.5%) and rubella (32.5%) were detected in patients only against the background of enterovirus infection (Fig. 2).

Rice. 2. Etiological structure of viral infections in newborns of the main group. Legend: 1 - mixed enteroviral infection; 2 - cytomegaly viruses; 3 - herpes simplex viruses type 1 and 2; 4 - influenza viruses; 5 - rubella viruses

In healthy newborns of the control group, enteroviruses were found in 10%, and cytomegaly viruses (10%) and herpes simplex viruses (15%) were not associated with picornoviruses.

Among the 54 newborns we examined, 31 children had congenital malformations (heart defects in 21 patients, malformations of the urinary system in 6, malformations of the central nervous system in 4). All children with congenital malformations were diagnosed with enterovirus infection, which was often combined with cytomegalovirus, herpetic and influenza infections. In congenital heart defects, the rubella virus was also detected in 42.8% of cases.

Perinatal lesions of the central nervous system, occlusive meningoencephalitis and hydrocephalus were detected in 49 examined newborns. During a virological examination of newborns with lesions of the central nervous system, as well as with developmental defects, enteroviruses were most often found (in 100% of cases), herpes (in 62.5-75% of cases), cytomegalovirus (in 75.3-87.5 % of cases) influenza (59.4-87.5%) infections (table).

Etiology of congenital infections of viral origin in newborns with lesions of the central nervous system

Viral infections	Perinatal lesions of the central nervous system		Hydrocephalus occlusive	Inflammatory diseases
Number of patients	Hypertensive-hydrocephalic syndrome (n = 49)	Convulsive syndrome (n = 6)
Enteroviral
Flu-like
Herpes simplex
Cytomegaly
Rubella

Thus, the results obtained showed that in the etiology of perinatal lesions of the central nervous system and congenital malformations of the central nervous system, urinary system and heart, the leading role belongs to associations of viruses, among which enteroviruses are of greatest importance. The above data suggest a relationship between anamnestic data, complications during pregnancy and childbirth, with the subsequent manifestation of intrauterine infection.

Conclusion

So, chronic predominantly enteroviral infections occupy a leading place in the etiological structure of intrauterine viral infections and the associated pathology of the mother, fetus, and newborn. Failure of adaptation to viruses that persist in a woman’s body is the most common cause of antenatal fetal death, congenital and perinatal pathology, prematurity and perinatal mortality. The main reasons for failure of adaptation: (1) - relatively high initial (before conception) level of activity of endogenous enterovirus infection, (2) - activation of endogenous enterovirus infection due to physiological restructuring of the immune system, (3) - acute infectious diseases during pregnancy.

The main links in the pathogenesis of chronic enterovirus infection in women, which determine the high risk of miscarriage, as well as congenital and perinatal pathology of the fetus and child: 1 - histotoxic hypoxia associated with the toxigenic activity of the virus, 2 - a virus-induced immunopathological process with pronounced autosensitization, 3 - immunodeficiency state, associated with the immunosuppressive activity of the enterovirus.

The widespread prevalence of both acute and chronic viral infections indicates the need for timely virological examination of newborns for a general group of viruses, and not for any specific taxonomic group of viruses. Directly when collecting an epidemiological history in the presence of corresponding high-risk factors for viral transmission, such as spontaneous miscarriages, chronic viral diseases of the mother and their exacerbation during this pregnancy, premature birth, stillbirth, as well as a complicated course of this pregnancy, which occurred with gestosis, threat of miscarriage, exacerbation herpetic diseases, acute respiratory infections and close contact with infectious patients can be suspected chronic form congenital viral infection in newborns.

Reviewers:

Agaev I.A., Doctor of Medical Sciences, Professor, Head of the Department of Epidemiology of AMU, Ministry of Health of the Republic of Azerbaijan, Baku;

Niftullaev M.Z., Doctor of Medical Sciences, Professor of the Department of Epidemiology of the AMU, Ministry of Health of the Republic of Azerbaijan, Baku.

The work was received by the editor on February 18, 2014.

Bibliographic link

Heydarova N.F. ASSESSMENT OF THE INFLUENCE OF ENTEROVIRAL INFECTION ON THE CONDITION OF NEWBORNS // Fundamental Research. – 2014. – No. 4-1. – P. 72-75;
URL: http://fundamental-research.ru/ru/article/view?id=33669 (access date: 02.22.2020). We bring to your attention magazines published by the publishing house "Academy of Natural Sciences"

Wikipedia gives the following definition of enterovirus infections: “This is a group of infectious diseases caused by various serotypes of enteroviruses from the picornavirus family. The name enteroviruses is associated with their reproduction in the intestines, but they rarely cause clinical enteritis.” This natural feature gave rise to the name “enterovirus” for the entire large group of viruses. Infection caused by these viruses has varied and numerous clinical manifestations.

Picornaviruses also include a virus that causes the corresponding disease, but active immunization helps prevent this infection. IN last years There has been a significant increase in diseases caused by non-polimyelitis enteroviruses. The relevance of identifying and treating this type of infection lies in the fact that they are uncontrollable due to significant variability and polymorphism, a high frequency of asymptomatic forms, prolonged viral carriage and the lack of specific prevention. The same pathogen can cause several clinical manifestations, and one syndrome can be caused by several types of enteroviruses. The same type of enterovirus can cause mild and extremely severe forms with damage to the nervous system. One type of virus can cause isolated diseases and large epidemics.

The incidence is recorded throughout the year, but spring-summer seasonality is more typical. Enteroviruses have been proven to be highly contagious and children aged 3 to 10 years are susceptible to their effects. About 85% of cases of infection are asymptomatic, and in 3% of cases a severe course is observed - this applies to young children and people with immunodeficiency conditions. Every 4 years, there are outbreaks of the disease caused by different serotypes of viruses. The serotypes dangerous to humans change every year.

Pathogenesis

The entry gate for viruses is the mucous membrane of the nasopharynx and intestines. Enteroviruses, which do not have a protein shell, easily pass the “gastric barrier” and concentrate on the cells of the intestinal mucosa. Their reproduction occurs in the lymphatic system of the intestine or nasopharynx (if the oral mucosa served as the entrance gate), and then the viruses enter the blood (viremia stage) and are spread throughout the body.

Possessing high degree tropism for many tissues (especially nervous and muscle tissue, including the myocardium), viruses cause characteristic clinical manifestations. At the same time, various organs are also involved in the process: the heart, eye vessels, liver, lungs, kidneys, intestines, which further expands the clinical picture of the infectious disease. By fixing on various tissues and organs, viruses cause swelling, inflammatory dystrophic and necrotic changes - that is, a secondary infection of target organs occurs. Clinically, this is manifested by a rash, isolated respiratory tract infection (ARVI), liver necrosis , And so on. The process of inflammation (systemic or organ) is triggered by products of free radical oxidation and proinflammatory cytokines .

Thus, three stages can be distinguished in pathogenesis:

• Impact of the virus on lymphatic system nasopharynx and intestines, which manifests itself in the clinic, and.
• Viremia, which is accompanied by fever and intoxication.
• Damage to various organs.

In response to exposure to viruses, immune restructuring occurs - immune reactions ( leukocytosis , increased number of monocytes and neutrophils active in phagocytosis).

Classification

By type of disease.

Typical shapes:

• damage to the nervous system;
• herpangina ;
• enteroviral fever;
• myalgia ;
• enterovirus;
• heart damage;
• respiratory form;
• hepatitis ;
• eye lesions;
• gastroenteric;
• hemorrhagic cystitis , orchitis , epidymitis ;
• vesicular stomatitis .

Atypical forms:

• erased;
• asymptomatic (the virus is in the intestines and does not penetrate the blood).

Mixed forms:

• combination and myalgia ;
• meningitis and herpangina ;
• exanthema And herpangina .

According to severity:

• light form;
• moderate severity;
• heavy.

According to the presence of complications:

• uncomplicated form;
• complicated.

Causes

As we found out, the cause of the infection is infection with enteroviruses, which are widespread everywhere. Microbiology defines enteroviruses as RNA-containing, small in size, heat-stable and resistant to acidic environments, bile and digestive juices. At a temperature of 37 C they remain viable for up to 65 days. When frozen, their activity remains for many years and is not lost during repeated freezing and thawing.

Overall genus Enterovirus includes more than 100 viruses dangerous to humans, including the virus and non-polimyelitis enteroviruses ( Coxsackie A And IN , ECHO, enteroviruses A , IN , WITH , D ), which cause infections with a polymorphic clinical picture. It could be ARVI, diarrhea , conjunctivitis , enteroviral exanthema , herpangina , damage to the nervous system ( meningitis , ), transverse myelitis . Factors that contribute to the disease are a decrease in local ( local immunity mucous membrane) and general protection body.

Epidemiology

Of greatest epidemiological significance are enterovirus Coxsackie A , IN And ECHO . The source of infection is a sick or asymptomatic carrier of the virus. Among children, the percentage of virus shedding is 7-20%, and in those under 1 year of age - 32.6%. It is healthy virus carriage that causes the constant occurrence of sporadic and widespread forms of diseases. The following factors are of great importance in the constant circulation of viruses: long-term virus carriage and the presence of susceptible populations. The risk of outbreaks increases when significant enteroviral contamination is “released” into the population.

In external environment pathogens are released from the patient’s intestinal tract (their main habitat and reservoir) and the nasopharynx (when coughing and sneezing). The virus is found in wastewater, water bodies, soil, and on products. Due to its high resistance to many factors, the pathogen persists for a long time in water and other environmental objects. Overcoming the water treatment barrier at stations, it enters the water supply network. It spreads quickly in the body, withstanding the action of gastric juice.

How is enterovirus infection transmitted? The main mechanism is fecal-oral, which is realized in various ways:

• Contact-household - infection through dishes used by the patient or through toys.
• Aquatic - when swimming in ponds or pools and ingesting water infected with a virus. Water transmission plays a leading role in the emergence of seasonal outbreaks, and this is facilitated by the asymptomatic carriage of enteroviruses by a wide range of people, their constant release in the environment and their almost constant circulation.
• Food - consumption of food contaminated with a virus or raw water. The factor of “dirty hands” is also important, as the main one in the transmission of pathogens among children. The virus thus enters the body through the mouth, nose or eyes.
• It is transmitted less frequently by airborne droplets (by sneezing and coughing with droplets of saliva).
• Separately, one can distinguish transplacental, when the enterovirus is transmitted from a pregnant woman to the fetus. Moreover, a woman does not necessarily have to experience the infection during pregnancy - it is enough to have it in a persistent form. Sudden infant death has been associated with congenital infection.

Direct contact with feces occurs when changing babies and diapers, making infants the most common transmitters of the virus. Indirect transmission occurs through contaminated water, food and household items when sanitary standards are not met. There are cases of infection from swimming in seawater contaminated by sewage.

The incubation period has different periods, which depend on the state of the human immune system and the characteristics of the type of virus. On average, its duration ranges from 2 to 10 days.

How long is a person contagious?

The most intensive release of the virus occurs in the first days of the disease. These days the pathogen is released in the highest concentrations. Considering that the virus is detected in the sick person several days before the onset of symptoms and the virus is excreted in the feces for another 3 weeks, it turns out that the person poses a danger for at least 3-4 weeks. It has been established that the duration of residence of viruses in the intestines is no more than 5 months. However, it is difficult to definitively establish how many days a sick person remains dangerous, since in immunodeficient individuals the virus can be excreted for several years, which means this contingent poses a danger in terms of infecting others.

