Sudden exanthema (roseola) in children and adults: symptoms, treatment. Cheat sheet for children's infections Symptoms and their treatment in children

This collection is intended for a wide range of readers. It talks about the most common acute infectious diseases in children. Along with such childhood infections as measles, scarlet fever, chickenpox, etc., we also include diseases that are equally found in adults, but pose a great danger to children. These are influenza and epidemic hepatitis (Botkin's disease), diseases that have attracted special attention in recent years.

What causes all these diseases, how they become infected and what measures can be taken to prevent them - this is the main content of this section.

This section is intended for a wide range of readers. It provides basic information about common infectious diseases in children. Particular attention is paid to caring for sick children at home and preventing infectious diseases.

Infectious diseases in children

Other diseases and injuries occurring in children

The fight against children's contagious (infectious) diseases has been and remains one of the main tasks of healthcare.

This fight is becoming especially important nowadays in connection with the decree providing for a sharp reduction in the incidence of infectious diseases and the complete elimination of some of them.

Numerous medical workers are engaged in solving this problem, starting with prominent scientists of all specialties (microbiologists, infectious disease specialists, pediatricians) and ending with nurses. However, for this struggle to be more successful, parents must take an active part in it. Without the conscious and active help of the general population, many preventive measures, that is, measures that help prevent the disease, become significantly less effective. But in order to provide this assistance, you need to know the main signs of these diseases, ways of spreading and measures to prevent them.

This section was written to familiarize a wide range of readers with the most common childhood infectious diseases and modern methods of their prevention and treatment. The so-called childhood infections include: diphtheria, scarlet fever, measles, whooping cough, chicken pox, rubella, mumps, polio. The name “childhood infections” has become widespread, but these diseases can also occur in adults, but most often they affect children aged 1 to 8 years. The predominant incidence of these infections in childhood is explained by the ease and speed of their spread with a high possibility of contact (especially in child care institutions, kindergartens, nurseries, and schools).

Many parents believe that every child must inevitably suffer from childhood infectious diseases, and the earlier he gets sick, the easier he will survive the disease. This is, of course, not true. It should be remembered that almost every disease can be prevented and that every disease, including infectious diseases, weakens the child’s body and inhibits its development, sometimes for a long time. The younger the child, the more harm the disease causes him. Therefore, the joint efforts of parents and medical workers should be aimed at preventing the occurrence of infectious diseases, especially in the first years of a child’s life.

The socio-economic significance of childhood infectious diseases is also very great: they disrupt the normal life of children's institutions, quarantines take mothers away from production, sometimes for a long time, which interferes with production, creates difficulties in family life and leads to large expenditures of public funds.

Propaedeutics of childhood diseases

In the third edition of “Propaedeutics of Childhood Illnesses,” all the main sections of the doctrine of a healthy child, his nutrition and care for him were revised anew and underwent some processing from the standpoint of the basic ideas of the physiological teachings of I. P. Pavlov. Additions and changes have also been made to all chapters in accordance with new literature data and our own experience.

We sought to give the student a short textbook that would allow him not only from the standpoint of creative Soviet Darwinism and the physiological teachings of I.P. Pavlov to learn the basics of the doctrine of a healthy child, but which would interest him and help him fall in love with his future specialty - pediatrics. We wanted the student - the future pediatrician - to understand the enormous importance of knowing the age-related characteristics of a healthy child and the decisive influence on the development of children and the resistance of their body to any negative influences of the correct organization of environmental factors, their care, their nutrition and upbringing.

In practical classes in the course of propaedeutics of childhood diseases, the student must acquire the correct skills for objective examination of the child in order to be able to detect even minor deviations from the norm in the initial phases of diseases in his future activities. Helping the student with this is also one of the objectives of the textbook.

A pediatrician in his daily work should focus on the prevention of childhood diseases and, already in his student years, “acquire a taste” for this work. This is one of the main tasks of proper education of a pediatric student; The textbook on propaedeutics of childhood diseases should help teachers in this work.

When presenting the methodology for studying children and the general semiotics of childhood diseases, we considered it necessary to dwell only on the features of using the main clinical methods for assessing the health status of children of different ages. The theoretical justifications for these methods are further presented in practical classes and described in detail in textbooks on diagnostics and propaedeutics of internal diseases. We sincerely thank all the comrades who sent us their critical comments, and are especially grateful to the members of the academic council of the Leningrad State Pediatric Medical Institute for all their valuable comments and instructions they made when discussing the second edition of our textbook.

All critical comments that will be made to us regarding the third edition of “Propaedeutics of Childhood Illnesses” will be accepted with sincere gratitude.

The published textbook - “Propaedeutics of Childhood Diseases” - is intended for students of pediatric faculties of medical institutes. When compiling the textbook, the experience of teaching propaedeutics of childhood diseases to students of the Leningrad State Pediatric Medical Institute was used and critical comments made regarding the chapters written for the “Manual of Pediatrics” by M. S. Maslov, A. F. Tour and M. G. were taken into account. Danilevich (vol. I, 1938). These chapters, largely revised, form the basis of this textbook.

It is possible that there will be defects in our work, so we will accept with gratitude all instructions and comments that will be made by heads of departments, practitioners and students themselves.

The fourth edition, the need for which arose two months after the publication of the third edition, is published without any significant changes and additions, and only occasional errors and typos have been corrected.

Contents and objectives of the course on propaedeutics of childhood diseases

The original content of pediatrics as one of the medical disciplines has expanded significantly. Pediatrics has long ceased to be a science only about the treatment of sick children and is now considered as the study of a healthy and sick child. This teaching covers the physiology, dietetics, hygiene, pathology and treatment of the child from birth to puberty. Modern pediatrics pays especially great attention to the prevention of diseases in children. Every children's doctor in his daily practical work must not only be a full-fledged attending physician, able to make an accurate diagnosis and correctly treat a sick child, but he must also be a good preventive doctor, who knows the child's diet very well, knows how to organize the necessary care and establish a rational regimen for an individual healthy child of any age, and for an entire group of children. A pediatrician should not be aloof from issues of raising children. The student must learn and study all these various aspects of the work of a pediatrician mainly when taking a course in clinical pediatrics. Propaedeutics of childhood diseases is an introduction to pediatric clinics.

The course of propaedeutics of childhood diseases includes the following four main sections: 1) anatomical and physiological characteristics of children, including the laws of physical and neuropsychic development of the child; 2) methods of objective examination of children, including features of taking anamnesis; 3) general semiotics of childhood diseases; 4) dietetics for a healthy child with the basic elements of baby food technology.

Without a clear knowledge of these sections, the preventive and therapeutic work of a pediatrician is completely unthinkable. A correct assessment of data from conventional physical, laboratory and other methods of clinical examination of a child and an understanding of the uniqueness of the pathology of children are possible only if there is sufficiently deep knowledge of the age-related anatomical and physiological characteristics of the child’s growing body. Without knowledge of the laws of physical and neuropsychic development of children, it is impossible to carry out the correct organization of public and individual protection of childhood, and, therefore, it is impossible to ensure the prevention of childhood diseases. This knowledge should form the basis of rationally organized physical education of children.

Clinical research of children requires a significant uniqueness of medical technique, the study of which should also be included in the course of propaedeutics of childhood diseases.

Brief information on the general semiotics of the most important diseases of childhood should provide the student with the correct orientation when taking courses in faculty and hospital pediatrics.

In the activities of a pediatrician, as mentioned above, preventive and therapeutic work are closely and inextricably linked. That is why, in the course of propaedeutics of childhood diseases, much attention should be paid to the diet of a healthy child and the basics of individual hygiene for children as the main elements in the daily preventive work of every practical pediatrician. The preventive side of the work of pediatricians has acquired particular importance in the Soviet Union, since in our country the vast majority of children, starting from a very early age, are served by preventive and therapeutic children's institutions, on the correct management of which their life and health largely depend.

It would be a big mistake to think that you can become a good pediatrician without a thorough knowledge of general theoretical disciplines (anatomy, histology, physiology, pathophysiology, etc.) studied in junior courses, and clinical disciplines in various sections of adult pathology studied in senior courses. courses. A pediatrician can only correctly and confidently navigate all the theoretical and practical issues of his specialty if he has good general medical training in all disciplines included in the program of a higher medical school. Only under this condition will he clearly understand all the features of the physiology and pathology of children at different age periods.

It must be especially emphasized that every pediatrician must know very well infectious diseases of childhood and must be well versed in issues of general and specific epidemiology.

The need for such versatile knowledge undoubtedly makes pediatrics a difficult specialty, but this path of study provides a good pediatrician with a broad outlook and extremely interesting and fruitful opportunities for practical and scientific activity.

A-Z A B C D E F G H I J J K L M N O P R S T U V X C CH W SCH E Y Z All sections Hereditary diseases Emergency conditions Eye diseases Children's diseases Men's diseases Venereal diseases Women's diseases Skin diseases Infectious diseases Nervous diseases Rheumatic diseases Urological diseases Endocrine diseases Immune diseases Allergic diseases Oncological diseases Diseases of the veins and lymph nodes Hair diseases Dental diseases Blood diseases Breast diseases ODS diseases and injuries Respiratory diseases Diseases of the digestive system Diseases of the heart and blood vessels Diseases of the large intestine Diseases of the ear, throat , nose Drug problems Mental disorders Speech disorders Cosmetic problems Aesthetic problems

Pediatrics is an independent field of medicine that studies age-related developmental characteristics of children, childhood diseases, as well as issues of organizing care for healthy and sick children. Initially, the subject of pediatrics was exclusively early childhood diseases and their treatment. In the modern understanding, pediatrics covers various aspects related to the normal development and diseases of children at various age periods (from birth to puberty). These areas include physiology, hygiene, dietetics, childhood diseases, their treatment and prevention.

In pediatric medicine, several areas are developing in parallel: preventive, clinical and social. The preventive direction includes the development and implementation of measures to prevent childhood diseases; clinical – direct examination and treatment of a sick child; social – gradual rehabilitation and integration of children into society. The anatomical and physiological characteristics of a growing organism determine the unique course of those diseases that occur in childhood.

In pediatrics, it is customary to distinguish several age periods of a child’s life: the neonatal period (first month), infancy (from 1 month to 1 year), early childhood (from 1 to 3 years), preschool (from 3 to 7 years), primary school ( from 7 to 11 years old), high school or teenage (from 12 to 17-18 years old) age. At different age periods of a child’s development, certain childhood diseases predominantly occur.

Thus, during the newborn period, childhood diseases caused by disorders of intrauterine development appear (asphyxia, hemolytic disease of the fetus, rickets

The most common symptoms of childhood diseases are rash, swollen lymph nodes, hyperthermia, runny nose, cough, vomiting, abdominal pain, and cramps. If these and other signs of the disease appear, it is imperative to consult your child with a pediatrician. Every parent should be familiar with the basics of pediatrics, know the main childhood diseases and their manifestations in order to be able to assess the seriousness of the baby’s condition and determine whether the ailment poses an immediate threat to life.

Pediatrics does not stand still: new methods for diagnosing and treating childhood diseases are emerging and being implemented, and understanding of the mechanisms of disease development in children is developing and deepening. The successes of modern pediatrics have made many once fatal childhood diseases recede. This was facilitated by the creation of vaccines against a number of childhood infectious diseases, the development of balanced artificial mixtures, the emergence of modern antibacterial drugs, and improved quality of diagnosis and treatment of children. However, childhood morbidity rates remain high; Diseases that were previously considered exclusively the lot of people of mature age have become significantly “younger”. Among childhood diseases, cardiovascular, endocrine, neurological diseases, neoplasms, and pathologies of the musculoskeletal system are increasingly common.

A child is not just a small copy of an adult. The child's body is in a state of continuous development, has a number of anatomical and physiological characteristics, physical and emotional immaturity, which determines the specific course of childhood diseases. The development of childhood diseases is always unpredictable: even a common runny nose in a child can become fatal if its causes are not recognized in time, the correct etiopathogenetic treatment is not selected, and specialist supervision is not organized. At the same time, thanks to the high compensatory capabilities of the child’s body, many diseases that cause chronic pathology or disability in adults can be successfully cured in children.

The origins of many adult diseases come from childhood. Therefore, the health status of an adult is largely determined by the conditions of growth and development of the little man, and by care for his health at the very beginning of life. Today, the emphasis in pediatric medicine is shifting towards disease prevention, which includes antenatal fetal protection, prevention of birth injuries, organization of careful care for the newborn (ensuring optimal diet, sleep and wakefulness, hardening), timely vaccination of children according to the national calendar of preventive vaccinations, screening programs for identifying hereditary pathologies, providing patronage and dispensary observation. Caring for children's health and preventing childhood diseases is a priority component of state policy.

Specialized care in the children's healthcare system is provided in children's clinics and hospitals, pediatric departments of multidisciplinary medical centers, and private children's clinics. It is impossible and ineffective to treat childhood diseases using “adult” methods, therefore, in recent years, narrow pediatric areas have been distinguished in pediatrics: pediatric cardiac surgery, pediatric traumatology and orthopedics, pediatric neurosurgery, pediatric hematology and oncology, pediatric anesthesiology and resuscitation, etc. The most important components of success in treatment Children's diseases are ensured by a professional approach, the use of high-tech diagnostic and treatment methods, and a trusting relationship between the doctor, parents and child.

Childhood illnesses cause natural anxiety in adults and a natural desire of parents to learn as much as possible about the causes of diseases and methods of treating them. The section of childhood diseases, located on the pages of the Medical Directory, introduces parents to the most common pathology in children of different ages, the causes and symptoms of diseases, necessary medical procedures and child care activities. On the pages of the site “Beauty and Medicine” you can find recommendations from pediatric specialists and the most up-to-date information about achievements in the field of prevention, diagnosis and treatment of childhood diseases.

In early childhood, the immune system continues to develop, so children are susceptible to frequent diseases. These are mainly infectious diseases: bacterial and viral. The child’s expanded social circle also contributes to their occurrence: on a walk with other children or in a child care facility.

In addition, not all children are taught the rules of hygiene at this age; there may still be a habit of putting various objects, toys or fingers into their mouths. Therefore, most children cannot avoid bacterial and viral diseases.

The most common childhood diseases at an early age are infections: endless colds, intestinal infections, flu, tubinfection (tubintoxication), etc.

It is advisable for parents to know their manifestations, which will help to suspect the disease in a timely manner and consult a doctor. Symptoms of intoxication at the beginning of infections may be similar, but there are still specific manifestations.

ARVI

According to statistics, ARVI is the most common disease in children, especially at an early age during the cold season. ARVI accounts for 90% of all infections in children. On average, a child can get a respiratory infection up to 6-8 times during the year.

This frequency is due to the fact that the body has not yet encountered the virus and has not developed antibodies to it. Frequent ARVIs are not a manifestation of an immunodeficiency state in a child; they only reflect the frequency of contact with the source of a viral infection.

Respiratory infections caused by parainfluenza viruses, influenza viruses, adenoviruses, enteroviruses, and rhinosyncytial viruses are more common. Over 300 varieties of pathogens are known, and there is no cross immunity between them.

Various respiratory viruses infect mucosal cells at different levels of the respiratory tract: rhinovirus - in the nasal cavity, parainfluenza - in the trachea and larynx, influenza - in the trachea and bronchi. The main cause of the disease is the underdevelopment of the immune system: interferon (a substance that provides local immune protection of the mucous membranes of the respiratory tract) is produced in children in smaller quantities and more slowly than in adults.

Children who were born and not breastfed (that is, not protected by maternal antibodies to viruses) are more susceptible to diseases; weakened children suffering from malnutrition and allergic diseases.

A child becomes infected by airborne droplets in public transport, in a store, or in a kindergarten. Viruses are contained in the exhaled air of a patient and are released when coughing and sneezing. The incubation period (the time from infection to the onset of manifestations of the disease) is often several hours, but not more than 3 days.

Symptoms of ARVI are:

• increased temperature - from low-grade fever to high fever (can last for several days);
• (because of her, the child becomes capricious);
• pain in joints and muscles;
• loss of appetite;
• catarrhal phenomena (nasal congestion, sore and sore throat, cough, hoarseness).

There are also distinctive features in symptoms, depending on the type of pathogen:

1. At parainfluenza the child’s general condition suffers less, the onset of the disease is usually gradual, the temperature rises within 37.5 0 C. Characteristic distinguishing signs are nasal congestion, hoarseness, dry rough (“barking”) cough, and a complication may be false croup or laryngeal stenosis, manifested by difficulty breathing.
2. Adenovirus infection more often causes severe intoxication (headache, lethargy, weakness, lack of appetite), high temperature and prolonged (up to 2 weeks) fever. The constant symptoms of this infection are: runny nose (due to inflammation of the nasal mucosa), sore throat (palatine tonsils become inflamed, tonsillitis develops), lacrimation (), multiple enlargement of the lymph nodes.

Upon examination, redness and enlargement of the tonsils, purulent discharge from the lacunae of the tonsils are revealed. Swelling of the eyelids and redness of the conjunctiva may appear first in one eye and then in the other, and persist for a week or more.