Symptoms of enterovirus infection

How does enterovirus infection manifest? It depends on the pathogen and signs of enterovirus can manifest as lesions:

• Respiratory tract ( acute respiratory infections , herpangina , pneumonia ). Caused by viruses Coxsackie A And B , enterovirus type 71, certain viruses ECHO. The lesions are characterized by either catarrhal symptoms of the upper respiratory tract, or interstitial pneumonia, or conjunctivitis.
• Nervous system (enteroviral meningitis , encephalitis ,transverse myelitis ). The causative agents of meningitis in the last 10-20 years are viruses ECHO 30 And ECHO 11. The most common recorded form of enterovirus infection was serous meningitis (66.1%). Poliomyelitis-like diseases are caused by Coxsackie A7 and enterovirus type 71.
• Muscular system - viruses Coxsackie B3 And B5 have myotropism (that is, they affect muscles).
• Cardiovascular system with development myocartitis , paricarditis , endocaditis .
• Skin - enteroviral exanthema or disease " hand, foot and mouth disease» (rash on arms, legs, in and around the mouth). The most common pathogens are Coxsackie A5 , 11 , 16 , 10 , B3 And enterovirus 71 (EV71 infection).
• Gastrointestinal tract - enteroviral diarrhea , called Coxsackie A (18, 20, 21, 22, 24) and three types ECHO (11, 14, 18).
• Eye - causes enterovirus type 70 .

The most common forms that occur without damage to the nervous system include respiratory diseases, herpangina , meningitis-like form, epidemic myalgia .

Enteroviruses are a common cause (in second place) of respiratory diseases affecting the upper respiratory tract. These respiratory diseases have a short duration incubation period(no more than 1-3 days) and proceed relatively easily. Pneumonia with this infection is rare.

Young people are more likely to get herpangina. It proceeds benignly, recovery occurs within a few days, only in rare cases in children it can be complicated by meningitis.

After identifying tropism Coxsackie viruses to muscle tissue, enteroviruses began to be given great importance in inflammatory muscle diseases. Myalgia (pleurodynia) occurs in outbreaks or sporadic cases. Muscle inflammation can be acute or chronic, but in chronic processes enteroviruses are rarely isolated. Most likely, enteroviruses trigger autoimmune inflammatory processes in the muscles, but then disappear.

Symptoms of enterovirus in adults

Enterovirus in adults most often causes catarrhal form and has the following clinical manifestations:

• acute onset;
• fever (up to 37.5-38 C);
• weakness;
• hyperemia of the pharynx of the face, neck;
• sore throat and sore throat;
• nausea,
• scleral vascular injection.

Enteroviral fever (minor disease)

This is another common form of infection in adults. It is a mild manifestation and is often not diagnosed because it is not severe and lasts no more than 3 days. Three-day fever is not accompanied by any local symptoms (only sometimes there is pharyngitis with regional lymphadenitis), general health is practically not affected, intoxication is moderate, so the patient does not seek medical help.

Acute hemorrhagic conjunctivitis

It also occurs among the adult population and mainly among young adults (20-35 years old) and adolescents. Patients report that there were people with conjunctivitis at home and after that they developed the disease. This infection is extremely contagious. It begins acutely and affects one eye first. The patient complains of a feeling of a foreign body or “sand” in the eyes, fear of bright light and lacrimation. In some cases, the second eye is affected after 2 days.

Upon examination, hemorrhages under the conjunctiva (small petechiae and even large spots), swelling of the eyelids, enlarged parotid lymph nodes and the presence of scanty serous discharge are revealed. The disease is benign, and the patient recovers for 2 weeks without visual impairment. In some cases it occurs or uveitis . Some patients with conjunctivitis develop neurological complications in the form of acute radiculomyelitis who required hospital treatment.

Pericarditis and myocarditis

The course of the disease with heart damage occurs in young people (from 20 to 40 years old). Moreover, it is mostly men who get sick. It manifests itself as pain in the heart, weakness and moderate shortness of breath, which occurs after an enterovirus infection caused by Coxsackie B. In general, it has a benign course, but in some patients acute inflammation heart muscle goes into a chronic process, progressing over time to dilated cardiomyopathy . In this case, the heart increases in size and its function suffers significantly.

Rash due to enterovirus infection is less common in adults than in children. It may accompany other forms of enterovirus infection (three-day fever) or be isolated. Externally, it resembles a measles rash (pink maculopapular), spreading throughout the body, involving the feet and face. Enterovirus rash disappears without a trace after 2-3 days.

Symptoms of enterovirus infection in children

If we consider the symptoms of enterovirus in children, we can say that their infection occurs in varying degrees of severity: from mild localized forms ( vesicular pharyngitis , herpangina ) to heavy ( serous meningitis And meningoencephalitis ).

According to statistics, children come to the fore serous meningitis , and then follows herpangina , epidemic myalgia And meningitis-like form . In infants and young children, the intestinal form is predominantly observed and enteroviral uveitis .

In all cases, the disease begins acutely: the temperature reaches 38-39 C, weakness, nausea, headache, vomiting, and enlarged lymph nodes (cervical and submandibular, as viruses multiply in them) appear. The temperature lasts 3-5 days and returns to normal, and after a few days the second wave of fever passes. When the temperature normalizes, the child's condition improves.

The further development of the disease depends on many factors - the virulence of the virus, its tendency to damage certain tissues and the state of the child’s immunity.

Herpangina

Most often detected in preschoolers and younger schoolchildren (up to 10 years). The onset of the disease is flu-like: fever, headache, and the child’s appetite also decreases. Pain may appear in the muscles of the legs, back and abdomen. Against this background, inflammation of the oral mucosa develops, accompanied by pain, which intensifies when talking and swallowing, excessive salivation, cough, and runny nose.

Against the background of the red mucous membrane, small papules (dense, rising above the mucous membrane) appear on the palatine arches, tonsils, palate, tongue and uvula. Gradually, the papules transform into vesicles - vesicles with serous contents. Subsequently, they open with the formation of grayish-white ulcers with a crown of redness. Larger ulcers may merge. Erosion of the mucous membrane is very painful, so the child refuses to eat and drink. Herpetic tonsillitis is accompanied by enlarged lymph nodes on both sides (parotid, cervical and submandibular). The duration of the disease is up to 10 days.

Signs of serous meningitis and encephalitis

This is a severe form of infection that occurs with inflammation of the membranes of the brain. The child's temperature rises significantly (up to 40.5°C or more), he is bothered by a severe headache and repeated vomiting, which does not bring relief. Meningeal symptoms appear: photophobia, sensitivity to loud sounds, increased headache when forcibly bringing the chin to the chest. Children become lethargic, apathetic, sometimes there is excitement and convulsions while maintaining consciousness. It often occurs, and when examining the abdomen, rumbling is detected. All these symptoms can last up to 10 days or more.

Often, against the background of a meningeal symptom complex, catarrhal syndrome, rash and diarrhea can be detected (it is characteristic only for ECHO-meningitis ), but they are of a secondary nature. This flow is called dissociated. For Coxsackie B-meningeal form, only a complete meningeal symptom complex is characteristic, and for ECHO meningitis - a dissociated meningeal symptom complex.

The clinical picture of meningitis depends on age: in younger children, meningeal symptoms disappear faster, and in children over seven years of age, the leading symptoms persist longer. In preschool children in the acute period, antiviral protection occurs due to innate immunity (active monocytes and neutrophils), so recovery occurs faster. After meningitis, residual effects may persist: increased, asthenic syndrome , oculomotor disorders, increased tendon reflexes and disorders of consciousness.

Encephalitis is inflammation of the brain. This is a dangerous disease with a high mortality rate. Children may experience cerebellar ataxia, motor seizures, and severe disease leads to coma . Based on localization, several varieties are distinguished: stem, cerebellar, hemispheric. In the cerebellar form, which is considered the most favorable, complete recovery is observed.

Epidemic myalgia

There is a second name for this infection - pleurodynia . Myalgia is characterized by severe pain in the abdominal muscles, back, arms and legs, and chest. Pain occurs when the temperature rises and its appearance is wave-like. When the temperature drops, muscle pain may disappear completely. The pain occurs in attacks, lasting from a few seconds to 20-25 minutes, and bothers the child for several days in a row. They intensify with movement, coughing and are accompanied by sweating.

In this case, the child experiences hyperemia of the pharynx, granularity of the mucous membrane, as well as cervical lymphadenitis. In some cases, an enlargement of the liver and spleen is detected. The average duration of the disease is from 3 to 7 days. If the disease takes on a wave-like course, the duration of the disease may increase by 2 weeks (3 exacerbations with breaks of 4 days).

Enteroviral uveitis

It is observed in children under one year of age. The main manifestations are rapid swelling and redness of the iris, disruption of its pigment, and deformation of the pupil due to damage to the muscles of the pupil. The disease often progresses and leads to the development of early and late complications in the form of partial or complete loss of vision.

Enteroviral diarrhea

The gastroenteric form is also common in children and is manifested by watery, loose stools (up to 10 times a day without pathological impurities), lack of appetite, bloating, vomiting (first days), abdominal pain (more in the right iliac region). At the same time, signs of intoxication (fever, weakness, loss of appetite) are moderate. In young children this form is accompanied catarrhal manifestations. The febrile period in children can last a whole week, and full recovery can take up to 2 weeks. But even with the duration of the disease, they do not experience significant dehydration. Sometimes the liver and spleen become enlarged. Older children recover by 3-4 days.

Pericarditis and myocarditis

It is believed that in 1.5% of cases, enterovirus infection occurs with heart damage, which more often develops in older children 1.5–2 weeks after the respiratory form. Often myocarditis develops complications and residual effects, has a benign course and a favorable prognosis. In some cases it is severe and leads to death.

The child has a slight increase in temperature, weakness, fatigue and pain in the heart area. Upon examination it is revealed moderate expansion borders of the heart, listen to muffled heart sounds in myocarditis and pericardial friction rub in pericarditis. Myocarditis is found at autopsies of children who died from fulminant infection caused by Coxsackie virus .

Enteroviral exanthema

This form occurs in children from 6 months to 3 years. It occurs in the form of an exanthema (rash), which appears on the skin on the 2-3rd day of illness, when the temperature drops. A rubella-like or maculopapular rash is localized on the trunk, arms, legs (less commonly) and face. The infection sometimes has a two-phase course.

The first phase is characterized by fever, skin rashes, and vomiting. The second phase is neurological complications that occur 3-5 days after the first manifestations of the disease and are regarded as a severe course of the disease. Neurological manifestations include aseptic meningitis , paralysis , rhombencephalitis . In mild cases, the disease passes through only one phase and the rash disappears without a trace in 2-3 days. Enteroviral exanthema can manifest itself as an independent clinical form, or accompany other forms of viral infections (serous meningitis, herpetic sore throat, gastroenteric form).

Enteroviral vesicular stomatitis

The second name is “arm, leg, mouth” syndrome, in which, against the background of a febrile reaction, a rash appears on the extremities and in the oral cavity on the 2-3rd day of illness. The onset of the disease is acute - with a rise in temperature to 40 C, which is accompanied by nausea, headache, vomiting and lasts up to 5 days.

Photos of enterovirus rash in children of various locations

It is also possible to experience abdominal pain, loose stools, catarrhal symptoms, runny nose and cough. From the second day from the onset of the disease, a spotted red-pink or vesicular (vesicular) rash appears on the arms, legs, around the mouth, on the lips and always in the oral cavity (vesicular stomatitis). Changes in the mucous membrane may be observed, as in herpangina . Vesicular stomatitis is characterized by the fact that blisters on the mucous membrane quickly turn into erosions; the child is bothered by pain, itching in the mouth and lip area. Skin rashes usually disappear after two to three days, leaving no traces, but manifestations of stomatitis can bother the child for up to 7-10 days.

Orchitis

In boys, inflammation of the testicles is possible. This disease appears 2 weeks after an infection that has other manifestations (respiratory variant, herpangina or diarrhea). The disease passes quickly and usually does not result in complications such as aspermia (lack of sperm) in adulthood. However, isolated cases of such a complication have been described.

The disease develops as a result of infection carried through the bloodstream into the testicle. Sharp pain appears, the scrotum on the affected side is noticeably enlarged, the skin of the scrotum is tense. The child's temperature rises and there are signs of intoxication. Touching the testicle is painful.

Poliomyelitis-like form

Children are predominantly affected. With this form, symptoms similar to polio occur, but they are caused not by the polio virus, but by enteroviruses 68–71 , Coxsackie And echoviruses . Acute paralysis develops in severe forms of the disease with damage to the central nervous system. As with, they lead to serious consequences.

Tests and diagnostics

Diagnosis of infection is established on the basis of epidemiological, clinical data and laboratory confirmation. Used:

• PCR study. Detection of RNA viruses PCR method in different biological materials is more reliable, has greater sensitivity and is the fastest research method. Stool samples, discharged vesicles or nasopharyngeal washings for PCR are collected in the first 3 days from the onset of the disease, and cerebrospinal fluid- in the first week of illness.
• The virological method is a direct method of identifying the pathogen - isolating it in cell culture. Isolation of enterovirus is carried out from sterile and non-sterile materials taken from the patient: cerebrospinal fluid, conjunctival and vesicular discharge, blood, oropharyngeal smear, fecal samples, smear of herpangina discharge. Isolation of the virus takes longer, and some viruses may not reproduce in cell culture.
• Serological. Blood is examined at the very beginning of the disease and after 2 weeks. This is the oldest but most relevant serological test for enterovirus, which detects specific antiviral antibodies in the neutralization reaction. It is carried out dynamically and determines the increase in antibody titer. Two samples of the patient's serum are examined using RTGA and RSC, taken with an interval of 14 days. A 4-fold increase in antibody titer is diagnostically significant. An accelerated modified m-RSC method has also been developed, which allows for rapid identification of enteroviruses.
• The ELISA method detects anti-enteroviral antibodies in the blood - markers of enteroviral infections. Early markers include IgM And IgA. Titer IgM indicates a recent infection and is detected 1–7 days after the onset of the disease. In 6 months IgM disappear while IgG persist and circulate in the blood for several years. However, the individual detection of anti-enteroviral IgM in blood serum is not a diagnostically significant indicator.
• The immunochromatographic method determines the presence or absence of antigen in feces or other test material. A negative antigen indicates that no traces of antigens were found, which means that the pathogen is absent.
• In the case of meningitis, the cerebrospinal fluid is examined, in which it is more often found neutrophilic pleocytosis (increase in cell number) or lymphocytic . During recovery, the indicators improve (the cerebrospinal fluid is sanitized), but this process is quite long. Thus, only on the 16-23rd day of illness does cerebrospinal fluid reorganization occur, and faster in young children than in school-age children. Sanitation of the cerebrospinal fluid indicates that the blood-CSF barrier has been restored. Its recovery is lagging behind clinical symptoms.

Treatment of enterovirus infection

Enterovirus infection in adults in mild form is treated on an outpatient basis. Mild forms include conjunctivitis , herpangina , three-day fever (with and without rash), vesicular pharyngitis , gastroenteritis , pleurodynia , uveitis . In healthy adults with strong immune systems, the infection does not develop to severe forms. Enterovirus in adults most often affects the respiratory tract (cold-like form) or occurs in the form of a three-day fever without catarrhal symptoms.

The characteristic symptoms were discussed above. Now let's look at the treatment and answer the questions: how to treat enterovirus and how to treat it?

• Bed rest is prescribed for the entire period of fever.
• Milk-vegetable diet, drinking plenty of fluids(2.5 l per day) and a balanced diet.
• The patient is given separate dishes and a towel, which are treated with boiling water.
• Toilets and sinks are treated with detergents and disinfectants for household use (Sanita, Nika-Sanit, Domestos). The exposure time of the drugs is doubled.

There is no etiotropic treatment. In mild cases, symptomatic therapy is carried out aimed at lowering the temperature, eliminating muscle and throat pain, and in severe cases, antiviral (interferons, ribonuclease, immunoglobulin), immunomodulating and anti-inflammatory hormonal therapy is carried out in a hospital setting.

Treatment of enterovirus infection in adults

Relief of hyperthermic syndrome

At temperatures above 38.5 C, antipyretic drugs from the group of non-steroidal anti-inflammatory drugs are prescribed: Acetaminophen , . At the same time, desensitizing drugs are prescribed for 5-6 days.

For epidemic myalgia

• within 5 days.
• Non-steroidal anti-inflammatory drugs.

In case of bacterial complications

Antibiotics are added to treatment -,.

Antiviral and immunomodulatory therapy

• Interferons, which have a wide antiviral spectrum. Natural and recombinant alpha-interferon preparations are prescribed. They are used topically and parenterally. Viruses do not develop resistance to interferons.
• Human immunoglobulin is normal - the solution is administered intramuscularly. Treatment of enterovirus in adults, which has caused severe damage to the nervous system, is carried out only in a hospital setting.

For meningitis and meningoencephalitis

• Dehydration therapy aimed at reducing cerebral edema and intracranial pressure. Intravenous drip administration is carried out for 3-5 days, with a transition to taking diuretics orally (,) in combination with potassium preparations.
• For anti-inflammatory and desensitizing purposes, hormonal drugs are prescribed according to the scheme (,) for a week.
• In case of seizures, treatment includes intramuscular/intravenous injections or.
• For the purpose of immunocorrection, intravenous administration is carried out for three days.

In paralytic form

• within 5 days.
• Subcutaneous administration in a monthly course. After a break of 14 days, a solution is prescribed intramuscularly.

An antiviral drug is considered an effective remedy Pleconaril , acting on picornaviruses and rhinoviruses. This etiotropic drug has undergone clinical trials abroad, but the drug is not registered in the countries of the former CIS, and therefore is not available to Russian citizens.

The drug is characterized by high bioavailability when taken orally (5 mg per kg of body weight 3 times a day, course 7 days). A high concentration of the drug is observed in the central nervous system and nasopharyngeal mucosa. Pleconaril can be used to treat enteroviral meningitis, encephalitis and respiratory lesions.

Treatment of enterovirus infection in children

How to treat enterovirus in children? As in adults, in mild forms treatment is carried out at home. To prevent the spread of infection, the child is provided with personal utensils and hygiene products; the room must be frequently ventilated and wet cleaned daily.

Catarrhal and eczematous forms, herpangina

Komarovsky believes that for these forms of enteroviral diseases, it is enough to carry out symptomatic treatment, since it is impossible to “kill” the virus with any drugs. The main treatment is drinking plenty of fluids, antipyretic and proper care for the child. For example, with herpangina, it is painful for a child to swallow, so he refuses to even drink. Warm and hot drinks increase sore throat, so you can give your child cool drinks and those that he prefers - the main thing is to prevent dehydration. After 10 days, the symptoms of herpangina or vesicular stomatitis in the “arm, leg, mouth” syndrome disappear - you just need to wait time. Catarrhal and eczematous forms usually do not cause much suffering to the child.

Gastroenteric form of infection

Concerning diarrhea in case of enterovirus infection, the doctor recommends, first of all, drinking large amounts of fluid with electrolytes (rehydration therapy - Humana Regidron Bio , Humana-electrolyte , Oralit , Glucosolan ), as well as cytomucoprotectors (these drugs protect the intestinal mucosa and restore it), for example,. If vomiting is present, drinks are given very often (15-20 minutes) and in small portions (1-2 sips). Children are recommended vegetarian puree soups, pureed or well-cooked porridge (rice, buckwheat, oatmeal) in water, mashed potatoes without milk, boiled lean meat minced through a meat grinder, crackers and dryers.

Often, with moderate and severe diarrhea syndrome, children are prescribed ( active substance-). The drug is active against pathogenic bacterial flora that can cause diarrhea: streptococcus, staphylococcus, salmonella, shigella, klebsiella, campylobacter and others. On the one hand, there is no need to prescribe it for diarrhea of ​​viral etiology. On the other hand, this drug is still prescribed because it prevents the occurrence of bacterial superinfection. Its purpose is indicated for young children with a burdened premorbid background. Nifuroxazide is almost not absorbed from the gastrointestinal tract, exerting its effect in the intestinal lumen, does not affect the saprophytic flora and does not disrupt the normal intestinal flora. Excreted through the gastrointestinal tract. It has a convenient release form: suspension (for children from 1 month) and capsules (from 7 years).

In case of moderate and severe diarrhea, immunopreparations (IPPs, ), which are prescribed for 5 days, and always probiotics ( , ) for a course of up to 14 days, are added to the treatment.

Indications for urgent hospitalization of children are:

• convulsions;
• peripheral paralysis;
• myocarditis ;
• lethargy ;
• headache with impaired consciousness;
• severe symptoms of intoxication;
• layering of secondary infection;
• severe background pathology;
• children under 5 years of age with vomiting after every meal, infants who refuse to drink or latch on to the breast, a history of convulsions, impaired consciousness.

An important point in the treatment of children in hospital conditions with symptoms of dehydration is reregistration (use water-salt solutions and glucose) and detoxification . Antiemetics are also used antihistamines, antispasmodics. In the presence of bacterial infection- . In severe forms with damage to the nervous system, corticosteroid drugs are indicated.

Therapy of enteroviral meningitis

• Dehydration is carried out - Mannitol , Diakarb , . Brings relief.
• In severe cases, administration is indicated (intravenously for up to 3 days).
• A complex is assigned B vitamins .
• In the acute period of the disease, immunomodulatory therapy is carried out. Any of the drugs is prescribed: (for a course of 6 tablets), (for a course of 5 injections), (intramuscularly, for a course of 5 injections), (rectal suppositories for 10 days). Inclusion during meningitis in children leads to a reduction in period meningeal symptoms and allows you to quickly achieve sanitation of the cerebrospinal fluid. Against the background of the prescription, the febrile period was shortened and the condition of the cerebrospinal fluid quickly improved. Usage Polyoxidonium leads to a shortening of the duration of fever, headache and meningeal symptoms. The drug also increases antibody formation and stops the inflammatory process. Clinical effect Cycloferon consists in reducing the duration of meningeal symptoms, the sanitation of the cerebrospinal fluid goes well. On the background Viferona sanitation of the cerebrospinal fluid is observed in 87% of children. According to clinical observations, the use of Viferona , Polyoxidonium , Anaferona , and for children over 7 years old - Anaferona , Amiksina, Polyoxidonium . Viferon is especially indicated for cytosis in the cerebrospinal fluid of more than 300 cells/µl. Also, observations have shown that a low level of initial pleocytosis of the cerebrospinal fluid (up to 50x106/l) is an indicator protracted process sanitation of cerebrospinal fluid and there is a basis for prescribing immunomodulators.
• In immunocompromised children, intravenous administration of gamma globulin has been successfully used.
• If used by children Pleconaril , the symptoms of meningitis disappeared 2 days earlier than in patients who did not receive this drug.
• With developed paralysis and polyneuritis , Consequently myelitis , encephalitis , drugs are prescribed that improve neuromuscular conduction and increase muscle contractility (,).
• If respiratory function is impaired, artificial respiration is performed.