At an early age, adenovirus infection may also cause manifestations from the digestive tract: watery stools with mucus for 3-4 days, and in rare cases, vomiting.

1. For respiratory syncytial infection (RSV infection) Damage to both the lower and upper respiratory tract is typical: a runny nose appears against the background of an increase in temperature; at first dry, and from 3-4 days with sputum, cough; shortness of breath with difficulty breathing.

Every fourth child develops pneumonia (). The appearance of cyanosis of the nasolabial triangle and shortness of breath indicates the severity of the infection and is an indication for hospitalization of the child. A complication may also be croup. The course depends on age: the younger the child, the greater the risk of severe course. The immune system is not stable, and it is possible to become infected with RSV again after some time.

1. Flu : Of the three main types of virus, viruses B and C most often cause disease in children. Distinctive signs are the predominance of intoxication symptoms: high fever with chills, pain in the eyeballs (children complain of “eyes hurting”), headache, lack of appetite, weakness. Among the catarrhal phenomena, a dry cough is noted (with damage to the trachea). On day 4-5 it becomes wet.

Children with ARVI should be treated by a pediatrician. Correctly prescribed treatment reduces the risk of complications. Hospitalization is required in case of severe illness. The child is recommended to rest in bed, drink plenty of warm fluids (juices, decoctions of dried fruits and rose hips, tea with lemon). This does not mean that the baby needs to be forcibly kept in bed. When he feels bad, he himself will try to lie down. As you feel better, let him move, but active games and gymnastics should be excluded.

Children under 3 years of age require drug treatment. All drugs for the treatment of ARVI are divided into 2 groups: and symptomatic drugs.

At an early age, the following antiviral drugs are used (but only as prescribed by a pediatrician):

• Grippferon (nasal drops) – has antiviral, anti-inflammatory, immunomodulatory effects;
• Viferon (rectal suppositories, nasal ointment);
• Anaferon for children is a homeopathic remedy in the form of lozenges (for children, the tablet should be dissolved in 1 tablespoon of water);
• Remantadine and Relenza for the treatment of influenza;
• Groprinosin - activates the immune system and prevents the spread of infection.

Antiviral drugs have the greatest effect when prescribed from the first day of illness.

Antibiotics have no effect on the virus. They are prescribed for severe illness, weakened children with the threat of bacterial infection, since in 10% of cases a viral infection is complicated by the development of a bacterial disease.

Symptomatic treatment consists of eliminating the manifestations of a respiratory disease. The temperature should not be lowered below 38 0 C: during fever, interferon, which suppresses the reproduction of the virus, is produced faster in the body. By lowering the temperature, the protective reactions of the body itself are inhibited. Only if there is a predisposition to febrile (that is, with an increase in temperature) convulsions, lower temperatures (above 37.5 0 C) are also reduced.

Drugs containing Ibuprofen and Paracetamol (Nurofen, Efferalgan-baby, Panadol-baby) are used as antipyretics. Aspirin is contraindicated for children. For nasal congestion, Otrivin-baby, Nazol-baby, etc. are prescribed, but for no more than 5 days. For inflammation of the throat, it is better not to use sprays before 2 years of age due to the risk of developing bronchospasm. If you can teach a child to gargle, then gargle with a solution of furatsilin or chlorophyllipt, as well as chamomile infusion.

To get rid of a dry cough, it is important to provide your baby with enough fluids and humidify the air. To facilitate the removal of sputum during a wet cough, mucolytics are used. At an early age (from 2 years old), you can use Ambroxol (Lazolvan, Ambrobene), Bromhexine in syrup, ACC.

Inhalations are effective in combating cough. They are convenient to carry out using (a device for inhalation, convenient for use at home; read how to use a nebulizer). At normal temperatures, you can use hot foot baths, after which you need to dry your feet thoroughly and pour mustard powder into your socks (can be left overnight).

Laryngitis

Laryngitis in young children can manifest itself not only as a cough, but also as difficulty breathing.

Inflammation of the larynx (laryngitis) is a fairly common disease at an early age. A type of it is croup or stenosing laryngitis, which can develop against the background of a respiratory infection or be of an allergic nature.

The frequency of croup is explained by anatomical features: swelling of the mucous membrane easily occurs in the area of ​​the vocal cords, therefore, with inflammation, accumulation of mucus, and reflex muscle spasm, the passage of air when inhaling becomes difficult.

Most often, croup occurs in children aged 2-3 years with parainfluenza, but it can also be caused by adenoviruses and rhinosyncytial viruses. Predisposing factors are excess body weight and allergic problems in the child.

Signs of croup (which can develop at night) are hoarseness or complete loss of voice, a “barking” cough, difficulty breathing, and restlessness in the child. If symptoms of croup appear, you should immediately call an ambulance.

Tactics of parents before the doctor arrives:

• the baby should be calmed, access to moist air and plenty of fluids should be provided;
• give an antipyretic (if there is a high temperature);
• restore breathing through the nose using drops.

The development of croup is an indication for hospitalization of a child in a hospital, where they can use: inhalations with bronchial dilators, mucolytics; administer corticosteroids depending on the severity of the croup.

Enterovirus infection

A common disease in children in the first 3 years of life also includes infection caused by enteroviruses. The virus is very stable in the external environment, it is released from the body of the patient and the virus carrier when coughing and talking, as well as with feces.

Infection is possible through airborne droplets, household contact (through toys and other objects), and fecal-oral route (through food and water) if hygiene rules are not followed. The incubation period is 2-10 days.

The onset of infection is acute. The fever is high and may be wavy. The infection is characterized by symptoms of damage to the respiratory and digestive organs against the background of intoxication. Since the virus multiplies in the lymph nodes, there is an increase in them in the neck and submandibular region.

One of the signs of the disease is a rash on the skin of the upper half of the torso and arms in the form of red spots or blisters. The rash disappears after 4-5 days, leaving light pigmentation.

Characteristic is damage to various internal organs with the development of the following forms of infection:

• sore throat with damage to the oropharynx (with a rash of bubbles with liquid contents on the mucous membrane, which open to form ulcers covered with a white coating);
• conjunctivitis with eye damage (redness of the mucous membrane, lacrimation, photophobia, swelling of the eyelids);
• myositis with damage to the muscles of the trunk or limbs (pain in the area of ​​these muscles);
• Enteritis with damage to the intestinal mucosa is manifested by loose stools of normal color without mucus and blood, with or without fever;
• in the heart, damage to different parts is possible: the heart muscle (with development), the inner membrane and valves (endocarditis), or all membranes (pancarditis); manifestation will be increased heart rate, heart pain, drop in blood pressure, rhythm disturbance;
• damage to the nervous system leads to the development of (inflammation of the lining of the brain) or encephalitis (inflammation of the brain substance), the signs of which are intense headache, repeated vomiting, convulsions, paralysis and loss of consciousness are also possible;
• damage to liver cells causes the development of hepatitis, the symptoms of which will be pain in the right hypochondrium, nausea, fever, weakness.

There are no specific drugs for the treatment of enterovirus infection; symptomatic treatment is carried out and diet therapy is prescribed. Measures are taken to prevent dehydration and detoxification therapy is prescribed. The duration of the disease is up to 2 weeks.

Whooping cough

The DTP vaccine will save you from whooping cough

This bacterial infection is caused by whooping cough. Infection by airborne droplets occurs through close contact with a patient, which can also be an adult, since immunity after vaccination is observed only for 5-10 years. Whooping cough is especially dangerous for children under 2 years of age. The prevalence of the disease has decreased due to planned vaccination, but it is still often recorded due to the refusal of some parents to vaccinate their child.

The incubation period is on average 5 days. The onset of the disease is acute. The symptoms are reminiscent of acute respiratory viral infections: low temperature, dry cough, and the state of health suffers little. Diagnosing whooping cough at this stage is difficult.

But gradually the baby’s condition worsens, the cough becomes paroxysmal and spasmodic. During an attack, the child's face becomes red and bluish in color. The intensity of the attacks increases; during an attack, temporary cessation of breathing (apnea) may occur.

Frequent coughing attacks lead to circulatory problems, including cerebral circulation. At the end of the attack there may be vomiting or the release of a lump of glassy mucus.

In severe cases, the child is hospitalized. Treatment includes antibiotic therapy (Augmentin, Azithromycin, Erythromycin, Rulid), oxygen therapy, sedatives, anticonvulsants, antiallergic drugs, mucolytics (thinning sputum), immunomodulators. In severe cases, corticosteroids are used.

Treatment of whooping cough is a very long process. Coughing attacks continue even after the destructive effect of an antibiotic on the whooping cough bacterium, which is associated with damage to the cough center by the toxins of the pathogen.

An attack can be triggered by any irritant. Therefore, you should provide the baby with a calm environment (avoid stress), and give crushed food in small portions. Early morning walks near a pond are very important, and in the apartment - ensuring an influx of fresh, moist air.

Scarlet fever

Scarlet fever is an acute bacterial infection caused by streptococcus, characterized by the appearance of a sore throat, rash, symptoms of intoxication, fever and the possible development of allergic and purulent-septic complications. The incidence is higher in the autumn-winter season. After illness, a strong immunity develops.

Children usually get sick after 2 years of age; they become infected more often in kindergarten, where outbreaks and epidemics can occur. The disease is usually transmitted by contact and airborne droplets, but foodborne infection is also possible. A sick child is dangerous to others from 1 to 21 days inclusive. The infection can be transmitted through a third party (when it is not the child himself who comes into contact with the sick person, but, for example, a parent who then transmits the infection to his child).

The incubation period is 3-7 days. The onset of the disease is acute, the baby becomes lethargic, a headache appears, fever with chills increases rapidly (temperature reaches 39-40 0 C), and vomiting may occur. On the very first day of the disease, a pinpoint bright pink rash appears against the background of redness of the skin.

The primary localization of rashes is on the lateral surfaces of the body, in natural skin folds (axillary, inguinal, buttock), and on the face. Scarlet fever is characterized by puffiness of the face and a pale nasolabial triangle, where there is no rash; feverish shine of the eyes; bright red lips.

A mandatory manifestation of scarlet fever is: enlarged tonsils and soft palate are bright red, there is pus on the surface and in the lacunae of the tonsils. The submandibular lymph nodes are enlarged and painful. Typical changes are noted in the tongue. At first it is coated, from 2-3 days it begins to clear, acquiring a characteristic appearance by the 4th day: bright red, with protruding papillae (“crimson tongue”).

In severe cases of the disease, the child may become agitated, delirium, or convulsions, which indicates damage to the central nervous system. The rash lasts about a week and disappears (without pigmentation). At 2-3 weeks from the onset of the disease, peeling of the skin is observed. A characteristic symptom of scarlet fever is lamellar peeling on the palmar surface of the hands and feet.

Infectious-allergic complications of the kidneys and heart rarely occur in young children. Pneumonia may develop. Bacterial carriage can persist for up to a month after the illness or longer (in the presence of chronic inflammation in the nasopharynx).

Children with scarlet fever are usually treated at home, providing the child with isolation (in a separate room for 10 days) and separate dishes. Bed rest is prescribed for up to 10 days to prevent complications. A mechanically and thermally gentle diet (mashed warm food) and drinking plenty of fluids are recommended. Children with severe forms of the disease are hospitalized.

Drug treatment includes:

• antibiotic therapy (the basis of treatment): penicillin antibiotics are used (orally or intramuscularly), and if they are intolerant, macrolides (Erythromycin, Sumamed, etc.) are used - the duration of the course and dose is determined by the doctor;
• antiallergic drugs (Cetrin, Suprastin, Tavegil, etc.);
• vitamin therapy;
• local treatment: gargling with infusions of chamomile, sage, calendula, furatsilin solution.

The child is admitted to the nursery after 22 days from the moment of illness. After scarlet fever, lifelong immunity is noted.

Rubella

A viral, non-severe infectious disease with airborne transmission. Children older than one year old get sick, since they were previously protected by antibodies received from their mother. The contagiousness of the virus is not high, so infection occurs only through close contact with a patient.

The incubation period is 2-3 weeks. Already at the end of this period, mild malaise and enlargement of the occipital, posterior cervical and parotid lymph nodes (a hallmark of rubella) are noted.

The onset of infection is acute with a moderate increase in temperature. Pink spots appear on the oral mucosa. Then a rash appears on the face. Very quickly, during the first day of illness, it spreads over the entire surface of the body and may be accompanied by mild.

The rash is abundant, most of its elements are on the child’s back and buttocks, but there are none on the palms and soles. The rashes look like spots, slightly raised above the surface of the skin. On the face, the rash tends to merge.

On the 3rd or 4th day, the rash turns pale and disappears without a trace. Minor peeling may remain. Enlarged lymph nodes persist for about 2 weeks. Atypical forms of the disease occur without rashes, but the infectious period is not shortened.

For rubella, symptomatic treatment is carried out (antipyretics, antiallergic drugs, drinking plenty of fluids). The prognosis is usually favorable, complications occur extremely rarely. The contagious period is 2 weeks (one week before the rash and one week after).

Chicken pox

A characteristic sign of chickenpox is a blistering rash all over the body.

The infection spreads through the fecal-oral route through water, food, household items, toys, dirty hands (some children at this age continue to put everything in their mouths). There is a seasonal increase in incidence in the summer-autumn period.

Clinical manifestations of acute intestinal infections in young children have much in common, regardless of the type of pathogen:

• acute onset of illness;
• symptoms of intoxication (fever, malaise, weakness, lack of appetite);
• intestinal dysfunction (nausea, vomiting, loose stools);
• stomach ache.

The nature of the stool may differ:

• abundant, watery – with acute intestinal infections caused by viruses and opportunistic microflora;
• scanty, with an admixture of mucus and streaks of blood - with dysentery;
• abundant, such as swamp mud - with salmonellosis, etc.

With rotavirus infection, catarrhal manifestations in the form of a runny nose and cough are often observed. A characteristic symptom of dysentery is a false urge to defecate.

Almost 70% of cases of ACI at a young age are mild to moderate. In severe cases, dehydration may develop due to frequent vomiting and large stools.

The doctor makes the diagnosis based on clinical manifestations and test results (bacteriological culture of stool and vomit, serological and immunological blood tests).

Mild forms of OCI can be treated at home. Moderate and severe forms require medical supervision, intravenous administration of solutions for the purpose of detoxification and replenishment of fluid and mineral losses, so children are treated in a hospital.

Treatment of OCI includes:

• bed or semi-bed rest;
• diet: exclude fresh fruits and vegetables, broths, fresh baked goods and juices; feeding in small portions (but often) is introduced; consumption of fermented milk products, slimy soups and cereals is recommended;
• rehydration (restoration of water-salt balance to normal): administration of solutions in the form of drinks (Regidron, Glyukosol, Oralit, carrot-raisin decoction, chamomile infusion) or drip administration of special solutions into a vein (in severe cases). The volume of fluid required is determined by the doctor depending on the degree of dehydration and the age of the child.
• antibacterial and antiviral drugs, their dosage and duration of the treatment course should also be selected by the doctor (Nifuroxazide, Ersefuril, Viferon are more often used);
• enterosorbents (promoting the removal of toxins from the body) – Smecta, Polyphepam, Enterosgel (after 2 years);
• restoration of normal intestinal microflora: probiotics are used (Bifiform, Bifidumbacterin, Enterol);
• symptomatic treatment (antipyretics, enzyme preparations, etc.).

Affective-respiratory attacks (ARS)

They talk about ARP when the baby literally “starts crying”, freezes while inhaling, his lips turn blue, and breathing stops briefly (for 30-60 seconds) (apnea). A spasm of the laryngeal muscles occurs, and such attacks resemble laryngospasm. In addition to “blue” attacks, there are also “white” ones, which develop in response to pain and are similar to fainting: the baby turns pale, the pulse slows down sharply or disappears for a short time.

Single ARPs, as a manifestation of strong negative emotions, are observed at an early age in every fourth completely healthy child, and in 5% of children they are repeated many times.

The appearance of ARP is promoted by a lack of calcium in the body, which leads to spasm of the larynx. With the syndrome of increased nervous excitability, the likelihood of seizures increases. A hereditary predisposition to their occurrence cannot be ruled out.

Typically, ARP occurs at 2-3 years of age. The frequency of attacks varies, from several per day to one per year. They arise reflexively and then can disappear without a trace, being an age-related feature. But such a child must also be shown to a psychologist.

Research has proven that ARP occurs equally often in capricious children with a tendency to hysteria and in children with normal behavior. Observation by a pediatric neurologist is necessary to exclude neurological and cardiac pathologies. There has also been evidence of a connection between ARP and blood diseases.

Tactics of parents in case of ARP in a child:

• during an attack, take the child in your arms, do not panic;
• to restore breathing, you need to pat the child on the cheeks, massage the ears, wipe the face with cold water;
• some children calm down faster if you leave them and move away;
• try to distract the child with some action, without focusing on his behavior;
• Do not indulge the baby’s whims and do not protect him from negative emotions; you should teach him to manage his emotions.

Drug treatment is usually not required. For repeated ARPs, you should seek the help of a psychologist.

Helminthic infestations (helminthiasis)

In the presence of pinworms Children are bothered by severe itching in the anus, especially severe at night. In their sleep, children scratch the skin in the perineal area, pinworm eggs get under the baby's nails, which causes repeated self-infection.