The doctors

Medicines

• Antipyretic drugs and NSAIDs: Paracetamol , Nice , Movalis .
• Desensitizing (anti-allergic): , Cytherizine .
• Hormonal agents: , .
• Interferons. Natural: Egiferon , Feron . Recombinant: Reaferon , Viferon , Realdiron , Roferon , Berofor , Inrek , .
• Immunoglobulins: Human immunoglobulin normal for IM administration
• Combined drugs (immunoglobulin plus interferon).
• Diuretics: Furosemide , .
• Anticonvulsants: , Phenobarbital .
• Infusion solutions: , Glucose 0.9% , .
• Antibiotics (for bacterial complications): Azivok , .
• M-anticholinergics (for lesions of the nervous system and spinal cord with paresis): , .

Procedures and operations

In case of bronchiolitis or severe pneumonia, meningitis and other life-threatening conditions, artificial ventilation and other resuscitation measures may be necessary. In case of cerebral edema it is carried out oxygen therapy . Surgeries for this infection are not indicated.

Prevention of enterovirus infection

Prevention of enteroviruses is ensured by compliance with sanitary and epidemiological requirements at the national level:

• Providing the population with quality water supply. This is possible by conducting routine laboratory tests of water (not only drinking water, but also waste water and open water bodies) to detect contamination by microbes and viruses. Hygienic requirements for drinking water have been developed - GSanPiN. According to them, the unit of measurement is the presence of enteroviruses in 10 dm3. Tap water from wells and packaged water should be free of enteroviruses. If necessary, hyperchlorination is carried out drinking water, in institutions (hospitals, kindergartens) a regime with mandatory boiling of water is established.
• Improvement of water supply sources and open reservoirs that are used for domestic and drinking water use.
• Maintaining the territory of treatment facilities in proper order and monitoring the quality functioning of treatment facilities.
• Providing high-quality and safe food products.
• Control of public catering establishments.
• Disinfection of sewage and control of enteroviruses in the environment to determine the preconditions for epidemic troubles.
• Organization and implementation of anti-epidemic measures in treatment and prevention, preschool and other institutions. Taking into account the high contagiousness (possibility of infection) of the infection, sanitary and epidemiological rules and regulations have been developed (SanPiN dated May 18, 2010 No. 58) for institutions carrying out medical activities. This is especially true for hospitals providing obstetric care (perinatal centers, maternity hospitals and departments). The rules include mandatory periodic disinfection of premises, furniture, and linen. Special requirements are imposed on catering units, storage conditions for products (separately dry, raw, meat and fish) and their processing.
• Man observing basic rules hygiene can prevent contracting this infection. This applies to frequent hand washing (necessarily before eating and after using the toilet), drinking high-quality bottled or boiled water, thoroughly washing vegetables and fruits that are consumed raw, treating dishes with boiling water, keeping kitchen utensils clean and frequently changing (processing) kitchen sponges or cotton rags (napkins).
• A memo on the prevention of enterovirus infection for parents includes the same accessible and feasible measures for observing normal rules of personal hygiene as for adults, but they must be carried out especially carefully.
• Mandatory hand washing with soap after visiting the toilet, before eating and throughout the day, since the “dirty hands” factor is the main factor in the transmission of pathogens in childhood.
• Treat with soapy water and hot water children's toys and other objects with which the child comes into contact.
• In outdoor conditions, on the street or in public places, wipe the child’s hands with antiseptic sanitary napkins.
• Eat only well-washed and processed (if possible) raw fruits, vegetables and berries. To treat vegetables and herbs, you can use the Aquatabs disinfectant.
• For drinking, offer your child boiled water or high-quality bottled water.
• In summer, swim in permitted bodies of water, the water in which meets sanitary safety standards.
• Make sure that your child does not swallow water while bathing. After bathing, if possible, take a shower; if not, wash the child and wash your hands with clean bottled water.

Prevention of enterovirus infection in kindergarten also consists of strict compliance with the rules of personal hygiene for children. In addition, very important aspect is the early detection of disease cases through daily medical examinations during the morning reception of children and the isolation of sick people.

• Isolation of patients with light forms for no less than 10 days. Those who have had a mild form of illness are allowed into the children's team without a virological examination.
• A restriction (or prohibition) on holding festive events is introduced in the team.
• If a kindergarten has a swimming pool or children regularly attend a city swimming pool, swimming is prohibited if a virus is detected in the water.
• Children's institutions are closed for quarantine and disinfection measures are carried out using drugs that have virucidal activity. They destroy the virus in the environment (wall and floor surfaces, dishes, toilets, pots, hard furniture, toys). In the outbreaks, “Nika-Chlor”, “Nika Neodez” (no need to wash off), “Zhavilar Plus” are used.
• Disinfectants are available in tablets that dissolve in water in different proportions. The items to be treated are either wiped with the prepared solution or soaked for a certain time.

Specific vaccines have not been developed due to the variety of virus serotypes. It is impossible to predict which serotype will circulate in a given region and at a given time. However, effective prophylaxis in children 1 to 14 years of age during outbreaks serous meningitis , poly-like form or uveitis , is possible by using a live polio vaccine containing attenuated strains (Sabin), which have an antagonistic effect on the enterovirus.

Vaccination is carried out once when the incidence rate rises. Within 2-3 days after vaccination, the intestines are populated by the vaccine poliovirus and pathogens are displaced serous meningitis . Prophylactic vaccination with live poliovirus vaccine significantly limits the scope of outbreaks.

After infection, those who have recovered from the infection develop lifelong immunity, but it is serospecific - only to the serotype of the virus that caused the disease. This immunity cannot protect a person from other types of enteroviruses, so the infectious disease can be transmitted many more times.

Enterovirus infection in children

Due to decreased immunity, children, especially infants, are more susceptible to the virus and their infection rate can reach up to 50%. With age, the level of immunity increases. The clinical picture of enteroviral infections in a child is diverse - from benign enteroviral fever to severe multiple organ lesions, which often lead to fatal outcome as a result of liver or heart failure. In infancy, the most characteristic are catarrhal symptoms of the nasopharynx and intestines. In severe cases, the infection manifests itself meningoencephalitis , pneumonia , myocarditis , hepatitis .

Some enteroviruses (eg. ECHO 11) cause severe generalized diseases in newborns. Generalized infections cause myocarditis or fulminant hepatitis which are accompanied by encephalopathy. Most often in newborns, symptoms of the disease appear on the 3rd-5th day of life. Boys and premature newborns have a more serious prognosis. The first symptoms are nonspecific: lethargy, lethargy, poor appetite. Hyperthermia is not observed in all babies.

In the case of myocarditis, heart failure develops rapidly with respiratory distress, an increase in heart size, and occurs. Mortality from myocarditis at this age reaches 50%. Death occurs within 7 days from the onset of the disease. Myocarditis is often accompanied meningoencephalitis , in this case characteristic symptoms appear: drowsiness or constant sleep, convulsions, protrusion of the fontanel, and when examining the cerebrospinal fluid, it is found pleocytosis . Infection with enteroviruses immediately after birth or up to one year of age causes a lightning-fast infection in an infant, which is called “viral sepsis,” which quickly leads to death.

Fortunately, in recent years, minor enteroviral disease has been detected more often. It occurs quickly, without pronounced symptoms and damage to the central nervous system or internal organs. This clinical form ranks first in frequency among other forms caused by enteroviruses. The disease begins acutely without a period of prodrome (predecessors). The temperature rises sharply , nausea, redness of the pharynx and conjunctiva often appears. The temperature lasts three days, after which all symptoms disappear. Parents should be aware of this form and, despite its relatively mild course, take all measures to prevent possible complications.

There is no specific treatment. Mild forms can be treated at home, but hospitalization is necessary for damage to the nervous system, heart, or high temperature that cannot be reduced for a long time. The child must remain in bed during the entire period of elevated temperature.

.

In the presence of loose stool give medications that restore water-salt balance: Regidron Optim , Regidron Bio (additionally restores the balance of microflora), Humana-electrolyte , Oralit , Glucosalan . At home, you can prepare a solution: dilute 1 tsp in 1 liter of water. salt, 8 tsp. sugar and juice of one lemon (citric acid on the tip of a spoon). Enterosorbents can be added to treatment -, Filtrum , . All these drugs have a high sorption capacity and remove viruses from the intestines. Typically, these actions significantly reduce the frequency and severity of stools.

Taking into account the viral etiology of diarrhea, a complex immunoglobulin preparation (CIP) can be used. It is used in children from one month of age in the presence of dysbacteriosis and immunodeficiency conditions. One bottle contains 300 mg of immunoglobulins ( IgG, IgA, IgM). After opening, add 5 ml of boiled water to the bottle and dissolve the powder. CIP is given to the child 1 dose once a day for 5 days, 30 minutes before meals.

The diet should be light, but rich in proteins (cottage cheese, fermented milk products, boiled meat). For diarrhea, food should be as gentle as possible - pureed meat and cereals, omelettes. It is necessary to give the child plenty of fluids. Recommends boiled water or mineral water, devoid of gas, dried fruit compotes, juices.

Komarovsky believes that there is no point in using antiviral drugs for this infection. First of all, because there are no drugs with proven effectiveness against enteroviruses. Antiviral drug Pleconaril , used for etiotropic treatment of this infection abroad, is not registered in Russia and Ukraine.

In case of severe infection (heart damage, encephalitis , meningitis , hepatitis ) in stationary conditions recombinant interferons are used ( Realdiron , Roferon , Viferon , Reaferon ) and immunoglobulins. These groups of drugs have shown their effectiveness in infections against the background of an immunodeficiency state and in newborns in the absence of antibodies to enteroviruses.

Of particular importance is the spread of infection in a kindergarten or school, where up to 50% of children can be infected. In order to timely identify and isolate patients in groups, it is necessary to examine the skin, pharynx and measure body temperature. Parents should monitor the child and in this matter they will be helped by a memo that indicates all the characteristic symptoms of infection and what to do if the child becomes ill. The first thing to do is to isolate the child, report the disease to a child care facility, where a quarantine is imposed for a period of 10-15 days.

Disinfection measures are carried out in the outbreak. All these actions will help localize the infection and prevent its spread. The important thing in the memo is measures to prevent the disease: teach the child to wash his hands after using the toilet and walking, drink boiled or bottled water, and it is unacceptable to use unwashed fruits and water from a lake or river. Children under 3 years of age who have had contact with the patient are given interferon drops into their nose for a week for prevention.

Enterovirus during pregnancy

During pregnancy, in addition to the usual manifestations of infection, a symptom complex with acute pain in the lower abdomen and fever, caused by an acute viral infection, is observed. mesadenitis . In practice, this is often interpreted as acute appendicitis or premature placental abruption, which leads to incorrect treatment tactics for the pregnant woman. Persistent enterovirus infection causes miscarriage and placental insufficiency. Intrauterine infection of the fetus is also possible. Transferred during pregnancy coxsackie infection causes congenital heart defects ( tetralogy of Fallot , tricuspid valve defects), digestive and genitourinary systems in a child.

A newborn can become infected in utero (hematogenously during the period of viremia) or during childbirth (ingestion of infected water). Intrauterine infection of the fetus is rare, and the outcome depends on the virulence of the circulating virus and the presence of maternally transmitted antibodies. The most dangerous are : lightning-fast infection (“viral sepsis”) and generalized infection with damage to the myocardium, central nervous system and lungs.

Diet for enterovirus infection

The patient's diet should be predominantly dairy-vegetable and organized within. Compliance is important drinking regime to reduce intoxication. In the case of diarrheal symptoms, it is advisable for the child to use a diet characterized by maximum sparing of the gastrointestinal tract.

Consequences and complications

The severity of manifestations and outcome of the disease depend on the ability of the immune system to respond to the pathogen. Timely comprehensive treatment, taking into account the patient’s form and immunity, ensures positive results and complete recovery. Among the consequences of meningitis, note long-lasting asthenic syndrome (weakness, headaches, fatigue), increased intracranial pressure, oculomotor disorders, increased tendon reflexes and disorders of consciousness.

Complications of enterovirus infection are most often associated with damage to the nervous system. In severe cases, the following may occur:

• cerebral edema ;
• dislocation syndrome (brain herniation, accompanied by cardiac and pulmonary arrest);
• encephalitis ;
• convulsive syndrome;
• hemiparesis (paralysis of one half of the body);
• development ;
• deterioration of hearing and vision.

Among other complications, it should be noted pneumonia , respiratory distress syndrome , acute kidney and liver damage.

Forecast

In most cases, the prognosis for infection is favorable. It is quite serious in myelitis and encephalitis, and very unfavorable in newborns with encephalomyocarditis . Loss of ability to work and hospital treatment for serous meningitis lasts up to 3 weeks.

Patients with damage to the nervous system are discharged from the hospital only after the composition of the cerebrospinal fluid has normalized, which lags behind the normalization of the clinical symptoms of the disease. Patients with damage to internal organs and the nervous system should be observed by appropriate specialists and undergo rehabilitation. After the disappearance of residual effects, the patient is removed from the dispensary register.

List of sources

• Nikonov O. S., Chernykh E. S., Garber M. B., Nikonova E. Yu. Enteroviruses: classification, diseases caused and directions for the development of antiviral agents // Advances in biological chemistry, v. 57, 2017, p. 119–152.
• Protasenya I.I. Enterovirus (Coxsackie and ECHO) infection in children /I.I. Protasenya, V.P. Molochny, V.I. Reznik //Far Eastern Journal of Infectious Pathology, 2003. - No. 2. - P. 51-54.
• Sutherland S. Enteroviruses. Congenital, perinatal and neonatal infections / Ed. A. Greenough, J. Osborne, S. Sutherland. - M.: Medicine, 2000. - P. 74-82.
• Heydarova N.F. Aggravating influence of enterovirus infection on the course and outcome of pregnancy / N.F. Heydarova // Ukrainian Journal of Clinical and Laboratory Medicine. – 2011. – No. 4, T. 6. – P. 70-74.
• Clinical and immunological features of enteroviral meningitis in children / V. V. Fomin, A. U. Sabitov, Yu. B. Khamanova, O. A. Chesnakova, JI. G. Besedina, Ya. B. Beikin // Bulletin of the Ural Medical Academic Science. - 2008. - No. 2 (20). - pp. 144-147.

IUI is one of the leading causes of perinatal morbidity and mortality. The frequency of IUI varies widely and depends on many factors: the type of pathogen, the condition of the fetus and newborn, gestational age, etc. Currently, the frequency of various manifestations of IUI is 10-53% (Fig. 102).

Rice. 102. Various manifestations of IUI

There are two concepts: IUI itself and intrauterine infection.

IUI is a disease in which the source of infection of the fetus is the organism of the infected mother and which has a variety of clinical manifestations in the form of pyoderma, conjunctivitis, rhinitis, hepatitis, gastroenteritis, pneumonia, otitis, meningoencephalitis, even sepsis. Infection has no clinical manifestations in the fetus and is expressed only in the penetration of pathogens into its body.

la. The disease in the fetus does not occur as a result of the mobilization of immunity and protective mechanisms in the mother-fetus system. In both cases, infection occurs in the antenatal period or during childbirth.

etiology of intrauterine infections

There is a well-known obstetric axiom: there is no parallelism between the severity of the infectious process in the mother and the fetus. A mild, mild or even asymptomatic infection in a pregnant woman can lead to severe damage to the fetus, including disability or even death. This phenomenon is largely due to the tropism of pathogens (especially viral ones) to certain embryonic tissues, as well as the fact that fetal cells with their highest level of metabolism and energy are an ideal environment for the reproduction (replication) of microbes. This is precisely what explains the great similarity of embryo- and fetopathies caused by various infectious agents.

To designate the IUI group, the abbreviation TORCH was proposed (based on the first letters of the names of infections, but the word “torch” carries a greater meaning - in English it is translated as “torch,” which emphasizes the danger and severe consequences of IUI).

Abbreviation TORCH is deciphered as follows. Toxoplasmosis- toxoplasmosis.

Others- other infections (it is absolutely proven: IUI is caused by pathogens of syphilis, chlamydia, enteroviral infections, hepatitis A and B, gonococcal infection, listeriosis; the probable culprits of IUI are measles and mumps; hypothetical - pathogens of influenza A, lymphocytic choriomeningitis, human papillomavirus).

Rubeola- rubella.

Cytomegalia- cytomegalovirus infection. Herpes- herpes virus infection.

The listed infections are most widespread among the adult population, including pregnant women.

Toxoplasmosis is observed in 5-7% of pregnant women, while in 30% of cases infection of the fetus is possible (encephalitis and its consequences, chorioretinitis, a generalized process accompanied by hepatosplenomegaly, jaundice and damage to the cardiovascular system).

Infection of the fetus with syphilis occurs at 6-7 months of pregnancy; spirochetes can penetrate the intact placenta. The result is a miscarriage of a macerated fetus or the birth of a still child with signs of visceral syphilis (liver damage, interstitial pneumonia, osteomyelitis, osteochondritis).

During pregnancy, chlamydia is detected in 12.3% of cases; about 50% of children born to mothers with chronic endocervicitis have signs of chlamydial infection.

Enterovirus infections are quite common. The ECHO and Coxsackie viruses are of greatest interest as causative agents of IUI. Enteroviruses are transmitted to pregnant women through direct contact with patients who have lesions of the upper respiratory tract, lungs, or manifestations of intestinal infection. The experiment proved the etiological role of Coxsackie viruses of group A (serotypes 3, 6, 7, 13) and group B (serotypes 3,4), as well as ECHO viruses (serotypes 9 and 11).

Up to 1% of pregnant women are carriers of the Australian (HBsAg) antigen, while the risk of infection of the fetus and newborn is 10%.

Perinatal infection with listeriosis occurs transplacentally, less often through the ascending route and through the amniotic fluid in case of listeriosis pyelitis, endocervicitis or influenza-like disease; the child is usually born with a generalized form of infection (granulomatous sepsis).

Measles is one of the most common infections and occurs in 0.4-0.6 cases per 10 thousand pregnancies.

The rubella virus is able to penetrate the placental barrier. The probability of fetal infection depends on the duration of pregnancy and is 80% in the first 12 weeks, 54% in 13-14 weeks and no more than 25% by the end of the second trimester.

Cytomegalovirus is a common cause of IUI (intrauterine infection in 10% of cases). The risk of infection of the fetus during recurrent cytomegalovirus infection in a pregnant woman is low due to the fact that the fetus is protected by antibodies circulating in the mother’s blood. Consequently, the risk group for congenital cytomegaly consists of children of seronegative mothers with seroconversion that occurred during this pregnancy.

Infection with the genital herpes virus is detected in 7% of pregnant women. Herpetic infection is characterized by lifelong carriage of the virus.

The particular relevance of herpes infection is associated with the emergence of AIDS patients. It has been established that herpes viruses can activate the HIV genome, which is in the provirus stage, and are a cofactor in the progression of HIV infection. Up to 50% of children born to HIV-infected mothers become infected antenatally, intrapartum, or in the early neonatal period through mother's milk.

ARVI suffered in the second half of pregnancy is a risk factor for the development of IUI due to transplacental transmission of the virus to the fetus. Respiratory viruses, which cause perinatal damage in 11% of cases, can persist and multiply in the placenta, fetal brain and especially in the choroid plexuses of the lateral ventricles of the brain.

pathogenesis of intrauterine infections

The pathogenesis of IUI is diverse and depends on many factors, primarily on the course infectious process in the mother (acute, latent, stage of remission or exacerbation, carrier state). At infectious disease In the mother during pregnancy, the embryo and fetus are affected not only by pathogens, but also by toxic products formed when the mother’s metabolism is disrupted, during the breakdown of the infectious agent, and, in addition, hyperthermia and hypoxia that occur during an acute process.

Gestational age plays an important role in pathogenesis. During the preimplantation period (the first six days after fertilization), under the influence of an infectious agent, the zygote dies or completely regenerates. During the period of embryo- and placentogenesis (from the 7th day to the 8th week), hy-

embryo whiteness, development of deformities, primary placental insufficiency. In the early fetal period (from 9-10 to 28 weeks), the fetus and placenta become sensitive to the pathogen. The development of deformities (so-called pseudodeformities), as well as sclerotic changes in organs and tissues, is possible.

IUI leads to disruption of the further development of an already formed organ. Thus, a urinary tract infection can lead to hydronephrosis, meningoencephalitis - to hydrocephalus due to narrowing or obliteration of the Sylvian aqueduct of the brain. After the 28th week of gestation, the fetus acquires the ability to specifically respond to the introduction of an infectious agent with leukocyte infiltration, humoral and tissue changes.

Exodus intrauterine infection may be different: prematurity, intrauterine growth retardation, antenatal death or various manifestations of local and generalized infectious process, placental insufficiency, adaptation disorders of the newborn; clinical manifestations of IUI can be observed in the first days of life (in the first four days, and in some types of specific infection - after the 7th day and beyond).

The localization of the infectious process in the fetus and newborn depends on the route of entry of the pathogen. Considered classic four ways of intrauterine infection:upward path- through birth canal(bacterial and urogenital infection); transplacental (hematogenous) route(bacterial foci of inflammation; viral infections; listeriosis; syphilis; toxoplasmosis); descending path(at inflammatory processes in the abdominal organs); mixed path.