There are general signs of helminthiases:

• decreased appetite;
• increased salivation;
• body weight deficiency with proper nutrition;
• frequent nausea, vomiting;
• abdominal pain (usually paroxysmal, in the navel area);
• bloating;
• unstable stool (diarrhea and constipation);
• pale skin;
• increased fatigue;
• allergic manifestations on the skin;
• restless sleep;
• causeless increase in temperature 37.1-37.5 0 C;
• imbalance and whims.

At ascariasis Due to migration in the body, worms can cause foci of inflammation of the lung tissue, which is manifested by paroxysmal dry cough, shortness of breath, bronchospasm and even hemoptysis. Skin allergic manifestations such as urticaria are also characteristic.

Abdominal pain can be so severe that it mimics acute surgical pathology (“acute abdomen”). A massive infestation of roundworms can cause either blockage of the bile ducts and jaundice.

In case of invasion whipworm One of the symptoms of the disease is anemia or swelling of different localizations.

Complications of enterobiasis often include recurrent vulvovaginitis (inflammation of the vagina) in girls, urinary incontinence, eczema of the perianal area, and appendicitis.

Children with helminthiasis are included in the group of frequently ill people (acute respiratory infections, stomatitis, pyoderma, etc.). Neurological manifestations often develop: headache, dizziness, obsessive tics (sniffing, blinking, grimacing).

The diagnosis can be confirmed by analyzing stool for worm eggs and scrapings from the folds of the perianal area (for pinworms). Sometimes the study has to be repeated several times.

In the treatment of helminthiases, chemotherapy, homeopathic remedies, and herbal remedies are used. Onions, pomegranates, pumpkin seeds, and walnuts have antihelminthic properties.

Of the medications, Vermox (Mebendazole) is most often used. Difezil and Quantrel are also effective drugs. But you should not self-medicate. Each drug has both indications and contraindications. Treatment should be prescribed by a pediatrician or infectious disease specialist.

Summary for parents

The main diseases in children from one to three years of age are viral or bacterial infections. A child at this age begins to go to kindergarten, the number of contacts increases, so protecting a child from diseases is not so easy.

The baby's immune system is still developing. Breastfeeding and the transfer of maternal antibodies to the child are of no small importance. You can strengthen your child's body by hardening it.

It is important that parents strictly observe the rules of hygiene and instill hygiene skills in their children from early childhood. Parents should know the signs of the most common childhood illnesses in order to promptly seek help from a doctor. Self-medication is dangerous!

Which doctor should I contact?

If the baby is sick, you need to contact a pediatrician, and in case of a serious condition (uncontrollable fever, repeated vomiting, drowsiness of the child and impaired consciousness, rapidly spreading skin rash and other severe symptoms), you need to call an ambulance. The child will likely need treatment in the infectious diseases department.

Additionally, consultations with specialized specialists may be required depending on the affected organs. So, in case of myocarditis, the patient is examined by a cardiologist, in case of meningitis, encephalitis - by a cardiologist, laryngospasm, otitis - by an ENT doctor. A gastroenterologist and pulmonologist advise the patient if hepatitis and pneumonia develop, respectively.

If a child suffers from colds more than 6 times a year, he may need to consult an immunologist.

1, average: 5,00 out of 5)

Childhood infections

Streptococcal infection.

One of the most common bacterial infections, the etiological agent of which is streptococcus, which is pathogenic for humans. This includes a group of streptococoses (acute and chronic lesions of the nasopharynx and middle ear, skin, rheumatism, GN).

Etiology: genus Strptococcus, form chains, gr+, aerobes. Groups: betta hemolytic, alpha hemolytic, non-hemolytic gama streptococcus. The most pathogenic are hemolytic gr A (scarlet fever, tonsillitis, erysipelas), betta hemolytic gr B (mastitis, urogenetic inf in women, newborns - generalization of the inf form with a severe wedge course (meningitis, sepsis), in older children - urinary organs, arthritis, pharyngitis , pneumonia).

Epidemiology: In newborns and infants - because. there is immunity from the mother - acute streptococcal infection, rheumatism, GN - does not develop!!! – z-e manifests itself: otitis media, rhinorrhea, cervical lymphadenitis. After 1 year of life, acute streptococcal infection of the skin and pharyngeal lymph ring appears. The maximum incidence rates with skin lesions are in preschool children, and with respiratory manifestations in primary school age children.

Source of streptococcal inf - healthy carriers, convalescent carriers, patients.

The transmission mechanism is air-drip, alimentary, or contact.

Immunity: antitoxic, antimicrobial character.

Scarlet fever.

Scarlet fever is an acute infectious disease, toxic and septic in nature, which is accompanied by general intoxication (fever, vomiting, damage to the nervous system and cardiovascular system), sore throat, pinpoint rash on the skin, and the development of complications of purulent-septic and allergic origin.

Etiology. Beta-hemolytic streptococcus gr A (65 serotypes). The source is a sick person, a carrier. Gate: nasopharynx, pharynx, skin. Most often children under 16 years of age.

Pathogenesis. Primary affect (angina) – blood (toxins, allergens) – toxic effect on the cardiovascular system, endocrine system, autonomic nervous system – general intoxication symptoms (fever, vomiting, rash, etc.)

Lines of pathogenesis: toxic, allergic, septic

Classification:

1. Typical

2. Atypical: erased, extrabuccal (no changes in the pharynx), agraval symptoms (hypertoxic, hemorrhagic - early death)

By severity:

1. Mild with transition to moderate - catarrhal sore throat, slight rash, temperature 38 (3-5 days)

2. Moderate to severe - repeated vomiting, fever (up to 40), rash, enanthema, sore throat with a yellow-white coating in the crypts (7-8 days)

3. Severe (toxic, septic, toxicoseptic) – repeated vomiting, fever, convulsions, mynegial symptoms, hemorrhages

With the flow:

1. Smooth course without allergy waves and complications

2. With allergy waves

3. With complications: - allergy, - purulent, - septicopyemia

4. Abortive

Clinic: Incubus period – 1-12 days, onset – acute, body temperature – up to 40*C, one-time vomiting, headache, weakness, painful swallowing, puffy face, increased lymph, hyperemia of the pharynx; Days 1-3 – rashes on the neck and chest (small-pointed, bright, red). During the day it covers the entire body (maximum – in folds and loose surfaces). The rash merges into one field of hyperemia. There is no rash on the chin and around the mouth. White dermographism. Rash 2-7 days; disappeared without a trace - the image of lamellar peeling (pityriasis). Sore throat (limited) – catarrhal (1 day), follicular (up to 5-7), necrotic (2-7 days, up to 10), fibrinous. Necrosis of a dirty gray or green appearance, on the soft palate - speckled enanthema. The oral mucosa is dry; the tongue is moist, covered with a gray-white coating; for 3-4 days – raspberry tongue (1-2 weeks); CVS – tachycardia, muffled sounds, increased blood pressure; increase heart and liver

Sympaticus (3-5 days) – tachycardia, increased blood pressure, dry skin, accelerated disappearance of dermogaphism, increased blood sugar

Vagus (5 days) – bradycardia, watering, decreased blood pressure, decreased sugar; Dermographism appears quickly and disappears slowly.

Blood: neutrophilic leukocytosis, increased ESR, from 4-6 days eosinophilia

In young children there are few manifestations, but septic complications are frequent.

Complications: lymphadenitis, otitis, sinusitis, mastoiditis, nephritis, arthritis, myocarditis (3-4 weeks), reinfection, superinfection.

Diagnostics: typical clinic

Differential diagnosis: Pseudotuberculosis: 2-8 days pinpoint rash, on the body and near the joints, “gloves and socks”, joint damage, dyspeptic symptoms

Rubella: sore throat is optional or unlimited; rash – pale pink, small maculopapular, mainly on the extensor surfaces, disappears within 3-4 days

Measles: prodromal period (rhinitis, conjunctivitis, bronchitis, Belsky-Filatov spots); rash – 3-4 days, maculopapular turning into hyperpigmentation

Hospitalization – 1 year of life, severe forms

Bed rest, semi-liquid diet

Antibiotics (penicillin 100-300 thousand units/kg, erythromycin, ampiox)

Detoxification (hemodez, glucose)

Vitamins, antihistamines (diphenhydramine, pipolfen) + treatment of complications

Prevention: - no specific, early detection, isolation for 10 days, quarantine - 22 days, contact - quarantine for 7 days after contact, 17 days when the sick child remains in the group.

Measles.

Measles is an acute infectious disease characterized by general intoxication, inflammation of the upper respiratory tract, oral mucosa, pharynx, eyes and maculopapular rash.

Etiology: vir. Paramixoviride genus Morrbiliviride. D-e hemolysis, hemoglutinating, symplast-forming.

Epidemiology: source – patient from 4 to 10 days of rash. Children under 3 months of age have innate immunity.

Pathogenesis: entrance gates – mucous membrane of the respiratory tract and conjunctiva. In the submucosal and lymphatic tracts, reproduction - blood - toxic-allergic damage to the respiratory tract, central nervous system, gastrointestinal tract.

Classification:

By type: typical, atypical (erased, marked, in vaccinated people, with AB and hormone therapy, hemorrhagic).

By severity: mild, moderate, severe (with or without hemorrhagic syndrome).

Downstream: smooth; not smooth - with complications (pneumonia, otitis media, croup, stomatitis, purulent skin lesions, colitis, meningoencephalitis); abortive.

Clinic: Incubus – 9-17 days (with immunoprophylaxis – up to 21). Periods:

1. Catarrhal: (3-7 days) t-38-39, headache, cough, weakness, sleep and appetite disturbances, catarrhal phenomena, development of croup syndrome, conjunctivitis, photophobia. Belsky-Filaty-Koplik spots.

2. Rash: (4-9 days) spots, enanthema, exanthema (maculopapular), pinpoint rash (appearance - 1 day - head, 2nd body, 3rd limbs), leukopenia, anxiety, drowsiness, delirium.

3. Pigmentation: (1-1.5 weeks) t-norm, pigmentation (as well as rash), asthenia, anergy.

Complications: pneumonia, otitis, croup, stomatitis (catarrhal, aphthous), purulent skin lesions, colitis, meningoencephalitis, laryngitis, larengotracheobronchitis, abscess.

Diagnostics: clinic, RZK, RGGA, RNGA, ELISA, leukopenia, lymphocytosis, eosinopenia, monocytopenia, ESR.

Differential diagnosis:

1. ARVI - rapidly developing acute intoxication, catarrhal symptoms, without characteristic rashes or spots.

2. Rubella - catarrhal period is absent, the rash is without localization, small on the extensor surfaces, blue-pink, disappears without a trace, enlargement of the cervical lymph nodes.

3. Enteroviral exanthema - on day 2, patty-papular, high t, no characteristic rashes, diarrhea, myalgia, hepatosplenomegaly.

4. Scarlet fever - tonsillitis, hyperemia of the pharynx, crimson tongue, no cough or runny nose, exanthema appears simultaneously on the folds and folds, nasolabial trigonum free of rash, on the 7-8th day pityriasis-like peeling, neutrophic leukocytosis, eosinophilia.

5. Mononucleosis - polymorphic exanthema on days 3-5, on the torso, quickly disappears, tonsillitis, polyadenitis, hepatosplenomegaly, leuko-, lympho-, monocytosis, atypical mononuclear cells.

6. Meningococcemia - rapid onset, high temperature, severe intoxication, hemorrhagic-necrotic rash throughout the body, especially on the ass and legs; neutrophilic hyperleukocytosis, meningococcus in the blood.

7. Allergic exanthemas - no catarrhal period and sequence, bright, polymorphic, scabies, eosinophilia.

8. Steven-Johnson syndrome – necrotic-ulcerative lesions of the mucous membranes (eyes, mouth, anus) exudative with the formation of large bullous elements.

1. hospitalization - up to 1 year, severe, complications, epidemiological indications (closed children's hospitals).

2. Isolation. Ventilation. Bed – 7-10 days. Drink plenty of fluids. Food. Hygiene of mucous membranes.

3. For a runny nose: naphthyzin, protargol.

4. Cough: bromhexine, libexin.

5. Vit. C, retinol, antihistamines.

Rubella.

Rubella is an acute infectious disease caused by a filterable virus (RNA-containing, a group of myxoviruses), characterized by a small-spotted rash, minor catarrhal symptoms and increased lymph nodes (posterior cervical and occipital).

Epidemiology. Source – patient 1 day of illness – 5 day of rash (with congenital rubella they are contagious for up to 1.5-2 years). Most often the disease occurs from 1 to 7 years, it is dangerous in pregnant women, if up to 3 months it is congenital. 4-6 months – innate immunity.

Pathogenesis: oral mucous membranes - blood - skin lesions, lymph nodes, changes in the blood (virus-neutralizing antibodies on the 2-3rd day of the rash), embryonic tissues (congenital malformations of the eyes, hearing, cardiovascular system, central nervous system).

Classification: - congenital, - acquired (by severity)

Clinic: incubation – 15-24 days; onset – lethargy, catarrhal phenomena (conjunctivitis, mild hyperemia of the pharynx, enanthema of the mouth), fever, headache; the rash on days 1-2 of the disease (face - whole body (extensor surfaces)) is small-spotted, pale pink, maculopapular, disappears after 2-3 days without a trace; increased l/u on the posterior cervical surface (painful, dense); blood – leukopenia, lymphocytosis, plasma cells.

Complications (rare): encephalitis, encephalomyelitis.

Diagnosis: clinic, RPGA.

Differential diagnosis:

Meeting measles - contact with a patient, administration of gama-globulin, characteristic rash, serodiagnosis.

Enteroviral exanthema - on the 2nd day, patty-papular, high t, no characteristic rashes, diarrhea, myalgia, hepatosplenomegaly.

Drug-induced exanthema – history, no intoxication, eosinophilia

Treatment and prevention: Symptomatic, isolation (for 5 days after the appearance of the rash, group quarantine for 21 days), in pregnant women - serology upon contact, in case of illness - abortion for up to 12 weeks; vaccination - 12 months, revaccination - girls - 14-15 years old.

Chicken pox

Chicken pox is an acute infectious disease that is caused by a filterable virus (DNA herpes zoster virus), transmitted by airborne droplets and characterized by fever, vesicular rash on the skin and mucous membranes.

Epidemiology: source – patient (1-2 days of incubation period. Up to 5 days after the appearance of the last rash); Transplacental transmission is possible.

Pathogenesis: mucous membrane of the upper respiratory tract – lymph/pathways – blood – epithelial cells of the skin and mucous membranes – formation of blisters on the skin (maximum concentration of the virus); formation of a bubble: damage to the cells of the spinous layer – hyperplasia – formation of oxyphilic inclusions – image of multinucleated giant cells – balloon dystrophy – necrosis – accumulation of interstitial fluid – blisters; in generalized forms, the gastrointestinal tract, liver, kidneys, central nervous system, etc. can be affected.

Classification:

By type: - typical, - atypical (- erased - roseolous-papular rash with small blisters; - pustular; - bullous; - hemorrhagic; - gangrenous (the last 4 in cachectic children of early age); - generalized - in newborns hyperthermia with expressive intoxication and damage to internal organs, often death).

By severity: - light, - medium, - heavy; indicators of severity: hyperthermia, rash, hemorrhagic syndrome, neurotoxicosis, croup.

According to the flow: - with complications, - without complications.

Clinic: lasts 3 weeks: incubation – 11-21 days; prodromal period – 24-48 hours (increased T*C, catarrhal symptoms, possible prodromal rash on the chest); 1-2 days of illness - variceal rash in the form of papules or spots, after a few hours single-chamber blisters - vesicles - form; some spots disappear, some turn into papules; rashes of spots, papules and vesicles occur in “jumps” from 3 to 5 times; after 1-2 days the bubble dries out (itching): vesicle - crust - crust disappears; simultaneously rashes in different stages of development - spots, papules, vesicles, crusts. Intoxication is mild.

Complications: encephalitis (hemiplegic, ataxic, damage to the subcortical ganglia), meningoecephalitis, myelitis, nephritis, myocarditis, bacterial complications (phlegmon, abscess, impetigo, bullous streptoderma, lymphadenitis, stomatitis. Purulent conjunctivitis, keratitis)

Diagnosis: clinic, laboratory - Aragao bodies (virus in vesicular fluid), RZK, ELISA, cultivation in embryonic cultures of human cells.

Differential diagnosis:

Herpetic infection - around the mouth (lips), nose - itching, vesicles.

Herpes zoster - one-sided pain along the nerves and rashes

Vesicular gamasoriketsiosis – tick bite, primary affect (necrosis with scab, erythematous wreath, lymphadenitis)

Treatment: hospitalization according to epidemiological and wedge indications (living conditions and severity), isolation until the 5th day after the last element of the rash, bed rest - 1 week, lubricating the vesicles with brilliant green or 0.04% gramicidin, eyes - rinse with 2% boric acid + drip albucid 15-20%, pharynx - furatsilin 1:5000; for severe cases - interferon, acyclovir, immunoglobulin; for purulent complications, antibiotics.