Bacterial IUI develops mainly due to the penetration of an ascending infection from the birth canal, with chorioamnionitis first occurring, the amniotic fluid becoming infected, and the fetus being affected due to the ingestion of amniotic fluid or its entry into the respiratory tract. Infection is possible when the fetus passes through the birth canal, which is typical for bacterial and urogenital infections. In case of hematogenous infection of the fetus, there must be a purulent-inflammatory focus in the mother’s body. The pathogen infects the fetal part of the placenta, breaking the placental barrier, and penetrates

into the fetal bloodstream. With hematogenous infection, generalized damage to the fetus often occurs - intrauterine sepsis. All true congenital viral infections are characterized by a transplacental route of infection, including such specific ones as listeriosis, syphilis, toxoplasmosis and cytomegalovirus infection. Transdecidual (transmural), descending and mixed routes of infection are observed much less frequently; the pathogenesis of fetal damage does not differ from that of hematogenous and ascending infection.

clinical picture

Clinical manifestations of IUI are mainly nonspecific and depend on the gestational age during infection, the number and virulence of pathogens, and the route of infection.

It is noted that the shorter the gestational age during infection, the more severe the course and worse the prognosis of IUI. The most severe damage to the liver and brain, which is disseminated in nature, is caused by pathogens that penetrate the fetus transplacentally. Clinically, this is manifested by spontaneous abortion, death of the ovum, premature birth, delayed fetal development, abnormalities of its development and the birth of a sick child. Such lesions are typical for: measles, rubella, chickenpox, cytomegaly, mumps, influenza, parainfluenza, herpes simplex type II, Coxsackie, parvovirus B19 (in early pregnancy), as well as HIV infection and some bacterial infections (listeriosis, streptococcal infection).

If infected in the first trimester of pregnancy, the fetus may develop micro- and hydrocephalus, intracranial calcification, malformations of the heart and limbs, and in the second and third trimesters - chorioretinitis, hepatosplenomegaly and jaundice, pneumonia, malnutrition.

The ascending route of infection is characteristic of opportunistic microorganisms, gardnerella, protozoa, fungi, chlamydia, mycoplasmas, etc. Pathogens multiply and accumulate in amniotic fluid, which is clinically manifested by the syndrome of “infection” or “infection of amniotic fluid”. During pregnancy with such an infection, polyhydramnios, malnutrition and

fetal hypoxia, edematous syndrome, enlarged fetal liver and spleen, hyperbilirubinemia; possible miscarriage, premature birth.

At the same time, asymptomatic colonization of amniotic fluid by various microorganisms cannot be ruled out. Asymptomatic chorioamnionitis should be assumed if treatment with tocolytics is unsuccessful in cases of threatened preterm labor.

TO nonspecific clinical manifestations of IUI in newborns may include respiratory distress syndrome, signs of asphyxia, hyaline membrane disease, congenital malnutrition, jaundice, edema syndrome, disseminated intravascular coagulation syndrome, as well as a symptom complex that requires careful differential diagnosis with manifestations of damage to the central nervous system of hypoxic-traumatic origin (general lethargy, decreased muscle tone and reflexes, regurgitation, breast refusal, intense weight loss and slow recovery, breathing problems, bouts of cyanosis).

In some newborns, the manifestations of IUI are different, specific character: vesiculopustulosis at birth, conjunctivitis, otitis, intrauterine pneumonia, enterocolitis, meningoencephalitis, gastrointestinal syndrome.

It should be noted that the possibility of developing IUI in children in the late period of development is associated with the persistence of the virus (chlamydial conjunctivitis, progressive cataracts with infection with the rubella virus, hydrocephalus with the persistence of Coxsackie viruses, chronic pyelonephritis and juvenile diabetes with chronic congenital enterovirus infection).

Features of clinical manifestations of certain diseases in pregnant women

Flu. When contracting influenza in the first trimester, miscarriages occur in 25-50% of cases. However, the incidence of fetal malformations is not increased.

Rubella. Fetal infection occurs in women who become ill with rubella for the first time during pregnancy. Infection of the fetus in the first 12 weeks of embryogenesis leads to the development of hereditary rubella syndrome (cataracts, microphthalmia, hearing impairment, micro- and hydrocephalus and heart defects).

If the disease occurs in the first trimester of pregnancy, the risk of miscarriages and congenital anomalies develops.

tia is high enough that the pregnancy should be terminated. When infected at a later stage, the organ of hearing is most often affected. After 16 weeks of gestation, the risk of infection decreases, but infection during this period can lead to the development of a chronic disease with impaired liver function, anemia, thrombocytopenia, central nervous system damage, immunodeficiency, and dental dysplasia. At the same time, the placenta is affected (inflammation of the villi and vasculitis), which disrupts the nutrition of the fetus. The risk of infection of the fetus by the rubella virus depends on the stage of pregnancy at which the mother was infected (Table 24). Measles.

The risk of miscarriage is increased (as with influenza), but fetal developmental abnormalities are not observed. During pregnancy, the risk of the disease and its severity are increased. Up to 25% of fetuses from sick mothers suffer from polio in utero. This virus does not cause fetal developmental abnormalities.

Mumps. Characterized by low morbidity and mortality. It occurs in a mild form. There is no risk of developmental abnormalities.

Hepatitis A (RNA virus). Oral-fecal route of infection. There are practically no complications during pregnancy if the disease is mild.

Hepatitis B (DNA virus). Routes of infection are parenteral, perinatal and sexual. Up to 10-15% of the population are chronic carriers of the hepatitis B virus. A pregnant woman infects the fetus during childbirth (the use of the fetal head for monitoring control during labor is not recommended).

Parvovirus. During pregnancy, the DNA virus passes through the placenta, causing non-immune edema syndrome in the fetus. The clinical picture in the mother is characterized by the presence of rash, arthralgia, arthrosis, and transient aplastic anemia. 50% of women have antibodies against parvovirus. If a pregnant woman does not have antibodies, then the greatest risk of miscarriage is observed before 20 weeks. Infection of the fetus occurs during the viremia phase. The virus has a tropism for erythrocyte progenitor cells. Clinical manifestations of IUI depend on the gestational age: early pregnancy - spontaneous abortion, late - non-immune fetal hydrops as a manifestation of a severe form of hemolytic anemia, intrauterine fetal death; The edematous syndrome that develops in the fetus occurs due to heart failure caused by anemia. An unfavorable outcome is observed in 20-30% of cases. In 70-80% of cases of serologically confirmed infection in the mother, no damaging effect on the fetus is observed, which can be explained by the neutralization of the virus by antibodies. There is no specific therapy.

Herpes. The greatest role in the pathology of pregnancy and intrauterine infection for the fetus is played by viruses of the family Herpesviridae.

Herpes viruses are transmitted in various ways, but the most important is the sexual route of infection. Primary genital herpes in the mother and exacerbation of chronic herpes are most dangerous for the fetus. If 0.5-1% of newborns are infected intranatally, then with acute genital herpes and exacerbation of chronic herpes (which is manifested by blistering lesions of the skin and mucous membranes of the genitals), the risk of infection of the fetus during childbirth reaches 40%. Adverse fetal outcomes are mainly associated with transplacental (hematogenous) transmission of the pathogen.

Infection of the fetus in the first trimester of pregnancy leads to hydrocephalus, heart defects, developmental anomalies of the gastrointestinal tract, etc. Spontaneous termination of pregnancy is often observed. Infection in the second and third trimesters is fraught with the development of hepatosplenomegaly, anemia, jaundice, pneumonia, meningoencephalitis, sepsis, and malnutrition in the fetus. With an ascending route of infection (from the cervix), the pathogen multiplies and accumulates in the amniotic fluid, and polyhydramnios is observed. Postnatal infection of newborns is also possible in the presence of herpetic manifestations on the skin of the mother, relatives or medical personnel.

Thus, infection of the fetus before 20 weeks of gestation leads to spontaneous abortion or fetal development anomalies in 34% of cases, in periods from 20 to 32 weeks - to premature birth or antenatal death of the fetus in 30-40% of cases, after 32 weeks - to the birth of a patient a child with damage to the skin (herpetic rashes, ulcerations, which are quite rare), eyes (cataracts, microphthalmia, chorioretinitis) and the central nervous system (microor hydrocephalus, cerebral necrosis). It should be noted the severity of the manifestations of the disease in a newborn when infected with the herpes simplex virus (meningoencephalitis, sepsis); death occurs in 50% of cases. Surviving children subsequently have severe complications (neurological disorders, visual impairment, delayed psychomotor development). Neonatal herpes occurs with a frequency of 20-40 cases per 100 thousand newborns.

Cytomegalovirus infection. Obstetric complications such as spontaneous miscarriages, premature birth, antenatal death and fetal abnormalities, polyhydramnios, and non-developing pregnancy are possible. The probability of infection during latent infection is practically absent; during reactivation and persistence it is 0.5-7% and during primary infection it exceeds 40%. Classic manifestations of cytomegalovirus disease are hepatosplenomegaly, thrombocytopenia, brain developmental disorders (microcephaly, intracranial calcification), encephalitis, chorioretinitis, pneumonia and intrauterine growth retardation. The mortality rate for congenital cytomegaly is 20-30%.

Coxsackievirus infection. In the first trimester of pregnancy, this infection is rare and leads to the formation of malformations of the gastrointestinal and urogenital tracts and the central nervous system. If infected in late pregnancy, a newborn may experience the following clinical manifestations: fever, refusal to eat, vomiting, hypotension, skin rashes, convulsions. Some newborns experience otitis media, nasopharyngitis, and pneumonia.

HIV infection. The possibility of intrauterine infection of the fetus from a mother infected with HIV is confirmed by cases of detection of virus antigens in fetal tissues and amniotic fluid. There are three ways for the virus to overcome the placental barrier: 1) transfer of free virus as a result of damage to the placental barrier and interaction with T4 receptors of fetal lymphocytes; 2) primary infection of the placenta, secondary infection of the fetus; carriers of the virus are

Hoffbauer cells of the placenta are formed, through which diaplacental transmission is possible; 3) the passage of the virus during childbirth from the affected cells of the cervix and vagina through the mucous membranes of the fetus. HIV infection is acquired by 20-30% of newborns from infected mothers. Children infected with HIV have skin lesions in the form of bacterial, fungal and viral exanthema.

Bacterial infection. The development of intrauterine bacterial infection is facilitated by the presence of focal foci (tonsillitis, sinusitis, carious teeth, pyelonephritis, chronic and acute lung diseases, etc.). Pathogens can penetrate the fetus through the placenta. Ascending infection most often occurs when the integrity of the amniotic sac is disrupted during pregnancy or childbirth. In addition, ascending infection is facilitated by colpitis, cervicitis, invasive methods for assessing the condition of the fetus (amnioscopy, amniocentesis, etc.), numerous vaginal examinations during childbirth, isthmicocervical insufficiency, and the threat of miscarriage. With generalized microbial contamination of amniotic fluid, chorioamnionitis is manifested by fever, chills, tachycardia, purulent discharge from the genital tract and other symptoms. The fetus is diagnosed with incipient hypoxia.

Among IUIs of a bacterial nature, STDs prevail. The most common causative agents of urogenital infections include Chlamydia trachomatis. Chlamydia primarily affects columnar epithelial cells. More than half of infected women have no clinical manifestations.

Clinical manifestations of chlamydial infection in newborns are conjunctivitis, which occurs at a time atypical for IUI - 1-2 weeks, and sometimes 5 weeks after birth, and interstitial pneumonia, which develops within 2-4 months from birth. Such long-term timing of infection indicates the predominant route of infection of the fetus with chlamydia through direct contact with the mother's birth canal, although an ascending route of infection through intact fetal membranes cannot be ruled out.

Mycoplasma infection. Mycoplasmosis during pregnancy develops mainly in people with immunodeficiency conditions. Urogenital mycoplasmosis can lead to IUI, which is

cause of miscarriage, stillbirth; In premature newborns, mycoplasmas cause the development of pneumonia, meningitis, and generalized infection.

Congenital syphilis. The disease is multisystem and has various forms. Its manifestations resemble secondary syphilis. Most children appear healthy at birth, some have vesicular bullous rashes on the palms and soles, but the following symptoms of the disease may appear 4 days to 3 weeks after birth.

Flu-like syndrome:

Meningeal symptoms;

Watery eyes (inflammation of the iris);

Discharge from the nose, the mucous membranes are hyperemic, edematous, eroded, replete with pale treponema;

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

Generalized arthralgia (no pain due to active movements in the extremities - Parrot's psuedoparalysis, the x-ray shows signs of osteochondritis, periostitis is often detected, in particular, of the tibia (saber tibia).

Enlargement of all groups of lymph nodes (cervical, elbow, inguinal, axillary, popliteal).

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

Rashes:

Maculopapular;

Fusion of papular lesions to form condylomas lata.

Listeriosis. In pregnant women, listeriosis can occur in the form of a flu-like illness, in a subclinical form with erased symptoms. Abortions or premature births, stillbirths or fetal deformities incompatible with life are observed. In fetuses, listeriosis manifests itself as granulomatous sepsis or septicopyemia with metastatic purulent meningitis; In newborns, sepsis and pneumonia are most common. The mortality rate of newborns with listeriosis reaches 60-80%.

Toxoplasmosis. The disease most often occurs through close contact with animals. Women are infected either by sporodonts from the soil (by

fallen there with the feces of animals, for example cats), from hands, furniture, floor, or cystozoids from Toxoplasma cysts contained in the tissues of intermediate hosts (when eating insufficiently heat-treated meat). The clinical picture is characterized by polymorphism (presence or absence of fever, enlarged lymph nodes, liver and spleen, myocarditis, pneumonia, etc.). With toxoplasmosis, the development of endometritis, damage to the placenta, threat of miscarriage, and fetal malnutrition are possible.

Candidiasis. Often develops during pregnancy urogenital candidiasis. This condition, like bacterial vaginosis, is a background for the addition of another bacterial and/or viral infection.

diagnostics

There are no reliable methods for diagnosing fetal IUI. One can only assume it based on indirect signs and establish infection of the fetus and gestational sac.

In a newborn, the infection manifests itself either from the moment of birth or within 3-4 days (with the exception of chlamydia and a number of other infections that may appear later). Its diagnostic signs depend on the localization or degree of generalization of the process.

In the diagnosis of IUI, the main ones are bacteriological and immunological methods. These include the detection of etiologically significant microorganisms in cultures in quantities exceeding 5x10 2 CFU/ml, and PCR, carried out to identify certain fragments of DNA or RNA of the pathogen cells.

Cultures and scrapings (to identify intracellularly located pathogens) in pregnant women are taken from the vagina and cervical canal. In pregnant women at high risk of developing IUI, they resort to invasive methods of obtaining material for bacteriological study (chorionic aspiration in early pregnancy, study of amniotic fluid after amniocentesis and umbilical cord blood obtained by cordocentesis). Bacteriological studies must be combined with identification of antigen in the blood serological methods determination of IgM and IgG, which are specific for that

or other pathogen. It is advisable to repeat the studies at least once every 2 months.

Currently, great importance is attached to ultrasound, which can be used to determine indirect signs of fetal IUI.

Indirect ultrasound signs of IUI

Symptom of fetal growth restriction.

Abnormal amount of amniotic fluid (usually polyhydramnios).

Signs of premature or delayed maturation of the placenta. Violation of its structure ( varicose veins its vessels, the presence of hyperechoic inclusions, placental edema, contrasting of the basal plate).

Irregularly shaped expansions of the intervillous space that do not correspond to the centers of the cotyledons.

Early appearance of placental lobulation.

Expansion of the pyelocaliceal system of the fetal kidneys.

Micro- and hydrocephalus.

Dilatation of the ventricles of the brain, increased echogenicity of brain tissue, cystic changes or foci of calcification (necrosis) in the periventricular zone of the brain, liver tissue.

Ascites, pericardial or pleural effusion, hepatomegaly, hypoechoic bowel, hydrops fetalis.

Screening tests for newborns at high risk of developing IUI include the study of smears of amniotic fluid, placenta, cord blood cultures and stomach contents of the newborn. In some cases, a blood culture test of the newborn is recommended, with capillary rather than umbilical cord blood collection being the most appropriate. The activity of alkaline phosphatase is determined, the number of platelets is counted (thrombocytopenia below 150x10 9 /l is considered a sign of infection), the ratio of young forms of leukocytes and neutrophils and radioisotope determination of B-lactamase (to detect infection with B-lactamase-producing microorganisms). Histological examination of the placenta is of great importance, although inflammatory changes do not always correspond to the child’s disease. In the diagnosis of viral infections, examination of formalin-fixed placental tissue using the PCR method can be useful. When conducting a serological examination of a newborn baby (IgG, IgM), the following principles should be remembered:

An examination of the newborn should be carried out before using donor blood products in the treatment of the child;

The results of the examination of the child should always be compared with the results of the examination of the mother;

The presence of specific immunoglobulins of class G in a titer equal to or less than the titer of the corresponding maternal antibodies does not indicate intrauterine infection, but the transplacental transfer of maternal antibodies;

The presence of specific immunoglobulins of class M in any titer indicates the primary immune response of the fetus or newborn to the corresponding bacterial/viral antigen and is indirect sign infections;

The absence of specific M immunoglobulins in the blood serum of newborns does not exclude the possibility of intrauterine or intrapartum infection.

A comparative analysis of the main methods for detecting IUI pathogens is shown in Table. 25.

prevention and treatment

Important importance in the prevention of IUI is given to identifying risk groups. Numerous risk factors can be divided into the following three groups.

Chronic infectious diseases: chronic infections of the respiratory system, digestive system, caries, tonsillitis; urogenital infections (pyelonephritis, colpitis, STDs); intestinal dysbiosis, bacterial vaginosis.

Complications of pregnancy: anemia, gestosis, miscarriage, isthmic-cervical insufficiency and its surgical correction, exacerbation chronic diseases and ARVI in the second half of pregnancy.

Complications of childbirth: ARVI during childbirth, prenatal rupture of water; weakness of labor; protracted labor; multiple vaginal examinations; delivery operations and benefits; long water-free period.

Method	Sensitivity	Specificity	Subjectivity of assessment	Advantages	Flaws
Cultural		Close to absolute	Present	High accuracy. Detects only living microorganisms. High reliability positive result	High cost, labor intensive. Available only for large centers. Strict requirements for collection, transportation, and storage of material. Unacceptable against antibiotics
	Close to absolute	Close to absolute	Virtually absent	High accuracy. High reliability of negative results.	Detects both live and dead microorganisms - a limitation for cure control. Risk of false positive results due to contamination
Enzyme-linked immunosorbent assay (ELISA):	Satisfactory	Satisfactory	Absent	Satisfactory accuracy at low cost.	Sensitivity and effectiveness vary for different excitatory

Continuation of the table. 25

antigen detection				Convenient for mass research	calves, and therefore there are test systems for diagnosing a limited number of infections. Ineffective for latent and chronic infections
Immunofluorescence reaction (RIF)	Satisfactory	Satisfactory		Does not require stringent conditions for laboratory organization and expensive equipment Satisfactory accuracy at low cost	Subjectivity in assessment. Low interlaboratory reproducibility
Cytological				Cheap, fast	Subjectivity in assessment. Low accuracy
Enzyme-linked immunosorbent assay (ELISA): detection of antibodies	Satisfactory		Absent	Detects the presence of infection of any location. Detects acute, chronic and latent forms of infection (IgM, IgG in dynamics)	Retrospective diagnosis (for IgG). A false negative result is possible in cases of immunodeficiency. Immunological trace - after cure, IgG remains positive for a long time

There are general principles of prevention and treatment for IUI.

1. Etiotropic antimicrobial (antiviral) therapy, taking into account the stage, general and local symptoms, duration of the infectious-inflammatory disease, the presence of a mixed infection, gestational age, clinical and laboratory signs of IUI.

2. Prevention (treatment) of dysfunction of the fetoplacental complex at 10-12, 20-22 and 28-30 weeks of pregnancy, as well as at individual critical periods and in the complex of prenatal preparation (metabolic therapy, vasoactive drugs and antiplatelet agents).

3. Immunomodulatory, interferon-corrective therapy: plant adaptogens, viferon.

4. Correction and prevention of microbiocenosis disorders in the pregnant woman’s body: bifidumbacterin, lactobacterin (at least 15 doses per day), floradophilus (1 capsule 2 times) enterally for 10-14 days; in combination with acylact or lactobacterin vaginally.

5. Pre-gravid preparation.

6. Treatment of sexual partners with STDs.

A number of preventive measures in most economically developed countries of the world, including the Russian Federation, have long been legalized by the state (Wassermann reaction, determination of Australian antigen, HCV antibodies and antibodies to HIV in blood serum). Children should be vaccinated against hepatitis B immediately after birth, after a week, after a month and after 6 months of life to prevent the development of severe forms of the disease. There are no specific treatments for hepatitis A. To prevent severe disease, you can use immunoglobulin 0.25 ml per 1 kg of body weight.

Women who have not previously had rubella, have not received rubella vaccination and, therefore, do not have antibodies to the rubella virus, are recommended to be vaccinated before pregnancy. Vaccination should be performed 3 months before pregnancy. A pregnant woman, especially one at risk, should avoid any contact with a patient with exanthema infection. In case of rubella infection in the first 16 weeks of pregnancy, its interruption is indicated.

If the infection occurred at a later stage, the tactics are individual; it is advisable to conduct an IgM study of umbilical cord blood (cordocentesis), a virological or PCR study of amniotic fluid.

niotic fluid or chorionic villus sampling (amniocentesis). If infection of the fetus is confirmed, termination of pregnancy is desirable.

For women who refuse to terminate a pregnancy at >16 weeks, administration of specific IgG may be a measure to prevent infection in the fetus.

Administration of gamma globulin to patients with rubella during gestation slightly reduces the incidence of fetal abnormalities. Vaccination of pregnant women is not carried out.

If a pregnant woman gets chickenpox 5-7 days before birth or in the first 3-4 days after birth, immediate administration of Zoster immunoglobulin or Varicella-Zoster immunoglobulin to the newborn is indicated. If the disease develops in a newborn (despite preventive measures), treatment with acyclovir is recommended at a dose of 10-15 mg per 1 kg of body weight 3 times a day. Treatment of sick pregnant women with acyclovir is carried out only in severe cases of the disease.

For mumps and measles, vaccination of pregnant women is not carried out, since a live attenuated vaccine is used. There is an inactivated vaccine available against influenza, types A and B. There is no risk to the fetus during vaccination. It is recommended to vaccinate pregnant women according to strict epidemiological indications in the second and third trimesters.

Since there is no specific therapy for parvovirus infection, it is recommended to use immunoglobulin to prevent severe complications.