Prevention: isolation until the 5th day after the last element of the rash, contact - isolation from 11 to 21 days of contact.

Herpes infection (herpes simplex)

Herpes simplex is a viral disease characterized by a long latent course with periodic relapses, which are accompanied by the manifestation of a vesicular rash, damage to the central nervous system and internal organs.

Etiology: herpes simplex virus (HSV), divided into HSV-1, HSV-2.

Epidemiology: source - sick carriers, HSV-1 - airborne and contact transmission (skin, mucous membranes), HSV-2 - sexual tract (genital and neonatal herpes). Maximum sensitivity – from 5 months to 2 years.

Pathogenesis: entrance gate (mucous) - reproduction in tissues of ecto- and endodermal origin - vesicular rash; HSV-1 persists in the nerve cells of the trigeminal nerve, HSV-2 - in the nodes of the sciatic nerve. Distribution is neurogenic, lymphatic and hematogenous. HSV-2 has oncological properties.

Classification: - congenital, - acquired (primary, secondary; localized, generalized)

Clinic: incubation period – 2-14 days; localized f-ma - itching, pain, vesicular rash against the background of hyperemia (possible fusion of vesicles with the formation of a large bubble, after opening - erosion), the content gradually becomes cloudy, at 3-4 days the vesicles dry out with the formation of a crust, at 5-7 days - disappear with the formation of slight pigmentation. In children with eczema - Kaposi's eczema herpetiformis (acute course, t-up to 40*, large vesicles on eczematous skin, enlargement of regional lymph nodes; often death). If the mucous membranes are affected - aphthous recurrent gingivostomatitis (in children 3-6 years old). The virus can infect the cornea in the form of herpetic keratoonjunctivitis, ulcers, and keratitis. Damage to the nervous system – encephalitis, meningitis, meningoencephalitis, meningoencephaloradiculitis.

Congenital herpes: extrauterine death, malformations (micro-, anencephaly, microphthalmia), herpetic sepsis.

Herpes in newborns: onset – 5-10 days of life, temperature –39-40*, intoxication, vomiting, acrocyanosis, agitation; on days 2-3 – impaired consciousness, meningeal signs, convulsions, patol reflexes, paresis; death.

Diagnostics: clinic, virological and cytological studies, RZK, RNGG, ELISA.

Differential diagnosis: herpes zoster, streptococcal impetigo, erysipelas, eczema, herpangina, mumps and enteroviral encephalitis.

Treatment: acyclovir, riboverine, alpizarin, helepin, flakosil, arbitol.

Prevention: isolate in the presence of rashes, for newborns in contact with a sick person - human immunoglobulin; herpetic vaccine 0.1-0.2 ml every 2-3 days 2 times a year. No activities are carried out in the outbreak.

Mumps (mumps)

Mumps infection is an acute viral disease caused by a virus (mumps, from the genus paramyxoviruses) spreads by airborne droplets and is characterized by systemic damage to the glandular organs (parotid, salivary), endocrine and NS.

Etiology: capable of agglutinating erythrocytes of Guinea pigs!!! Gee-gee...

Epidemiology: source - the patient at the end of the incubation period and before the 9th day of illness.

Pathogenesis: entrance gate - membrane of the mouth, nose, throat (reproduction in epithelial cells) - lymphatic pathways - blood (primary viremia) - salivary, pancreas and endocrine glands, NS (replication) - blood (secondary viremia) - damage to other organs.

Classification:

1. Typical:

Glandular isolated (parotid, submandibular, testicles)

Isolated damage to the central nervous system (serous meningitis, meningoencephalitis)

Combined

2. Atypical: erased, asymptomatic.

By severity: light, medium, heavy.

Clinic: incubation period 11–21 days (until 23-26). Weakness, myalgia, headache, sleep disturbance and appetite, nausea, vomiting, constipation, m/w diarrhea, coated tongue, chills, t up to 40, enlarged salivary glands (painful, pasty), dry mouth, ear pain, chewing and talking time increases. Filatov's syndrome (pain expressed in front and behind the ear), swelling of the neck, Murson's syndrome (hyperemia of the mucous membrane near the stenon duct). CNS lesions: meningus signs, headache. CVS: bradycardia, muffled sounds, systolic murmur, decreased blood pressure. Blood: leukopenia, lymphocytosis, ESR. Indicators of severity: degree of gland damage (swelling, swelling, pain), damage to the central nervous system (severity of meningeal signs), degree of general intoxication.

With bilateral architis, infertility may occur.

Serous meningitis: 3-9 years, acute onset, increased t, repeated vomiting, headache, convulsions, minor meningeal signs, increased cerebrospinal fluid pressure, cytosis of lymphocytic character, Pandey's r. - weakly positive.

Meningoencephalitis: the same + general hyperesthesia, impaired consciousness, psychomotor agitation, hallucinations.

Diagnosis: clinic, epidemiological history, RZK, HORN, spinal puncture

Treatment: hospitalization for severe cases. There is no etiotropic. Symptomatically: drinking plenty of fluids, liquid food, rinsing the mouth, dry heat on the glands, for hyperthermia - analgin, etc., for pancreatitis - a dairy diet, cold on the epigastrium, pancreatin; meningitis: magnesium sulfate, diacarb, contrical, gordox, trasylol, glucose, vitamin C, albumin, plasma, prednisolone, human leukocyte interferon, AB in purulent process. For architis: bed, cold on eggs, suspensions, antihistamines, anti-inflammatory drugs (aspirin, prednisolone), ribonuclease 0.5 mg/kg *4 times/day – 10 days.

Prevention: isolation for 9 days after recovery, in a children's institution - quarantine for 21 days. Contact – non-admission to the team from 11-21 days from the moment of contact. Special professional – live mumps vaccine (15-18 months) – s.c. 0.5 ml. Duration of immunity is 3-6 years.

Whooping cough.

Whooping cough - acute infection in a cat develops with a whooping cough bacillus and is characterized by damage to the respiratory tract with the presence of a typical clinical symptom - spasmatic (convulsive) cough.

Etiology: Bordet-Gengou bacillus (Haemophilus pertussis).

Epidemiology: source – patients (especially atypical forms) – from 1 day to 4-5 weeks. Routes of transmission: airborne droplets during close, prolonged contact. Newborns and up to 3 years of age are most often affected. High mortality up to 2 years.

Pathogenesis: epithelium of the respiratory tract (reproduction) – release of toxin – intoxication of the nervous system, central nervous system, DS – spasm of the respiratory muscles, spastic contraction, respiratory failure (neurosis of the respiratory tract) – disturbance of ventilation and breathing – hypoxia, hypoxemia, acidosis. Constant agitation - spastic manifestations (vomiting, spasm of the diaphragm, peripheral vessels, convulsive syndrome) - damage to the central nervous system - pertussis encephalopathy. An allergic reaction with an asmatic component is possible.

Classification: typical (mild, moderate, severe), atypical (erased, subclinical (in vaccinated)).

By periods:

1. incubation (3-15 days).

2. catarrhal (6-14 days) – dry cough, runny nose, t up to 38.

3. period of spasmodic cough (2-5 weeks) - increased cough, paroxysmal, characterized by reprisals (deep convulsive sighs after coughing on exhalation), glassy mucus, vomiting, nosebleeds, face engorged with blood, lacrimation, tongue boat, frenulum is injured , involuntary defecation and urination. Ro – increased transparency of the lungs. Leukocytosis, lymphocytosis. Mild degree – 10-15 attacks + 3-5 reprises; average degree – 20-25 attacks + up to 10 reprises; severe degree – 40-50 attacks + more than 10 reprises + apnea;

4. period of resolution (1-3 weeks) – spasmodic character and recurrences disappear.

The duration of the disease is 1.5 – 4 months.

Features of 1 year. Incubus 4-6 days. Catarrhal –5-7 days. (+runny nose, sneezing, no cough), period of spastic cough (2-3 months) – appearance of cough, no recurrence, attack ends with apnea, convulsions and encephalopathy syndrome.

Complications: secondary infection (auto-, super-), central nervous system lesions (encephalopathy), convulsions, pneumothorax, emphysema, hernias, nasal bleeding, hemorrhages in the skin and conjunctiva, atelectasis, epilepsy, paralysis, tic, pneumonia.

Diagnosis: clinic with characteristic cough, leukocytosis, lymphocytosis. Bacteriology – sputum culture, ELISA, RZK, RPGA.

Differential diagnosis:

1. Parapertussis – infection caused by parapertussis bacillus (Bardetella perapertussis) and clinical manifestations similar to mild whooping cough. Epid: source – patient, transmission – airborne; more often children 2-7 years old; There is cross-immunity-pertussis - parapertussis. Clinic (incubation period - 5-15 days), increasing cough to the point of spasmodic character, repeated episodes, vomiting, t - normal, cough for 2-3 weeks, no complications, diagnosis - culture from the nasopharynx and AT titer in the serum. Treatment is symptomatic.

2. ARVI - significant catarrh phenomenon, cough for 5-7 days, followed by a decrease. No reprises.

Treatment: hospitalization - up to 1 year, complications, severe. Fresh air, breathing exercises, nutrition. Etiotropic: ampicillin, erythromycin, levomycin, gentamicin. Pathogenetic: aerotherapy, vitamins A, C, gr. B, desensitization. Up to 1 year – Ig 3 ml, neuroplegics (aminosine, seduxen, propazine), oxygenation (oxygen tent), inhalations.

Prevention: isolation for 30 days from the onset of cough (20 from the onset of spasmodic cough), contact up to 7 years - isolation for 14 days. Special prof – ACDP (3 months 0.5 ml, every other month 3 times IM; booster vaccine – 18 months), passive prof – Ig 3 ml 2 days.

Diphtheria

Diphtheria is an acute bacterial anthroponotic infection, which is characterized by an inflammatory process with the formation of a fibrinous film at the site of pathogen invasion, symptoms of general intoxication and damage to the CVS and NS.

Etiology: Corynebacterium diphteriae, gram +, facultative aerobe; options – gravis, mitis, intermedius.

Epidemiology: source – patient, carrier (infectious throughout the entire period of illness). The transmission fur is airborne.

Pathogenesis: penetration into mucous membranes - release of toxins - damage to cells at the site of inoculation - inflammation, slowing of blood flow, formation of fibrinous film + toxins - damage to the heart, nervous system, endocrine, kidneys.

Classification:

Classification of diphtheria (Rozanov 1944)

1. by localization:

Typical:

Diphtheria of the oropharynx (localized island, local membranous, widespread, toxic (1,2,3 stages))

D upper respiratory tract (larynx (localization of croup), larynx and trachea (widespread croup), larynx + trachea + bronchi (descending croup))

D nasopharynx

D of the nose (lok membranous, spread)

D eyes (lobar, widespread, toxic)

D skin (lok membranous, toxic)

Dyra (widespread, localized)

D of the genital organs (localized, widespread, toxic)

Combined

Atypical:

Subclinical

D oropharynx catarrhal

D oropharynx hypertoxic

Nose catarrhal, catarrhal-erosive

D eyes catarrhal

D skin is filmless, pustular, impetigo-like, panaritium, phlegmon, panarichia.

2. By severity:

Mild: localized forms - oropharynx, island, nose, eyes, ear, skin, genitals.

Moderate: localized forms - oropharynx, nasopharynx; common - nose, eye, ear, skin, genitals.

Severe: toxic, hypertoxic forms.

3. Downstream:

No complications

With complications (myocarditis, PNS (paresis, paralysis), adrenal gland damage)

4. Bacterial carriage

Convalescent

Transitional

Short-term (2 weeks)

Protracted (more than 1 month)

Chronic (more than 6 months)

According to the degree of intoxication: - non-toxic, - subtoxic, - toxic, - hemorrhagic, - hypertoxic.

According to the distribution of plaque: - local; - common

Oropharyngeal diphtheria:

Catarrhal syndrome (atypical): enlarged tonsils, slight hyperemia of the mucous membranes, low-grade fever, slight intoxication

Insular f-ma: islands of whitish plaque with irregular edges (1-4 cm), tightly connected to the surface of moderately enlarged tonsils, T*C - up to 38*, pain when swallowing, enlarged lymph nodes, moderate intoxication

Membranous f-ma: acute onset. T*C up to 39*, headache, decreased appetite, vomiting, chills, pain when swallowing, the surface of the tonsils is hyperemic, covered with a whitish-gray coating with a smooth surface; tightly fused to the surface, swelling of the palatine arches, uvula; sometimes paratonsillar tissue; regional lymph nodes are enlarged and painful, T*C decreases after 2-3 days while plaque persists for up to 6-7 days

Common f-ma: as with membranous f-ma + more pronounced intoxication plaques beyond the boundaries of the amygdala (anterior arches, uvula, sometimes lateral and posterior walls of the throat)

Toxic f-ma: also + severe intoxication T*C up to 41*

Hypertoxic f-ma: also + severe intoxication of the central nervous system, the appearance of ITS, possible DIC syndrome

Toxicity levels:

1. Swelling along the pancreas above the enlarged lymph nodes to the middle of the neck

2. Swelling up to the collarbones

3. Swelling below the collarbones

Features of diphtheria in children of the first year of life: rare, usually up to 6 months; localization - nose (instead of films there is a catarrhal-erosive process), skin, larynx (weak cough, stenotic breathing is not expressed, short stages), oropharynx; with toxic - a slight increase in l / u, unexpressed swelling of the pancreas, pronounced intoxication, significant swelling of the mucous membranes, early widespread film formation.

Diphtheria of the larynx (croup): often in the first year of life, they are distinguished: - localized croup A (larynx + trachea), - widespread croup B (larynx + trachea + bronchi). Stages:

Catarrhal (1-3 days, T*C up to 38*, cough, hoarse voice, swelling of the mucous membranes);

Stenotic: - compensated (difficulty in breathing, aphonia, intoxication, hypoxia, cyanosis, 2-3 days); - subcompensation (respiratory failure, stenosis, shortness of breath); - decompensated (excitement, cyanosis, decreased breathing, tachycardia)

Asphyxial (terminal)

Diagnostics: clinic, bacteriological examination, RNA, RPGA, bacterioscopy.

Differential diagnostics:

Lacunar tonsillitis - more severe intoxication, more pronounced hyperemia of the tonsils, closer to the uvula; purulent effusion, easily removable films

Follicular tonsillitis - more pronounced intoxication, more pronounced hyperemia of the tonsils, easily removable films, etc.

Fungal tonsillitis - pinpoint, spot or total plaques, more severe intoxication, more pronounced hyperemia of the tonsils, easily removable films

Necrotizing tonsillitis

Simanovsky-Rauchfuss' sore throat

Aphthous stomatitis

Peritonsillitis

Retropharyngeal abscess

Mumps

Infectious mononucleosis

Croup during ARVI - suddenly appears in the midst of complete health, there is no aphonia, quickly eliminated (on its own or with treatment)

Treatment: specific - antitoxic anti-diphtheria serum (PDS) - administered according to the scheme depending on the wedge form. An intravenous test (sensitivity to foreign protein) is performed first. The total dose per course is 10-120 t MO (first dose 10-80 t MO, repeat dose 0-40 t MO). In one place no more than 10 tons MO. For toxic forms, half is administered intravenously. For combined forms, the dose is determined by the localization and level of toxicosis. For mild forms of AB (erythromycin, rifampicin, pinicillins, cephalosporins). Detoxification – native plasma, rheopolyglucin 5-10 ml/kg. Vit B1, RR. Prednisolone 2-3 mg/kg. For ITS - PDS 100-130 thousand MO, prednisolone, dopamine 1-3 mg/kg, heparin, contrical, gordox, correction of metabolic acidosis. For croup - 1st (sodium bromide, euphilin, diuretics), 2st (AB, hormone, sedatives, intubation).

Prevention: ADP (from 3 months - 0.5 * 3 times every month, 1 revacc - 18 months 0.5 ml 2 - 6 years), ADP-M (11.14 years), ADP, ADP-M. Contact are subject to ADP-M, ADP + AB.

Shigelosis (dysentery)

20-21 Shigelosis is an acute infection caused by bacteria of the genus Shigella, characterized by damage to the mucous membranes of the distal colon, general toxicity, abdominal pain, pathological impurities in the feces (mucus, blood, pus).

Etiology: subgroups: A (Sh. Dysenteriae - Grigorieva-Shiga -), B (Sh. Flexnery), C (Sh. Boydi), D (Sh. Sonnei).

Epidemiology: source – patient, carriers. Mm fecal-oral transmission. Transmission routes: Grigorieva-Shiga - contact-household, Sh. Flexnery - water, Sh. Sonnei - dirty hands.

Pathogenesis: Entrance gate - gastrointestinal tract (per os) - in the stomach part dies with the formation of endotoxin - the rest in the colon - reproduction (intracellular).

Classification:

by type: typical, atypical (erased, dyspeptic, subclinical, hypertensive)

By severity: mild, moderate A (with a predominance of local process), B (with toxic conditions), C (mixed)

Indicators of severity: symptoms of intoxication (meningoencephalitis, CVS, metabolic disorders), local symptoms (chronicity, frequency, stool, abdominal pain, prolapse of the mucous membrane, anal gaping).

Course: acute (up to 1 month), prolonged (up to 3 months), chronic (more than 3 months) (continuous, recurrent).

Clinic: Incubus period – 1-7 days.

The typical form is acute onset, t=38-39, nausea, single vomiting, anxiety, abdominal pain, frequent bowel movements, liquid stool, greenish with mucus, blood. At the end of 2 days - spastic colitis (pain in the left half, stool up to several dozen times a day, false urges, tenesmus, rectal spitting. The tongue is dry, the sigmoid is palpated - a dense painful cord. Blood - leukocytosis with neutrophs, ESR .

Characteristics in young children: acute onset, t up to 40, toxicosis with damage to the NS, CVS, neuratotoxicosis, blood in the form of streaks or impurities, bowel movements always have a fecal character, often a long course, m/w conjunctivitis, sepsis, meningitis.

Complications: prolapse of the mucous membrane, bleeding, perforation, peritonitis, intussusception, secondary infection.

Diagnosis: clinic, bacteriology, scatological examination, RNGA.RPGA, RA (diagn titer zone 1:100, Flexner 1:200).

Differential diagnosis:

1. Salmonellosis - more frequent bowel movements, foul-smelling, swamp-like, no tenesmus, pain in the bowels, vomiting.

2. Enteroinvasive escherichiosis – T-norm, watery, frequent stools, mucus, blood.

3. Staphylococcal enterocolitis - often up to 6 months, fever, weight loss, liquid bowel movements with mucus and blood, long-term course.

4. Intussusception – acute onset, T-norm, pain, no stool.

Treatment: diet, oral rehydration, etiotropic therapy (AB for severe and severe degrees, up to 1 year - polymexin M - 100 mg/kg/day, gentamicin 4-6 mg/kg, rifampicin 20 mg/kg; for mild stage - nitrofurans - furazolidone, furadonin) Application of bactisubtil, lacto- and bifidobacterin. Enterosorption, enzymes. Detoxification orally (leg, medium) parenterally (heavy). Treatment of complications.

Prevention: discharge after 1-2 negative blood tests (2 weeks after the end of treatment). Observation 3-6 months. Contact – 7 days + bacteriology.

Salmonella

An acute infectious disease of people and animals, caused by salmonella in cats.

Etiology: Gr-, AG – flagella (H), wall cells (O), membranes (Vi).

Epidemiology: Source - meat, patient, bird eggs. In children under 1 year - contact and everyday life: staff, mother, inf things.

Pathogenesis: GIT – endotoxin – non-vascular, NS – reproduction – secondary desemination.

Classification:

By type: typical, atypical.

Cln form: 1. Gastrointestinal (gastritis, enteritis, colitis, mixed), 2. Typhoid-like, 3. Septic, 3. Erased, 4. Subclinical.

By severity: light, medium, heavy

Course: acute (up to 1 month), prolonged (up to 3 months), chronic (more than 3 months).

Clinic: incubation period – 2-3 hours – 5-7 days.

Acute onset, increased temperature, chills, nausea, vomiting (first food - then bile), diarrhea (watery, with mucus, foul-smelling, green), m/w neurotoxicosis; if colitis may be caused by tenesmus. Duration 5-7 days.

Features up to 1 year – most often enterocolitis, blood in the stool, toxicosis is pronounced, often complications (septic form, meningitis, encephalitis, osteomyelitis, infection), severe course, often fatal. With development up to 10 days – normal, no vomiting, hepatolienal syndrome, flatulence, toxicosis.

Complications: ITS, acute renal failure, disseminated intravascular coagulation, dysbacteriosis, reactive arthritis.

Diagnosis: clinical epidemiology, laboratory - blood, bacteriology, RPGA (1:80-1:320).

Differential diagnosis:

1. Dysentery – short-term fever, colitis syndrome, stool character.

2. Colinfection – enteritis phenomena.

3. Viral diarrhea - acute, fast-acting, possibly cararious, watery bowel movements without pathological impurities.

4. Intussusception - acute onset, T-norm, pain, no stool

5. Typhoid-paratyphoid fever - undulating fever, intoxication, rash.

Treatment: hospitalization for 1 year, severe, moderate forms. Etiotropic (severe, generalized) – rifampicin 20 mg/kg, gentamicin 15 mg/kg, (mild) – polyvalent salmonella bacteriophage 10-20 ml. Pathogenetic – rehydration. For ITS – rheopolyglucin, dopmin, corticosteroids, diuretics. For neurotoxicosis - aminazine, dipyridoxine, diazepam, dropiridol. Also complex Ig enterosorbents, enzymes, vit, biological products.

Prevention: admission after a negative bacteriological examination (2-3 days after discontinuation of AB), medical examination for 3 months.

Escherichiosis

– acute diseases of the gastrointestinal tract, most often in young children, caused by different strains of Escherichia coli.

Etiology: Gr-, AG – somatic (O), membranes (K), flagellar (N). Subgroups: enteropathogenic (EIE - O11, O55, O44, O127... - only up to 1 year), enteroinvasive (EIE - O28, O124, O151, O144... - dysentery-like), enterotoxigenic (ETE - O1, O8, O9, O20... - cholera-like ), entnrohemorrhagic (EGE - O157, O159 - hemorrhagic colitis).

Epidemiology: source – patient, carrier. Food, contact-household.

Pathogenesis: infection - thin tissue (less often thick) - enterotoxin - damage to enterocytes, blood vessels, NS - increased vascular penetration, increased secretory activity of the epithelium - loss of water - acidosis - kidney damage, hemodynamic disturbances.

In young children, EPE incubation period is 5-8 days. Onset is acute, increased t, intoxication, diarrhea (watery stools, yellow (orange), + mucus) - maximum on days 5-7, toxicosis, exicosis, stools up to 10-15 times a day, vomiting, restlessness, sleep disturbance, decrease body weight. In severe cases - + neurotoxicosis, toxicosis with dehydration.

In older children: EIE (dysentery-like course) – Incubation period – 2-3 days. – acute, increased t, intoxication (first 1-2 days), abdominal pain, weakness, no tenesmus, frequent bowel movements, with mucus and blood. ETE - (acute gastroenteritis) - incubus - hours - 3 days - acute, watery stool, base of odor and impurities, epigastric pain, normal, duration 3-5 days.

Diagnosis: clinic, laboratory - bacteriology (defecation, vomiting, washing water), IFA, RNGA.

Diff. diagnosis:

1. Salmonellosis - fetid stools, green, no tenesmus, soreness in the stool

2. Intestinal staphylococcal infection - often after maternal death, secondary damage, gradual development.

3. Viral diarrhea - acute, fast-flowing, possibly carrious, watery bowel movements without pathological impurities.

4. Simple dyspepsia – inappropriate complementary feeding, after eating, regurgitation, bowel movements with a sour smell. Correction of nutrition - restoration of function.

AB-severe – polymexin-M, biseptol, levicytin, gentamicin.

Biological products – bifidumbacterin, colibacterin, lactobacterin, acipol, bacteriophage.

Rehydration – during the first 6 hours – amount of fluid (ml/hour)?m?p/6?10 (m-body weight, p-%weight loss). After maintenance therapy (? 80-100ml/kg) - glucosolan (NaCl 3.5+Na bicarbonate 2.5+KCl 1.5+ glucose 20g - per 1 liter of water), rehydron (NaCl 3.5+ KCl 2.5+Na citrate 2.9+ glucose 10g+1l of water) – 1-2 teaspoons every 5-10 minutes. +sweet tea, rice broth. Oral rehydration – 1-2 tbsp. At 3 tbsp - intravenous colloid solutions (1/3 volume of liquid) - composition: for isotonic dehydration 10% glucose: salt solutions = 1:1 (up to 1 year 2:1), for salt deficiency (1:3(1:2)), with water deficiency (3:1(2:1)). Under the control of bcc and electrolytes. Reduction of K, Na, Cl.

Prevention: san-gig regime, source isolation...

Acute intestinal infections caused by conditionally pathogenic flora.

1. intestinal infections of Proteus etiology - damage such as gastroenteritis, enterocolitis. Proteus – facultative anaerobe, AG – somatic (O), flagellar (P). Epidemiology: source – patient, carrier, other animals. Pathogenesis: develops against the background of decreased immunity, dysbactenia. In case of massive infection, endotoxin causes general symptoms of intoxication. In other cases, the process is slow, it may enter the bloodstream with the development of secondary foci of infection. Clinic: incubation period – 2-5 hours. In the older ones - food toxic infection, in the younger ones (incubus - 2-5 days) - enteritis, enterocolitis - stool - liquid, green, admixtures of mucus, blood. Diagnosis: clinical picture, blood (leukopenia, neutropenia, lymphocytosis, ESR), sigmoidoscopy, bacteriology, RA, RNGA. Treatment – ​​AB – only for severe cases.

2. intestinal infections caused by Klebsiella - proceeds according to the type. Etiology: AH – somatic (O), capsular (K). Epidemiology: source – patient, carrier, other animals. Newborns often need care items. Potogenesis: portal of entry – gastrointestinal tract – with massive infection – toxemia – invasion – massive bacteremia. Clinic: incubation period: 3-5 days, acute – T-max up to 39-40, vomiting, diarrhea (watery, greenish, with undigested pieces of food), toxicosis, exicosis, stomach is moderately swollen. Diagnosis: culture, RA, RZK. Treatment: the same.

3. intestinal infections caused by Pseudomonas aeruginosa - often a nosocomial infection (usually pneumonia, meningitis...). Etiology: uxotoxin, hemolysin, enterotoxin, leukocidin, collagenase, elastase. Epidemiology: source - patient, carrier, nosocomial infection (purulent wounds, pneumonia...), or animals. Pathogenesis: primary (gastritis, enteritis, enterocolitis), secondary. Clinic: incubation period: 3-5 days, gradual development, deterioration of general condition, subfibrile T, bowel movements 5-20 times/day (liquid, greenish, fetid, mucus, blood). The course is long and undulating. In older people - gestroenteritis (foodborne toxic infection). Diagnosis: bacteriology, RPGA, RA. Treatment: AB – gentamicin, polymexin M sulfate.

4. intestinal infections caused by campylobacteria - Etiology of Campilobacter (vibrio). Epidemiology: source - animals. Pathogenesis – entrance gate – gastrointestinal tract – reproduction in thick and thin tissue – bacteremia, toxemia – generalization is possible. Clinic: incubation period: 2-5 days, acute – T – up to 39-40, repeated but not frequent vomiting, anorexia, lethargy, anxiety, diarrhea (watery, foul-smelling – 2-20 times/day – mucus and blood appear later), pain in the abdomen, after bowel movement it decreases, the abdomen is moderately distended. Diagnosis: coprogram, culture, RA, RPGA, RZK. Treatment: the same.

5. intestinal citrobacter inf – source – patient, carrier. m/w pets. Young children get sick. Elderly people rarely suffer from food poisoning. Clinic: in young children – enterocolitis (feces, blood in the stool, intoxication). Diagnosis: bacteriology, RPGA, RA. Treatment: the same. Prevention: not developed.

1. OKI caused by staphylococcus

Etiology: gr+, S. Aureus, S. Epidermidis, S. Saprophyticus.

Epidemiology: source of information – patients, carriers.

Classification:

By localization: Localized forms (respiratory tract, gastrointestinal tract and biliary tract, kidneys, central nervous system, ...), generalized.

Damage to the gastrointestinal tract: gastroenterocolitis (thymus toxicoinfection), enterocolitis (primary, secondary).

By severity: mild, moderate, severe.

Clinic: Primary enterocolitis - after exogenous infection, more often in children of the first year of life. Often there is a history of pre-existing omphalitis, purulent conjunctivitis, staphyloderma, maternal obstruction (purulent lactation mastitis), unfavorable premorbital condition (rickets, malnutrition). The onset of obstruction is often gradual (m/w acute), t - subfibrile, m/w one-time vomiting, bowel movements up to 10 times a day (yellow or greenish, with mucus, streaks of blood rarely), flatulence. Duration up to 4-5 weeks. The current is wavy. Possibly intestinal toxicosis occurs with exicosis of 1-2 degrees, t up to 39, repeated vomiting, bowel movements up to 15 times a day (watery), pallor, sunken eyes and fontanelles, dry mucous membranes, bloated abdomen, weight loss, hepatosplenomegaly, weakening of tones. Blood leukocytosis, neutrophilia, shift to the left, ESR.

Secondary: for sepsis, pneumonia, gn. otitis, may be due to dysbacteriosis. Clinic + we are the main clinic.

Diagnosis: clinical picture, bacteriology, AT level in blood serum.

1. AB (7-10 days) – oxacillin sodium salt IM, IV 50 – 100 mg/kg * 4 times a day, carbinecilin, gentamicin, brolomycin, garamycin.

2. Immunotherapy: passive – anti-spaphylococcal plasma, hyperimmune anti-staphylococcus Ig; active – adsorbed staphylococcus toxoid, staphylococcus antiphagin, autovaccine.

3. Biological products – bifidumbacterin, lactobacterin, bificol.

4. Correction of CBS, rehydration.

Rotovirus infection

Rotavirus infection is a acute infectious disease caused by a virus that dates back to the origin of the reoviruses, the genus of rotaviruses, and is characterized by intoxication syndrome, disorders of the lateral tract, and high blood pressure levels.

Etiology: rotavirus gr A (4 serotypes).

Epidemiology: dzherelo – illnesses and noses, transmission mechanism – contact-casual; peak of sickness - leaf fall - fierce.

Pathogenesis: mouth – herbal tract – enterocytes of the small intestine (reproduction) – inflammatory process – diarrheal syndrome.

Clinic: incube – 1-5 dB; cob of gostria for 1 dose - gastroenteritis and enteritis (watery and emptied ribs, weakly packed foam, without pathology, with an insignificant amount of mucus, with a pungent odor - 5-20 times per dose; imperative position before defecation; vomiting; life pain ; T*S – 38-39*). Duration of diarrhea is 7-10 days. Weakness, weakness, adynamia, headache. Some patients develop catarrhal symptoms for 3-4 days. Respiratory syndrome: hyperemia and granularity of the throat without a tendency to increase Possible exicosis 1-2 tbsp. Children under age 1 have a more difficult life.

Diagnosis: typical clinic, epidemiological history, follow-up laboratory (ELISA, RN, RTGA with rotavirus antigen).

Differential diagnostics: GKI – low-syndromic rotaviral gastroenteritis; cholera - with rotavirus infection, diarrhea, abdominal pain, flatulence, catarrhal symptoms; salmonellosis – intoxication syndrome, green discharge from mucus and blood, hepatolienal syndrome.

Diet: diet with limited carbohydrates, more protein; sorbents, eubiotics; recommend - cholesterol, smecta; if necessary, re-draftation.

Prevention: no specific; identification and isolation of patients.

PSEUDO-TUBERCULOSIS

Acute infectious disease, zoonosis, with intoxication, fever, scarlet fever-like rash, damage to other organs and systems.

ETIOLOGY – Iersinia psevdotuberculosis. Capsule, endotoxin (soluble fraction of O-AG). Sensitive to dryness, sunlight. Behind somatic S-AG and R-AG and flagellar R-AG there are 6 serovars (usually 1,3,4). Highly invasive properties - easily penetrates through natural barriers.

EPIDEMIOLOGY Source - wild and domestic animals (mainly mouse-like rodents - they infect water and food). The path is food (salad, fruit, milk, water). Does not occur in children under 6 months. Seasonality - all year with a maximum in February and March.

PATHOGENESIS Pathogen - intestines through the mouth (infection phase) - invasion into the mucous membrane (enteral phase) - inflammation in the mucous and lymph apparatus (regional infection phase) - blood - internal organs (liver, lungs, heart, kidneys - generalization phase ); allergic component (rash, arthralgia, erythema nodosum).

CLASSIFICATION OF CLINICAL FORMS

Typical forms: scarlatiniform, abdominal, arthralgic, icteric, combined, generalized

Atypical: catarrhal, erased, subclinical

Severity: light, medium, heavy. Indicators of severity – a) meningoencephalic syndrome, b) hemorrhagic, c) significant liver damage, d) abdominal, e) articular, f) generalization

Course: smooth, with exacerbations and relapses, with complications.

CLINIC Incubate period - 3-19 days (6-8), acute onset, increasing T to 38 - 400C. Intoxication, catarrhal syndrome, rash for 2-4 days. Manifestations of all syndromes (see classification, depending on the form - the clinic of this syndrome prevails).

DIAGNOSTICS Culture of blood and swabs from the oropharynx (1st week), sputum, feces, urine - to isolate Yersinia. Serology – RA, RSK, RPGA (diagnostic titer 1:200), RTGA. Using the paired serum method - in the first days and 2-3 weeks, the titer increases 4 times.

TREATMENT Bed rest, a complete diet, AB for moderate and severe forms - chloramphenicol, tetracycline, gentamicin intramuscularly. Detoxification – 5% eye with insulin, albumin, plasma, rheopolyglucin. Hormones: prednisolone 1-2 mg/kg/day - for severe arthritis, erythema nodosum. Methyluracil, pentoxyl, Vit C. For polyarthritis - NSAIDs; cardiovascular – corglycone, cordiamine; hemorrhoids syndrome - heparin, aminocapron.