If a pregnant woman has a herpetic infection, the nature of preventive and therapeutic measures, obstetric tactics will depend on the type of disease, its form (typical, atypical, asymptomatic, duration), as well as on the presence of genital lesions, the condition of the membranes, etc.

In case of primary infection of a pregnant woman in the early stages of pregnancy, it is necessary to raise the question of its termination. If the pathology occurs at a later date or the woman was infected before pregnancy, preventive measures consist of dynamic ultrasound monitoring of the development and condition of the fetus, prescribing a course of therapy, including a metabolic complex, cell membrane stabilizers, and unithiol.

The basic antiviral drug is acyclovir (Zovirax). Despite the lack of evidence of its teratogenic and embryotoxic

clinical effects, it is advisable to limit the prescription of acyclovir to pregnant women suffering from genital herpes to the following indications: primary genital herpes; recurrent genital herpes, typical form; genital herpes in combination with a permanent threat of miscarriage or symptoms of IUI. Acyclovir is prescribed 200 mg 5 times a day for 5 days. The issue of longer use of the drug and repeated courses of treatment is decided individually. The drug is highly effective in preventing perinatal infection. Pregnant women with frequent relapses of infection have had positive experience with permanent therapy with acyclovir (suppressive therapy). In case of complicated herpetic infection (pneumonia, encephalitis, hepatitis, coagulopathy), treatment is carried out together with an infectious disease specialist. Intravenous administration of the drug is required at a dose of 7.5 mg/kg every 8 hours for 14 days. At the same time, it is advisable to use immunoglobulin therapy, interferon preparations, antioxidants (vitamins E and C). Among interferons, preference should be given to viferon; adaptogens are also prescribed plant origin. It is possible to use laser blood irradiation, plasmapheresis and enterosorption. It is also necessary to treat bacterial diseases accompanying genital herpes (most often chlamydia, mycoplasmosis, trichomoniasis, candidiasis, bacterial vaginosis). After complex therapy complications for mother and fetus are reduced by 2-3 times.

The tactics of labor management in women with primary and recurrent herpes deserve special attention. C-section as a prophylaxis for neonatal herpes, it is necessary in the presence of herpetic eruptions on the genitals or primary genital herpes in the mother 1 month or less before birth. In the case of abdominal delivery due to rupture of the membranes, the anhydrous interval should not exceed 4-6 hours.

Treatment and prevention of cytomegalovirus infection is quite difficult. Treatment consists of courses of passive immunization. It is possible to use anti-cytomegalovirus immunoglobulin 3 ml intramuscularly once every 3 days, 5 injections per course. Treatment with human immunoglobulin is more effective (intravenous administration of 25 ml every other day, 3 infusions per course). Intraglobin-F is administered at the rate of 4-8 ml per 1 kg of body weight once every 2 weeks for prophylactic use. Number of preventive

infusions, as well as the preventive treatment regimen are determined individually. Cytotect for proven cytomegalovirus infection with therapeutic purpose administer 2 ml per 1 kg of body weight every 2 days under the control of serological parameters. Preventive prenatal preparation includes infusion of 5 ml of cytotect 2 times a week for 2 weeks. In any case, the expected benefit from the use of immunoglobulins should exceed the risk of possible complications (allergic and pyrogenic reactions, production of antibodies - antigammaglobulins, exacerbation of infection). The specific antiviral drug ganciclovir is used according to strict vital indications for the mother and newborn. Viferon is also used to prevent complications.

Currently, zidovudine and other nucleoside analogs with antiviral activity are used to treat AIDS. No evidence of the teratogenic effect of these drugs has been established, but their use in HIV-infected people in the early stages of pregnancy should be strictly justified. The main purpose of prescribing drugs to seropositive pregnant women is to prevent transmission of the virus to the fetus (it occurs through the placenta or to the newborn - when passing through an infected birth canal, and especially often through breast milk and in close contact with the mother). Zidovudine is prescribed at a dose of 300-1200 mg/day. Although experience with its use is limited, the administration of zidovudine to HIV-infected pregnant women may be an effective method for preventing the development of HIV infection in young children. Breastfeeding stops.

If there are signs of a bacterial intrauterine infection, intensive antibiotic therapy (penicillins, cephalosporins) is carried out. A newborn born with signs of IUI is prescribed antibacterial therapy, initially with the same antibiotics, and then depending on the isolated microflora and its sensitivity to antibiotics.

Prevention of congenital chlamydia is of a similar nature. During pregnancy, macrolides are used to treat the disease (erythromycin 500 mg orally 4 times a day for 10-14 days). Josamycin (vilprafen) is close in its spectrum of antimicrobial action to erythromycin, has virtually no side effects, is not destroyed in the acidic environment of the stomach, and has antichlamydial action.

equal to doxycycline. The drug is prescribed 2 g per day in 2-3 doses for 10-14 days. Spiramycin (rovamycin) is used at a dose of 3,000,000 units 3 times a day (at least 7 days). In case of individual intolerance to natural macrolides, it is permissible to prescribe clindamycin orally at 0.3-0.45 g 3-4 times a day or intramuscularly at 0.3-0.6 g 2-3 times a day.

Treatment of patients with urogenital infection caused by Mycoplasma hominis And Ureaplasma urealytica, it is necessary to begin immediately after confirmation of the diagnosis by laboratory methods. The pregnant woman and her husband are being treated. It does not differ significantly from that with urogenital chlamydia. During pregnancy, preference should be given to rovamycin and vilprafen. Against the background of antibacterial therapy, it is advisable to prescribe eubiotics (acylact, lactobacterin). It should be noted that a more effective prevention of IUI caused by mycoplasmosis and chlamydia is the treatment of women outside pregnancy, when it is possible to use a wider range of antibacterial (tetracyclines, fluoroquinolones, etc.) and immunostimulating agents (decaris, prodigiosan, tactivin, etc.) .

Prevention of congenital toxoplasmosis

Identification of women infected for the first time during a given pregnancy (by an increase in antibody titer in paired sera), timely resolution of the issue of termination of pregnancy.

Treatment during pregnancy to prevent transmission of infection to the fetus.

Examination and treatment of newborns.

Serological monitoring of uninfected women throughout pregnancy.

Treatment is carried out with sulfonamides.

The drug of choice for the treatment of listeriosis is ampicillin (penicillin), used in doses of 6-12 g/day for severe forms of the disease and 3-4 g/day for minor manifestations - daily for 2-4 weeks. Pregnant and postpartum women should be isolated. Treatment of newborns with listeriosis is very difficult and should begin as early as possible. The drug of choice is ampicillin, prescribed intramuscularly at 100 mg/kg 2 times a day during the 1st week of life and 200 mg/kg 3 times a day at age

grow older than 1 week. The duration of treatment is 14-21 days.

Treatment of patients with syphilis during pregnancy is carried out according to the general principles and methods of treating this infection. With each subsequent pregnancy, a patient with syphilis must undergo specific treatment. A three-time serological examination of each pregnant woman is mandatory in the first and second half of pregnancy and after 36 weeks of pregnancy.

For urogenital candidiasis in pregnant women, it is preferable to use local therapy (clotrimazole, miconazole, isoconazole, natamycin). The feasibility of enteral administration of antifungal agents is determined by the presence or absence of gastrointestinal candidiasis. Recurrent vaginal candidiasis is an indication for examination for viral and bacterial sexually transmitted infections. Patients should be informed that they and their sexual partners are recommended to undergo examination and, if necessary, treatment, abstinence from sexual activity until recovery, or the use of barrier methods of contraception.

Bacterial vaginosis is a clinical syndrome characterized by the replacement of the normal vaginal microflora, which is dominated by lactobacilli, by opportunistic anaerobic microorganisms. When treating pregnant women, intravaginal administration of clindamycin phosphate in the form of 2% vaginal cream 5 g at night for 7 days or 0.75% metronidazole gel 5 g at night also 7 days from the second trimester of pregnancy is preferable. If local therapy is insufficiently effective, oral use of the following drugs is possible: clindamycin 300 mg 2 times a day for 5 days or metronidazole 500 mg 2 times a day for 3-5 days. It is advisable to use eubiotics, vitamins and other agents that help normalize the microbiocenosis of the vagina and intestines.

Issues of prevention and treatment for IUI cannot be considered completely resolved. The validity of prophylactic antibiotics for pregnant women and newborns at high risk of developing IUI is still a subject of debate, although most clinicians consider such measures appropriate.

Due to the inability to carry out massive complex antibacterial therapy in pregnant women when planning

The child's family should treat the couple long before pregnancy as preconceptional preparation.

Pre-gravid preparation scheme

1. Comprehensive examination with the study of immune, hormonal, microbiological status, diagnosis of concomitant extragenital diseases, consultations with related specialists.

2. Immunostimulating, immunocorrective and interferon-correcting therapy:

Drug therapy (pyrogenal, prodigiosan, taktivin, immunofan, specific immunoglobulin therapy and vaccine therapy, ridostin, larifan, viferon), laser therapy, plasmapheresis;

Herbal medicine (ginseng, eleutherococcus, aralia, lemongrass, etc.)

3. Etiotropic antibacterial or antiviral therapy according to indications:

Tetracyclines;

Macrolides;

Fluoroquinolones;

Clindamycin, rifampicin;

Cephalosporins;

Acyclovir, ganciclovir.

4. Eubiotic therapy:

For oral use - bifidumbacterin, lactobacterin, floradophilus, solcotrichovac;

For vaginal use - bifidumbacterin, acylact, lactobacterin, “Zhlemik”, “Narine”.

5. Metabolic therapy.

6. Correction of menstrual irregularities and concomitant endocrinopathies.

7. Mandatory treatment of a sexual partner in the presence of STDs, using individual regimens for chronic inflammatory diseases of the genitals.

Thus, the greatest danger of intrauterine infection faces those children whose mothers are primarily infected with IUI during pregnancy. For infections such as rubella and toxoplasmosis, primary infection of a pregnant woman is the only option for infecting the fetus. As calculations show, identifying women

Women at risk at the stage of pregnancy planning and implementation of appropriate preventive measures can reduce the risk of IUI with severe consequences by 80%.

Carrying out mass screening for IUI is currently hardly possible for financial reasons. However, in cases where the expectant mother approaches the birth of a child with full responsibility and turns to an obstetrician-gynecologist at the pregnancy planning stage, it is necessary to prescribe a minimum amount of research for IUI - determination of IgG to the main pathogens - cytomegalovirus, toxoplasma, herpes simplex virus, rubella virus . The results of the study will make it possible to find out whether a woman belongs to any risk group. Carrying out preventive measures (for example, vaccination in case of rubella), as well as compliance by a woman at risk with recommendations for preventing infection during pregnancy will significantly reduce the risk of IUI in the unborn child.

The second important aspect of examination for IUI before pregnancy is the possibility of proving primary infection of the pregnant woman. Its presence is evidenced by IgG seroconversion, which requires the use of invasive methods of examining the fetus or termination of pregnancy in the early stages. If a pregnant woman first applies for registration in the second or third trimester, the determination of IgG class antibodies to IUI loses its relevance, more informative in this case, determination of IgM class antibodies, which are an indicator of primary infection and reactivation of chronic infection, as well as PCR research.

In this case, laboratory methods should be considered secondary to clinical examination (including ultrasound). For diagnosing genital herpes, chlamydia, mycoplasmosis in pregnant women, direct methods (PCR, etc.) are more effective.