PREVENTION Duration of hospitalization - up to 7-10 days of normal T + normal blood and normal clinic. Observation in the outbreak for 3 weeks, prohibition - raw vegetables without heat treatment. Rodent control.

YERSINIOSIS

Acute infectious disease. Anthropozoonosis with intoxication and primary damage to the gastrointestinal tract, liver and joints.

EPIDEMIOLOGY Source: mice, rats. The route of transmission is food, contact, aerogenic. Factors - milk, meat, vegetables, fruits, hands, dishes, care items. Seasonality – all year round, maximum from October to May. Mostly children aged 3-5 years are affected.

ETIOLOGY Iersinia enterocolitica (Gr - rod or coccobacterium), facultative aerobe, no disputes. Resistant to low T, 5 biovars, 30 serovars for O-AG.

PATHOGENESIS Pathogen - mouth - small intestine (primary localization) - reproduction, maximum - in the terminal part of the small intestine - inflammation (from catarrhal to ulcerative-necrotic) - peripheral lymph nodes (hyperplasia, necrosis or microabscesses) - ending, or: – blood – abscesses of the liver, spleen, lungs, bones. Allergic manifestations - exanthema, arthritis, arthralgia, myalgia, myositis, heart damage, erythema nodosum, Reiter's syndrome.

CLASSIFICATION

Forms: intestinal (mainly), abdominal, hepatitis, septic, articular, erythema nodosum.

CLINIC Incubus period 5-19 days (7-10). The onset is acute, T 38-39, intoxication, diarrhea (3-15): green mucus, sometimes blood. The duration of the disease is 3-15 days. There will always be shit, and other manifestations will depend on the form. For the most part, the course is mild to moderate. Symptom of “hood”, “gloves”, “socks” - rash. Generalized form: acute onset, intoxication, 2-3 days - rubella- or scarlet fever-like rash, maculopapular, around the joints, hepato-, splenomegaly, bilirubin is increased due to bound. Urine: albumino-, cylinder-, pyuria. ESR 50-70. During the attenuation period, peeling: large-plate - palms, feet, pityriasis - torso, limbs. A constant sign of the disease is pain around the navel and in the right ilium. Hepatitis - high T does not decrease during the icteric period, diarrhea, abdominal pain, dark urine on days 3-5, jaundice. The liver is enlarged, diseased, dense. Erythema nodosum (children over 10) - acute, with intoxication, increased T, rash on the legs, in the form of painful pink cyanotic nodes. Disappears within 9-22 days.

DIAGNOSTICS Bacteriological method - isolation from poop, blood, urine, pus, mucus from the throat, l/u (1st 2-3 weeks). Serology: RA with live or dead Yersinia culture (1:40 – 1:160), RPGA 1:200.

TREATMENT Levomycetin succinate for 7 days, if there is no effect then gentamicin for 7 days. Also, see treatment of pseudotube.

PREVENTION Those who have been discharged are allowed to work after being discharged after 3 negative bacterial examinations of their poop. In the outbreak - final disinfection (after isolation of the patient), contact contacts are monitored for 18 days. Veterinary control of domestic and agricultural animals.

MONONUCLEOSIS

Acute febrile illness with polyadenitis, mainly cervical lymph nodes, enlarged spleen, liver, tonsillitis, virocytes in the blood.

ETIOLOGY Epstein-Barr virus (EBV) multiplies in B lymphocytes without cytolysis.

EPIDEMIOLOGY is ubiquitous, incidence is sporadic. Seasonality – all year round, especially spring and autumn. The source is a patient, a virus carrier. The mechanism is air-drip, contact. The entrance gates are the mucous membrane of the oropharynx and the upper respiratory tract. Immunity is strong.

PATHOGENESIS EBV is tropic to the lymphoid-reticular system, the virus penetrates the lymph, blood, then into the lymph nodes, liver, and spleen. Damage to the palatine and nasopharyngeal tonsils - swelling, hyperemia, difficulty in nasal breathing. Tonsil damage + bacteria = sore throat. Sensitization of the body is an allergic reaction. Fixation of EBV on the surface of the B-lymphocyte - activation of T-killers, NK cells, K-cells - increased activity of T-suppressors - inhibition of proliferation and differentiation of B-lymphocytes (therefore they do not become malignant). In icteric forms, single bile thrombi and deposition of bile pigment in the hepatocytes of the central zones of the lobules.

CLASSIFICATION Typical forms: there are light, medium, heavy. Atypical - erased, asymptomatic, visceral. Severity indicator – degree of intoxication, ? lymph nodes, changes in the oropharynx, difficulty in nasal breathing,? liver and spleen, changes in the blood.

CLINIC Incubate period is several days – 1-2 months. The onset is acute, ? T up to 38-40, intoxication, pain in the muscles, joints. Fever of the wrong type 1-3 weeks. Pain while swallowing. Tonsillitis from catarrhal to ulcerative-necrotic with the formation of fibrin films. Polyadenitis, sometimes mesadenitis, possible measles, scarlet-like, urticarial, hemorrhagic rash (lasts 1-3 days). ? liver, spleen from 3-5 days. Puffiness of the face, swelling of the eyelids, tachycardia, muffled sounds, sometimes systolic murmur. Fever from 3 days to 3 weeks. At the end of the 1st week, plaque from the tonsils and hyperemia of the pharynx disappear. L/u? h/w 2 weeks – several months. Virocytes are detected in the blood from 6 weeks to 4-6 months.

DIAGNOSTICS Blood: leukocytosis 9-15*10 9/l, virocytes 15-50%, ESR 20-30. Serology: Paul-Bonnell-Davidson (with sheep red blood cells), Lovrik-Wolner, Hoffa-Bauer (with horse erythrocytes) - rapid diagnostic method. IgG,M against viral capsid Ag. Anti-EBnuclear IgG,M.

TREATMENT Diet – do not eat: spicy, fried, extractive foods. Drink a lot. Vitamins. Rinse your mouth with 2% NaHCO3, chamomile decoction, brush your teeth, put vasoconstrictor drops in your nose. AB – children under 3 years of age at risk? microbes, older ones - with massive deposits on the tonsils (macrolides). Hormones - for severe forms with a pronounced allergic component, 1-2 mg/kg/day for 3-5 days. For weakened young children - normal human Ig - 1-2 doses.

PREVENTION No special treatment is carried out; contacts are monitored for 20 days.

ENTEROVIRAL INFECTION

Caused by enteroviruses - Coxsackie, ECHO, characterized by a variety of clinical signs associated with intoxication, fever, damage to the nervous system and the muscular system.

ETIOLOGY Coxsackie, ECHO is a group of intestinal viruses with single-stranded linear RNA. Coxsackie - group A (24 serovars), B (6 serovars). ECHO – 34 serotypes. From humans they are isolated from nasopharyngeal swabs, poop, blood, and cerebrospinal fluid. In the environment - in wastewater, flies, some domestic animals.

EPIDEMIOLOGY Source – b-noy or virus carrier. The route of transmission is fecal-oral, airborne. Seasonality – all year round, maximum – summer, autumn.

In newborns, the typical form is encephalomyocarditis; in the first months of life – enteroviral diarrhea; 1-3 years – paralytic poliomyelitis-like forms; pre- and schoolchildren – meningitis.

CLINICAL FORMS General clinic: incubation – 1-10 days, acute onset, T 39-40 (3-5 days). Intoxication SDM, hyperemia of the face, neck, sometimes with a maculopapular rash, hyperemia of the pharynx, posterior wall of the pharynx, conjunctiva. Blood - ? ESR, relative neutrophilia, lymphopenia.

Serous meningitis: children aged 5-9 years, serous inflammation of the soft membranes, ependyma with hydrocephalic-hypertensive swelling. Nausea, repeated vomiting, abdominal pain, delirium, convulsions. All – see general clinic, + granularity of the soft palate. From the 1st day there were meningeal signs. Abdominal reflexes? In young children, the fontanel is tense and pulsating. Sometimes asymmetry of the face, tendon and skin reflexes. The liquor is clear, under? pressure, cytosis - 0.1-0.5 per 109/l (normal 1-6 per 106/l), initially neutrophilic-leukocyte, from 7-8 days lymphocytic, ? from 10 pm. Protein is normal, sugar, chlorides are normal. ESR moderate?, fever for 1-10 days, normal cerebrospinal fluid for 3-4 days.

Epidemic myalgia: Coxsackie B virus, see general clinic + sharp pain in the muscles of the chest, upper abdomen, limbs, spastic in attacks for 10-30 minutes, ? when coughing, moving. Because of this, breathing becomes shallow and frequent. Sometimes pain in the hypochondrium, iliac region, near the navel. Photophobia, ? submandibular, cervical lymph nodes, lonely dry or moist rales in the lungs, inconsistent? liver and spleen. It proceeds in waves for 3-5-7-14 days. Relapses are possible. Blood – leukopenia, neutrophilia, ? ESR.

Paralytic form: Coxsackie A. ECHO - children 4-8 years old. The course is mild, T-normal, central nervous system – flaccid monoparesis of the limbs, weakness of the buttocks and thighs, calf muscles, and sometimes facial muscles. Muscle tone, tendon reflexes, cerebrospinal fluid – normal. The 7th pair is affected peripherally and recovers quickly. May mimic polio.

Herpangina: Coxsackie A, B, ECHO. T – 39-40, headache, vomiting, abdominal pain. Pharynx: hyperemia, on the arches, tonsils, uvula, back wall of the pharynx - papules, quickly turning into vesicles - bursting - shallow gray-yellow ulcers with a red rim (5-10 or more). It hurts to swallow. Submandibular lymph nodes, sensitive. Blood - ? ESR. Lasts 1-7 days, ulcers heal in 4-7 days. Full recovery.

Enteroviral fever: Coxsackie, ECHO. Rough for 3 days, moderate headache, sometimes nausea, vomiting, paroxysmal abdominal pain. Hyperemia of the pharynx, coated tongue, ? l/u, liver, spleen. Measles-like rash. Lasts 2-3 weeks.

Epidemic exanthema: Coxsackie, ECHO. Older children. Incubation 4-5 days. T 37.5-38. Headache, muscle pain. Hyperemia of the pharynx. After 2 days T?, the condition improves, a rash appears on the face, chest, and limbs - erythematous, maculopapular. Disappears within 2-4 days. On the mucous membranes there is spotted enanthema. The disease lasts up to 1 week. Pigmentation lasts 5-6 days, no peeling.

Summer flu: Coxsackie A, B, ECHO. ?T, headache, runny nose, dry cough, nausea, vomiting. Hyperemia of the face, pharynx, conjunctivitis, ? l/u, liver. Mild course for 1-5 days.

Enteroviral diarrhea: children under 4 years old, T 38-39, vomiting, abdominal pain, snot. The poop is sparse, watery, sometimes greenish. From the 1st day, diarrhea is combined with a runny nose, hyperemia of the mucous membranes, and dry cough, lasting 2 weeks.

Encephalomyocarditis of newborns: Coxsackie V. Infection from the mother or patients, or intrauterine. The onset is acute, 38-40, lethargy, drowsiness, vomiting, snot, heart-vessel failure + encephalitis develops with tonic or clonic convulsions, impaired consciousness. Liquor – cells 0.1-0.3*109/l, ? squirrel. ECG - ? voltage, negative T, sharpening of P, widening of QRS, shift of ST. In 1-2 days - death.

DIAGNOSTICS Virology - in the 1st days, nasopharyngeal washouts, poop, cerebrospinal fluid. Serology - RSK using the method of paired sera on the 1st days and 2-3 weeks (? more than 4 times).

TREATMENT? -globulin 1-6 ml on the 1st days, RNase 3-20 mg 6 times a day. Symptomatic: fever, dehydration, detoxification, pain. For encephalomyocarditis - hormones. Thermal procedures – for myalgia, paralytic form. AB – with 2-stage infection.

PREVENTION Hospitalization up to 10 days. Isolation of contacts for 14 days.

MENINGOCOCCAL INFECTION. PURULAR MENINGITIS. MENINGOCOCCAEMIA ETC.

An acute anthroponotic disease, caused by meningococcus (hereinafter referred to as “m-coccus”), is characterized by clinical polymorphism (from nasopharyngitis and simple carriage to generalized forms).

ETIOLOGY The causative agent is Neisseria meningitidis. Diplococcus Gr-. According to the AG structure there are 13 serotypes (A, B, C, D). In patients, it grows on the mucous membrane of the nasopharynx, cerebrospinal fluid, and is released from the blood. Can form L-shapes. The greatest virulence is in serogroup A (due to high invasiveness).

EPIDEMIOLOGY Source – patient and carrier. The most dangerous are patients with meningococcal nasopharyngitis; they secrete m-coccus for 3-4 weeks. Healthy carrier period from 2 to 6 weeks (there are many more). The transmission mechanism is airborne, promotes coughing, sneezing, and runny nose. The vozb-l is unstable in the environment. The maximum incidence is February – April. Contagiousness index 10-15%. Post-infectious persistent type-specific immunity.

PATHOGENESIS M-coccus – mucous membrane of the nasopharynx, pharynx – nasopharyngitis, locally? barrier permeability – lymph, blood (bacteremia). At this stage it may be limited, if there are no pathological phenomena at the site of invasion - a healthy nose. Intense bacteremia, ? org-ma reactivity - lymphogenously penetrates into the blood, dissemination often into the brain and spinal cord through the choroid plexuses of the cerebral ventricles - encephalitis, ventriculitis, meningitis. If m-coccus is introduced into other organs and tissues (skin, joints, heart, kidneys, lungs) – meningococcemia (m-coccal sepsis). Endotoxin is a vascular poison (spasm of capillaries, their permeability). Pathogenesis of ITS: occurs due to massive bacemia and toxinemia. Endotoxin – disturbance of hemodynamics, microcirculation – DIC-sdm. As a result, hemorrhagic SDM (adrenal infarctions, hemorrhages into the mucous membranes). Inflammation of meningeal membranes that do not stretch + ? intracranial pressure = displacement of the GM and wedging of the cerebellar tonsils into the foramen magnum - death from respiratory paralysis. Cerebral collapse leads to the development of subdural effusion.

CLASSIFICATION Localized forms: meningococcal carriage and acute nasopharyngitis. Generalized forms: a) typical – meningococcemia, meningitis, meningoencephalitis, combined; b) atypical – serous meningitis, hyperacute m-coccal sepsis, fulminant and fulminant m-coccemia. Rare forms: m-coccal endocarditis, arthritis, synovitis, iridocyclitis, pneumonia.

CLINIC Incubus period 2-20 days.

Nasopharyngitis: acute onset, T – normal, subfebrile, or febrile (1-3 days). Headache, sore throat, nasal congestion, lethargy, adynamia, pallor. In the pharynx there is hyperemia of the mucous membrane, granularity of the posterior pharyngeal wall (hyperplasia of lymphoid follicles). Blood – in 50% of cases – neutrophilic leukocytosis. Biological examination of mucus from the nasopharynx, epidemiological situation.

Meningococcemia: acute onset, T 38-39, intoxication, pain in the muscles of the back, limbs, thirst, pallor. After 4-6 hours, a hemorrhagic rash appears on the buttocks, thighs, legs, torso, followed by necrosis, its rejection and scar formation. Hemorrhagic SDM: hemorrhages in the sclera, conjunctiva, mucous membrane of the pharynx, uterine, nasal, gastric. ? headache, cerebral scream, repeated vomiting, consciousness may be impaired, convulsions. Damage to small joints. Pleurisy, arthritis, thrombophlebitis, endomyopericarditis, acute renal failure, glomerulonephritis, pyelitis. In the hyperacute form - Waterhouse-Frederiksen SDM. Cardiovascular failure (cyanosis, thread-like pulse, blood pressure, collapse). ITS develops, degrees: 1 – compensated: T 38-40.5, tachycardia, ? RR and BP are normal. Convulsive readiness, hypercoagulability. 2 – subcompensated: skin is pale gray, cold, moist, acrocyanosis, T 37.2. ? Heart rate? ChD, ? HELL. Muffled tones, oliguria, confusion, acidosis, stage 2 DIC (hypocoagulum). 3 – decompensated: unconscious, total cyanosis, multiple hemorrhagic-necrotic elements, venous stasis like cadaveric spots. Pulse thready, shortness of breath, ? Heart rate, blood pressure – 0. Muscle hypertension, hyperreflexia, pathological reflexes. Pupils are constricted, photoreaction?, meninges, convulsions. Anuria, acidosis, DIC 3-4 degrees. Possible pulmonary edema, GM. 4 – agonal state: no consciousness, areflexia, atony, dilated pupils, do not respond to light, ? edema of the GM, lungs.

M-coccal meningitis: suddenly? T up to 39-40, headache in the forehead and back of the head is aggravated by irritants - sound, light, vomiting without nausea, psychomotor agitation is replaced by inhibition, drowsiness. Pain along the spine, general hyperesthesia. "Spotting dog" pose. + with Kernig, Brudzinski, Guyen, Lesage, Babinski, Gordon. The cerebrospinal fluid is clear or slightly opalescent on the 1st day, then cloudy and purulent. Cells – 1000 per µl. Protein?, sugar, chlorides?.

M-coccal meningoencephalitis: encephalitic symptoms predominate: motor agitation, impaired consciousness, convulsions, damage to pairs 3,6,7,8. Hemi- and monoparesis, bulbar paralysis, and ataxia are possible. The current is very difficult.

M-coccal meningitis and M-coccemia: the most common variant of generalized forms of M-coccal infection. One of the forms dominates. The severity is due to pronounced bacteriaemia and changes in the central nervous system and other organs and systems.

Clinic of edema and swelling of the brain: impaired consciousness, vomiting, psychomotor agitation, clonic-tonic convulsions, facial hyperemia, cyanosis, hyperthermia, extinction of corneal reflexes, constriction of the pupils,? r-ii to the light, ? Does your heart rate change? Heart rate. HELL?, then?.

In young children, m-coccal infection is accompanied by cerebral hypotension, toxicosis and exicosis with diarrhea. It develops acutely, within a few hours. State? before our eyes. The face becomes sharp, repeated vomiting, convulsions, muscle hypotonia,? reflexes. When the medulla oblongata is pinched, the pulse is rare, arrhythmic, Cheyne-Stokes breathing. Death from pulmonary edema, respiratory arrest. Ependymatitis occurs in early or late stages of meningitis: drowsiness. Motor agitation, prostration, stupor, or coma. Hypertonicity of the muscles, tremor of the limbs, convulsions, hyperesthesia. In infants there is a bulging of the large fontanelle, divergence of the seams, legs are elongated and crossed. The fingers are bent into a fist. Characteristic is emaciation, bordering on cachexia (with normal nutrition). The liquor is xanthochromic, ? protein, cellular composition is normal. The cerebrospinal fluid from the ventricles is purulent, with the presence of polynuclear cells and m-cocci.

DIAGNOSTICS Isolation of excretion from the blood, nasopharynx, and cerebrospinal fluid. Express method - thick drop bacterioscopy, coagglutination method, enzyme antibodies, counter immunoelectrophoresis method. Serology – RNGA with meningococcal erythrocyte diagnosticum of serogroups A, B, C. Blood is examined over time at intervals of 5-7 days + general analysis of cerebrospinal fluid.

M-coccal infection in 1-year-old children: most often M-coccemia and its fulminant forms. With meningitis, meningeal symptoms are weakly expressed or absent, the general symptom predominates: hyperesthesia, clonic-tonic convulsions, tremor of the hands, chin, repeated vomiting, Lesage symptoms, “cooper dog” pose. First anxiety, then weakness, crying, piercing scream. In infants, encephalitis, ependymatitis, blockage of the cerebrospinal fluid tract - hydrocephalus. The course is slow and protracted. Sanitation of the cerebrospinal fluid is delayed, often leaving residual effects and complications. Attachment of 2-part microflora.

TREATMENT Carriers: gargling with 0.05-0.1% permanganate, 0.02% furacillin, ultraviolet radiation, for 4-5 days erythromycin, chloramphenicol, Vit, antihistamines. Generalized: chloramphenicol 25 mg/kg, anti-influenza β-globulin 1-2 doses. For meningeal sdma - lasix 1-2 mg/kg. Excitement, convulsions - seduxen. If there is a threat of ITS - prednisolone 2-3 mg/kg, if ITS - prednisolone 5-10 mg/kg. Detoxification – reopoli, albumin, 10% glucose. Meningococcal meningitis: benzylpenicillin - IM 200,000-400,000/kg (children under 6 months - 300,000-500,000) every 4 hours, in the first 3 months - every 3 hours. For endotoxic shock - chloramphenicol succinate 80-100 mg/kg/day every 6 hours. Treatment of ITS – depending on the degree, hydrocortisone 20-40-80 mg/kg/day, prednisolone – 5-20 mg/kg/day, then successively reopoli 10 ml/kg, 10% albumin 5-10 ml/kg, 4% soda – 2 ml/kg, 10% CaCl or glucanate 1 ml per year of life. Cocarboxylase – 50-100 mg, 5% Vit C 5-10 ml, for convulsions – seduxen. To stabilize blood pressure - dopamine 2-10 mcg/kg/min, for acute cerebral edema - mannitol 1-2 g/kg, furosemide 1-2 mg/kg, 10% albumin, concentrated plasma - 5-10 ml/kg, hormones , anticonvulsants, oxygen. Treatment of DIC – intravenous heparin 100-50-15 IU/kg according to the phase (in phase 4 – contraindicated), contrical, Trasylol – 1-2 thousand IU/kg, fresh donor blood, thrombomass; dicinone 12.5% ​​0.5-2 ml every 4-6 hours; for bleeding, prothrombin, aminocapron.

PREVENTION For group illnesses in closed groups, quarantine for 10 days (temperature measurements and ENT examinations every day). All contacts are examined for nasopharyngeal mucus - children 2 times with an interval of 3 days, adults - 1 time. All patients are isolated and treated. Carriers are not allowed into children's institutions. In the center of information - current disinfection. In the hospital, staff wear masks. Specific profile: polyvalent vaccine of serogroups A, B, C. Observation of convalescents: after meningococcemia 6 months, meningitis - 1 year.

Polio

Poliomyelitis is an acute infectious disease characterized by general toxic manifestations and damage to the central nervous system such as flaccid peripheral paralysis.

Etiology – Poliovirus hominis (enterovirus).

Epidemiology – Source of infection – patients or virus carriers. The virus is excreted in mucus from the nasopharynx (up to 2 weeks) and in feces (up to 1.5 months). The main routes of transmission are fecal-oral and airborne. Mostly children under 7 years of age are affected; Children in the first months rarely get sick - transplacental immunity. After an illness, lasting immunity.

Pathogenesis – infection – per os – active reproduction in the intestines and regional lymph nodes (enteric phase) – transition into the blood (hematogenous phase of viremia) – hematogenous spread through the perineural, lymphatic and perivascular spaces into the nervous system: anterior horns of the spinal cord (damage to motor neurons is not uniform , asymmetrical paralysis is possible), the zone of the nuclei of the cranial nerves, the hypothalamic region, the cerebellum. BBB breakthrough occurs in 1% of infected people, the rest are virus carriers. The development of the pathological process is closely related to the state of reactivity of the organism. Periods of the disease: preparalytic (2-5 days), paralytic, recovery, residual. The lumbar spine, thoracic and cervical regions are most often affected.

Clinic – incubation period – 5-26 days (Wednesday 10-12 days). Forms: without damage to the NS (subclinus, abortive), with damage to the NS (non-paralytic poliomyelitis - meningeal form, paralytic poliomyelitis - spinal, bulbar, pontine and encephalitic forms). The onset is acute, T – 38–39, intoxication, catarrhal symptoms; m\b abdominal pain, gastrointestinal and vegetative disorders; pain appears in the legs, arms, spine, especially when trying to sit down. A forced position is a symptom of a tripod (support with your hands behind you when sitting). (+) Brudzinsky village, Lassegue; decreased reflexes, muscle spasms, tonic or clonic convulsions, movement disorders. a decrease in T, the appearance of paralysis (a paralytic period begins) - the lower extremities are affected (80%), less often the upper extremities, muscles of the trunk, abdomen, and neck; later – muscle atrophy, joint laxity, osteoporosis? recovery period (2 weeks)

Pontine form - damage to the trigeminal, facial and abducens nerves; bulbar – damage to the trunk and nuclei of the cranial nerves; inparant (without clinical manifestations, ? antibody titer); abortive - without paralysis; meningeal – clinic of serous meningitis.

Diagnosis - the presence of flaccid paralysis after fever, virological examination (nasopharyngeal lavages, blood, feces, cerebrospinal fluid), serology - the method of paired sera (titer increase 4 times). Lumbar puncture: cell-protein dissociation in the first 5 days, and pronounced protein-cell dissociation on days 10-14.

Differential diagnosis - polyradiculoneuritis, myelitis, congenital myotonia, neuritis of the facial nerve of another etiology, serous meningitis with Coxsackie and ECNO.

Treatment: Bed rest, β-globulin (0.5 ml/kg for 2-3 days), diuretics, lumbar puncture, analgesics, bromides; from 3-4 weeks - prozerin 0.0005-0.001 2 times a day, dibazol 0.001-0.005 per day; galantamine up to 20-30 days. + physiotherapy, massage, gymnastics, orthopedic treatment.

Prevention – isolation for up to 21 days from the onset of the disease, contact – quarantine for 20 days; vaccination – Sebin live attenuated polio vaccine from 3 months, 3 times at monthly intervals simultaneously with DPT vaccination. Revaccination – once at 2, 3, 6 and 14 years of life.

Flu

Acute infection with damage to the mucous membranes of the upper respiratory tract, intoxication and fever.

Etiology – orthomyxovirus A, B, C strains. Antigens: hemagglutinin, neuroamindase.

Epid – a tendency to epidemics and pandemics, type-specific immunity to circulating strains of the virus. During epidemics - variability of the virus, a new variant - increased susceptibility of the population; source of infection – patient, contagious from the first hours of illness, max – 2-3 days; transmission mechanism – airborne. In children under 6 months of age, immunity comes from the mother.

Pathogenesis – epitheliotropy – reproduction in the epithelium of the upper respiratory tract, formation of autoantigens – autoimmune cytotoxic reactions. From the site of primary localization - entry into the blood, viremia, general cytotoxic effect, mainly aimed at the central nervous system, damage to precapillaries and capillaries; development of hemodynamic disorders. In the central nervous system – encephalopathy, in the lungs – hemorrhagic edema. General toxic effect - inhibition of cellular and humoral immunity, activation of infection. Allergic and autoallergic reactions are possible.

Clinic: incubation period – hours, 1-2 days; chills, increased T to 38-40, muscle pain. Typical forms are catarrhal, subtoxic, toxic, toxic-catarrhal; atypical – erased, hypertoxic, fulminant; options - croup syndrome, asthmatic syndrome, primary lung disease, segmental lung disease, cerebral syndrome, abdominal, hemorrhagic syndrome. The severity of the pull is light, moderate, heavy. Typical clinical picture – general intoxication + catarrhal symptoms of the upper respiratory tract; fever, general weakness, headache, pain in the eyeballs, muscles, photophobia, sweating, sleep disturbance. Up to 38? - mild course, 39 and more - severe. Rhinitis, laryngitis, tracheitis. After 2-3 days - decrease in T, improvement in general condition.

Complications - purulent laryngotracheobronchitis, focal or segmental pneumonia, meningitis, meningoencephalitis, encephalitis, neuralgia, neuritis, polyradiculoneuritis, cardiac dysfunction (myocarditis).

Features of the course in children of different ages - in newborns - a gradual onset, erased clinical picture, pallor, breast refusal, weight loss, vomiting, often complications; 1-3 years - especially severe, intoxication, central nervous system damage, meningoencephalitic syndrome, catarrhal symptoms - mild, often lung damage, croup syndrome, asthmatic syndrome.

Diagnostics – clinic, epidemiological history; virus isolation - rinsing from the nasopharynx; serologically (RTGA – titer increases 4 times in dynamics).

Differential diagnosis – typhoid fever, typhus, psittacosis, measles, enterovirus infections, intestinal infections, infiltrative form of tuberculosis.

Treatment – ​​fasting regimen, etiotropic: rimantadine (influenza A) – 50 mg 3 times a day; anti-influenza immunoglobulin - up to 2 years - 1 ml, 3-6 years - 2 ml, after 6 - 3 ml; leukocyte interferon – 5 drops intranasally every 2-3 hours for 5 days. Warm drink, Vit, ascorutin. When an infection occurs, antibiotics are used.

Emergency help for hyperthermia and convulsions syndrome - paracetamol 0.01/kg, physical cooling of the body; if there is no effect, use lytic mixtures.

Parahippus

Acute respiratory tract obstruction, moderate intoxication, symptoms of damage to the mucous membrane of the upper respiratory tract.

Etiol – Paramyxavirus. Antigens – hemagglutinin, neuraminidase. Stability of antigenic structure.

Epidemic – the greatest concern in children under 2 years of age, depends on the time of year, the level of concern for influenza and other acute respiratory viral infections. Source of information – patient. Isolation of the virus occurs during the acute period of the disease (7-10 days). The route of transmission is airborne.

Pathogenesis – contact with the mucous membranes of the upper respiratory tract, penetration into the epithelium – destruction of the epithelium, accumulation of mucous exudate, swelling; viremia, general toxic effect. Sensitization by viral antigens, addition of infection. In the central nervous system – encephalopathy, in the lungs – hemorrhagic edema. General toxic effect - inhibition of cellular and humoral immunity, activation of infection. Allergic and autoallergic reactions are possible. Vascular and microcirculatory disorders are minor, the larynx suffers more.

Clinic – incubation period – 2-7 days – increased T, minor intoxication and catarrhal symptoms; weakness, disturbances of appetite, sleep, headache; increase in catarrhal symptoms - persistent loud dry cough, sore throat, runny nose, Krupp syndrome. Severity – light, medium, heavy. T – max up to 3 days, cough, runny nose – up to 7-10 days.

Clinic of stenosing laryngotracheitis - in the midst of complete health, more often at night the child wakes up from a loud cough + hoarseness of voice, noisy breathing.

Diagnostics – epidemiological + clinic + serology – RSK, RPGA, RN (titre increase 4 times)

Treatment: symptomatic at home, hospitalization for croup syndrome and severe complications.

Adenovirus infection

Acute respiratory disease caused by adenoviruses, severe intoxication, damage to the mucous membranes of the upper respiratory tract, conjunctiva, sclera and lymphoid tissue

Etiol – DNA-containing viruses, antigens: A – group-specific, B – carrier of toxic properties, C – type-specific.

Epidemic – Source of the disease – patients + carriers, virus release – in the first 2 weeks of the disease; transmission mechanism – airborne, possibly alimentary. Children of the first months of life have passive transplacental immunity. After suffering from a disease - active immunity.

Pathogenesis – entrance gate – URT, conjunctiva, intestine. Reproduction in the epithelium - viremia - damage to the nasal mucosa, back of the throat, tonsils, regional lymph nodes. Inflammation is accompanied by a pronounced exudative component, possibly penetrating into the lungs, developing pneumonia and bronchitis.

Clinic - incubation period - 2-12 days, the onset is acute, the symptoms appear sequentially: first - increased T, catarrhal symptoms, lethargy, loss of appetite, headache? significant serous nasal discharge? mucopurulent. The nasal mucosa is hyperemic, nasal breathing is difficult. Characteristic lesion of the mucous membrane of the back wall of the throat (granular pharyngitis). Often accompanied by a wet cough; typical damage to the mucous membrane of the eyes - conjunctivitis can be catarrhal, follicular, membranous. Possible intestinal disorders in young children.

Wedge shape: according to the main syndrome: catarrh of the upper respiratory tract, nasopharyngoconjunctival fever, conjunctivitis and keratoconjunctivitis, membranous conjunctivitis, pneumonia; by additional syndrome: croup syndrome, asthmatic syndrome, diarrhea syndrome, lymphadenopathy, exanthema syndrome; flow form: light, moderate, heavy.

Diagnostics: wedge + epid, serology: RSK, RPGA (titre increase 4 times in paired sera). Express diagnostics – fluorescent antibody method.

Treatment - at home, hospitalization - for young children with severe forms and complications. Treatment is symptomatic - desensitizing drugs, multivitamins, 0.05% deoxyribonuclease solution, 3-4 drops every 3 hours for 2-3 days.

Respiratory syncytial + rhinovirus

RS-inf – acute viral illness, accompanied by moderately severe symptoms of intoxication, predominance of damage to the upper respiratory tract, frequent development of bronchiolitis.

Etiol is an RNA-containing paramyxovirus. 2 serovars that share a common complement-binding antigen.

Epid is a source of inf – patients, rarely – virus carriers. Isolation of the virus within 10-14 days by airborne droplets. The highest susceptibility is in children from 4-5 months to 3 years, immunity is unstable and specific.

Pathogenesis – damage to the epithelium of the upper respiratory tract (in young children and urinary respiratory tract – the pathological process quickly spreads to small bronchi and bronchioles)? epithelial hyperplasia, hypersecretion, blockage of the bronchi with thick viscous mucus? violation of the drainage function of the bronchi, development of microatelectasis, impaired oxygen metabolism, oxygen starvation, shortness of breath, tachycardia, addition of tank inf.

Clinic – incubation period 4 days. Symptoms of damage to the upper and lower respiratory tract. The severity depends on the age of the patient, the state of the body's reactivity at the time of injury, and the primary or secondary encounter with the virus.

Wedge-shaped, different age groups: older age – the course is mild, like acute catarrh of the upper respiratory tract, often without an increase in T or low-grade fever, the main symptom is a dry persistent cough; duration – 2-3 weeks; children of the first year - acute onset, elevated T, dry cough, nasal congestion, pallor, hyperemia of the mucous membranes of the anterior arches, the back wall of the throat? the addition of bronchiolitis: paroxysmal prolonged cough, at the end of the attack - thick, viscous sputum. In severe cases, respiratory failure occurs.

Diagnostics – clinic + epidemiology

Treatment - home conditions, symptomatic, for obstructive syndrome - aminophylline with diphenhydramine, other antihistamines, expectorants.

Rhinovirus – acute infection of the respiratory tract with predominant damage to the mucous membrane of the nasal cavity and nasopharynx.

Etiol – RNA-containing picornavirus

Epid is a source of information – patients, virus carriers. Isolation of the virus within 5 days by airborne droplets. The least susceptibility is in children under 6 months due to passive transplacental immunity; immunity is unstable and specific.

Pathogenesis – entrance gate – nasal mucosa? reproduction? swelling of the mucous membrane + hypersecretion, addition of a tank infection

Clinic – incubus lane – 1-5 days, acute onset: malaise, low-grade fever, nasal congestion, coughing, body aches? excessive watery mucus discharge from the nose? on days 2-3 – mucopurulent discharge (add tank inf). The illness lasts 5-7 days.

Wedge shapes of different age groups: in newborns - according to the type of catarrh of the upper respiratory tract, in children of younger age - tracheobronitis is more common, in older children - a milder course of the type of catarrh of the nasopharynx.

Diagnostics – clinic + epidemic, laboratory – virus isolation on tissue culture; express diagnostics – immunofluorescence method.

Treatment is symptomatic, vasoconstrictors in the nose, warm plenty of fluids, hot foot baths. On the first day - leukocyte interferon intranasally.

Viral hepatitis

Viral hepatitis is a group of anthroponotic viral diseases with different mechanisms of transmission and characteristics of pathogenesis, united by the hepatotropic nature of the pathogens and the resulting similarity of clinical manifestations (jaundice, intoxication, hepatosplenomegaly).

Etiology: Currently, the existence of seven viruses belonging to different groups has already been proven, which are the causative agents of the same viral hepatitis (VH): hepatitis A virus (HAV), the causative agent of viral hepatitis A (HAV), hepatitis B virus (HBV), the causative agent of HBV, hepatitis virus C (HCV) is the causative agent of HCV, hepatitis D virus (delta virus HDV) is the causative agent of HDV, hepatitis E virus (HEV) is the causative agent of HEV, hepatitis F virus (HFV) is the causative agent of BHF, hepatitis G virus (HGV) is the causative agent of BGG.

Peculiarities

Hepatitis A

Hepatitis B

Hepatitis C

Hepatitis D

Hepatitis E

Preferential transmission mechanism

fecal-oral

parenteral, sexual, vertical

parenteral

parenteral

fecal-oral

Transfer factor

water, food

all human biological fluids

mostly blood

mostly blood

Features in different age groups

Mostly children and young people get sick; children 1 year old do not get sick due to placental immunity

Children aged 1 year are more likely to get sick; after 3 years, neglect decreases significantly (reduced parenteral manipulations)

Children aged 1 year are more likely to get sick; after 3 years, neglect decreases significantly (reduced parenteral manipulations)

The greatest - in young children and chronically ill patients. hep B

Children are not the dominant age group.

Spreading

ubiquitous

ubiquitous

ubiquitous

everywhere, but mostly Asia

Previously – Asia, Africa; Now – in Europe there are not only imported cases

Maximum infectiousness

as long as there is viral RNA

all the time while there is HBsAg and, especially, HBeAg

the last days of the incubation period and the first days of the pre-icteric period

Seasonality

summer autumn

all year round

all year round

all year round

summer autumn

Carriage

Chronization

Pathogenesis: The main pathogenetic features of VH are caused by dysfunction of hepatocytes, the main target of viruses. The mechanism of damage to hepatocytes is different in cases of hepatitis of various etiologies. With HAV, there is a direct impact of the virus that has penetrated the cell, and the multiplication of the virus leads to its death. In cases of HBV, the main role belongs to immune reactions: immune cytolysis with the participation of killer T-lymphocytes, subsequently antibody-dependent immune cytolysis, autoimmune reactions. With HCV, many mechanisms are similar to those with HBV, but HCV, unlike HBV, is capable of causing a cytopathogenic effect itself, like HAV. In addition, the role of autoimmune reactions is great, but antibody-dependent immune cytolysis is less pronounced. The hepatitis D virus has a direct cytopathogenic effect, immune inflammation is mild, which explains the lack of effect from the use of immunosuppressive drugs. With HEV, as with HAV, the direct cytopathogenic effect of the virus on the cell predominates, but cholestasis and glandular transformation of cells are more common.

CAA – acute inf., characterized by minor manifestations of intoxication, liver dysfunction and a benign prognosis.

Classification wedge of forms: typical (mild, moderate and severe forms), atypical (anicteric, erased, subclinical).

Clinic: incubator lane – 10-45 days – no wedge manifestations; prodromal (pre-icteric period - 3-5 days) - acute onset, T - 38-39, weakness, headache, nausea, vomiting, malaise, minor catarrhal symptoms, possible dyspeptic disorders? disappearance of symptoms of intoxication after 1-2 days, do anorexia, nausea, enlarged liver, its sensitivity, pain remain? the appearance of yellowness of the skin, sclera, mucous membranes, acholia of stool, darkening of urine. Jaundice period - the appearance of jaundice - improvement in general well-being, disappearance of intoxication; duration 10-12 days, enlargement of the liver, spleen, dysfunction of the cardiovascular system (bradycardia, decreased blood pressure, weakened heart sounds, significant HD disturbances. - decline in clinical manifestations - improved appetite, increased diuresis, lightening of the skin, shrinkage of the liver (up to 40 days or more Period of convalescence - no complaints, health is good, the functional state of the liver is restored; astheno-vegetative disorders are possible (2-3 months).

Diagnostics: epidemiological history + clinic, laboratory: increase in ALT, AST, increase in bilirubin with a predominance of direct bilirubin, increase in thymol test. Specific methods: determination of HAV in feces, the presence of growth of antiviral antibodies and antibodies against the IgM class virus antigen.

Treatment: diet No. 5, vitamins, choleretic drugs at the end of acholia, in severe cases - detoxification therapy, essential.

Prevention: discharge on 21 days from the onset of jaundice in the absence of symptoms of intoxication, liver shrinkage, normal levels of bilirubin, enzymes. Dispatch observation – 6 months. Contacts - observation for 35 days, in children's institutions - quarantine for 35 days.

Viral hepatitis in children of the first year.

Etiology: Most often caused by HBV (HCV, HDV), which is transmitted parenterally during various manipulations. Sometimes vertical transmission of infection is possible (infection of a fetus or newborn by a mother who is sick or a virus carrier).

Pathogenesis: In cases of HBV, the main role is played by immune reactions: immune cytolysis with the participation of killer T-lymphocytes, subsequently antibody-dependent immune cytolysis, autoimmune reactions. With HCV, many mechanisms are similar to those with HBV, but HCV, unlike HBV, is capable of causing a cytopathogenic effect itself, like HAV. In addition, the role of autoimmune reactions is great, but antibody-dependent immune cytolysis is less pronounced. The hepatitis D virus has a direct cytopathogenic effect, immune inflammation is mild, which explains the lack of effect from the use of immunosuppressive drugs.

Clinic: Incub. period 60-180 days (usually 70-90). The initial period is 5-7 days. Phenomena of general intoxication, loss of appetite, increased body temperature, loss of body weight, lethargy.

With the onset of jaundice, the symptoms of intoxication intensify, jaundice increases gradually over 5-7 days. At the same time, the liver enlarges and thickens, the abdomen is moderately swollen, the stool is acholic, the urine is dark, and splenomegaly is possible. The intensity of jaundice may not correspond to the severity of the disease. The duration of the icteric period is 7-10 - 30-45 days. In the post-icteric period, as a rule, hepatosplenomegaly persists, scleral icterus, skin subicterus, ALT and AST activity decreases, and dysproteinemia persists. During convalescence, the functional state and morph are restored. liver structure.

A characteristic feature of HBV in 1-year-old children is the high frequency of severe and malignant (fulminant) forms and high mortality.

Diagnostics: wedge + epid. Lab.: increase in ALT, AST, bilirubin (due to the direct fraction). Increased in urine. urobilin, bile enzymes. Specifics: RPG, RPGA, ELISA, RIM - detection of HBV antigens (HBsAg, HBeAg), antibodies to them (antiHBs, antiHBe, antiHBc).

Indicators of a malignant form: neuropsychic disorders - hepatic encephalopathy (severe agitation with motor restlessness, hand tremors, clonic-tonic convulsions. Within 1-3 days - hepatic coma develops, jaundice increases significantly. Characteristic: bilirubin-enzyme dissociation (increase in bilirubin when enzyme activity decreases), this means prothrombin in the blood serum decreases, hemorrhagic manifestations appear, the size of the liver decreases, it becomes soft, often not palpable at all; a “liver odor” appears.

Outcomes: HBV in children often ends with recovery with complete restoration of the functional state and morphology of the liver structure; recovery with an anatomical defect (liver fibrosis) or the development of complications with paralysis of the biliary tract and gastroduodenal zone may be observed. HBV can result in the formation of CPG or CAG. In the fulminant form, the prognosis is difficult. Recovery is usually observed under the conditions of using complex intensive treatment in the precursor stage of hepatic coma.

Delta infection

HBV - acute or chronic liver damage associated with a defective virus without an envelope, the cat contains RNA and requires HBV for its existence

Etiol and epidemiological features: source of information - patients with HBV and carriers of HBsAg infected with HDV. Transmission through blood and drugs, transplacental transmission. Young children and patients with chronic hepatitis B are most susceptible

Clinic: there is a mixed form (acute HBV+IOP) - co-infection and chronic HBV and IOP-superinfection.

Co-infection: incubation period - 8-10 weeks, severe clinical manifestations of HBV with the development of hepatodystrophy, a protracted form with exacerbations and wavy progression.

Superinfection: incubator per – 3-4 weeks? deterioration of general condition, enlarged liver, appearance or intensification of jaundice, increased levels of bilirubin and enzymes. The progression of the disease is severe, chronic hepatitis and cirrhosis often develop.

Diagnosis: the appearance of an exacerbation in a patient with Chron HBV, circulating HBsAg, delta virus and delta antigen in the liver tissue, detection of anti-HBc specific antibodies to the delta virus.

Treatment: Hospitalization, interferon therapy?-interferon, glucocorticosteroid drugs in children of the first year of life in fulminant forms and precoma, coma + detoxification therapy, proteolysis inhibitors (trasylol, gordox, contrical), cocarboxylase, ATP, Vit C, Vicasol for hemorrhagic syndrome, heparin for DIC, soda for acidosis, gastric lavage, high siphon enemas; exchange blood transfusion, hemosorption, plasmaphoresis, hemodialysis, hyperbaric oxygenation, symptomatic treatment.

Prevention: Mandatory screening of donors for HBsAg; prohibition of blood transfusions and the use of blood products not labeled for HBsAg; transition to the use of disposable instruments.

Specific prof: the use of specific immunoglobulin with a high titer of anti-HBs antibodies for children born from mothers with HBV.

The purpose and task of immunoprophylaxis. The role and tasks of the doctor

The goal is to reduce morbidity and mortality caused by infectious diseases (poliomyelitis, diphtheria, tetanus, measles, mumps, rubella, tuberculosis, whooping cough, etc.), which can be prevented through immunization.

Tasks: maximum coverage of preventive vaccinations among the child population in order to increase immunity to infectious diseases through active immunization.

The clinic doctor performs:

1. systematic monitoring of persons with a complicated medical history, recommendations for their vaccination

2. takes part in the work of the vaccination commission of the clinic, which should include the head of the clinic and an immunologist, allergist and neurologist

3. conducting the first briefing regarding immunization issues for all medical workers who are enrolled to work in the clinic, kindergartens and schools in the clinic’s service area

4. organization and conduct of planned training regarding advanced training of medical workers of the clinic on the specifics of the profession, followed by taking the test

5. providing medical assistance in drawing up monthly plans for immunoprophylaxis at sites, kindergartens, schools

6. monitoring the work of nurse vaccinators in the clinic

7. in order to monitor the vaccination of children, periodically visit kindergartens and schools according to the schedule approved by the head physician

8. control of the formation of the vaccination card file

9. control of the completeness and quality of vaccinations for people at risk

10. conducting monthly and annual analysis of the implementation of the vaccination plan for each infection

11. participation in the study of the causes and analysis of all cases of post-vaccination complications

12. Drawing up a vaccination plan for the year for the clinic

13. compiling a report on preventive vaccinations for the quarter, half-year and year (F No. 5)

14. Control of the use and storage of vaccine-serum preparations

15. Carrying out health education work among the population

Vaccination calendar:

1. Against tuberculosis: Vacc – 3-5 days of life; revak: 1st - 7 years old, 2nd - 14 years old (children with (-) Mantoux district)

2. Against polio: Vac – 3 months three times with an interval of 1 month; revak – 18 months, 3 years, 6 years and 14 years

3. Against whooping cough, diphtheria, tetanus: Vac – 3 months three times with an interval of 1 month; revak – 18 months

4. Against diphtheria, tetanus: Revak – 6, 11, 14, 17 years

5. Against measles: Vak: 12 months, revak – 6 years

6. Against mumps: Vac 12 months

7. Against rubella: Vak 12 months, Revak – 15-16 years (girls)

8. Against hepatitis B: Vac: 1, 2, 7 months.

Activities based on maximum coverage:

Clear cooperation between pediatric and epidemiological services;

Full-fledged work in the family

Characteristics of vaccine preparations (against diphtheria, tetanus, whooping cough, polio, measles, mumps). The normal course of the post-vaccination period and possible pathological post-vaccination reactions, their prevention and treatment.

Whooping cough, diphtheria, tetanus: the following drugs are used:

1. Adsorbed pertussis-diphtheria-tetanus vaccine (DTP) - is a homogeneous suspension of phase I pertussis microbes killed with sodium merthiolate, purified and concentrated diphtheria and tetanus toxoids, adsorbed on aluminum hydroxide gel. 1 ml of vaccine contains 20 billion pertussis microbial bodies, 30 fluctuating units of diphtheria and 10 binding units of tetanus toxoid.

2. Adsorbed diphtheria-tetanus toxoid (ADT) - a mixture of purified and concentrated diphtheria and tetanus toxoids adsorbed on aluminum hydroxide gel. The drug contains in 1 ml 60 fluctuating units of diphtheria and 20 binding units of tetanus toxoid.

3. Adsorbed diphtheria-tetanus toxoid with reduced antigen content (ADS-M) - a mixture of purified and concentrated diphtheria and tetanus toxoids adsorbed on aluminum hydroxide gel. The drug contains in 1 ml 10 fluctuating units of diphtheria and 10 binding units of tetanus toxoid.

4. Adsorbed diphtheria toxoid with reduced antigen content (AD-M) - purified, concentrated diphtheria toxoid adsorbed on aluminum hydroxide gel. The drug contains 20 fluctuating units of diphtheria toxoid per 1 ml.

5. AP-toxoid – purified, concentrated tetanus toxoid, adsorbed on aluminum hydroxide gel. The drug contains 20 toxoid binding units per ml.

The preparations are a uniformly turbid whitish liquid, which, after settling, separates into a clear liquid and a loose sediment, which completely breaks up when shaken.

Vaccination - at 3 months. DTP vaccine. The vaccination course is 3 intramuscular injections of 0.5 ml with an interval of 30 days. Revak. – at 18 months. At 6 years old revak. – ADP-anatoxin, at 11, 14 and 18 years old – revak. ADP-M-anatoxin. Interval between vaccines and 1st revak. - Not< 12 мес. и не >2 years.

Reactions to administration: local (hyperemia of the skin, swelling of soft tissues or slight infiltration at the injection site), general (increased body temperature without deterioration of the general condition).

Complications:

1. Allergic: Quincke's edema, urticaria-type rash, exacerbation of allergic diseases; rarely reactions such as anaphylactic shock.

2. Collapse.

3. Encephalopathy: impaired brain function, intracerebral pressure, impaired consciousness, convulsions, pathological reflexes, paresis of the limbs, encephalitis.

4. Residual condition: the occurrence of seizures at t?<39?C, если они отсутствовали в анамнезе и проявились в течении года после вакцинации. Острый нефрит, миокардит, серозный менингит (очень редко).

5. Sudden death.

6. Exacerbation (or first manifestations) of chronic diseases and revival of latent infection (provoking role of vaccination).

Poliomyelitis: a vaccine is used, which is a trivalent preparation of attenuated strains of Sebin poliovirus types I, II, III, obtained on a primary kidney culture of African green monkeys; intended for oral use.

The vaccine is a transparent liquid of a reddish-orange color, without sediment or foreign impurities, available in bottles of 2 ml (10 doses) and 5 ml (25 or 50 doses). The ratio of virus types in the vaccine dose is 71.4% (I), 7.2% (II), 21.4% (III).

Vaccination begins at 3 months, carried out three times with an interval of 1 month (not > 6 months). Revaccination – at 18 months, 3, 6 and 14 years. Between vaccination and revaccination - no< 6 мес.

Vaccination is carried out on the same day as vaccination with DTP vaccine (ADS or ADS-M toxoid).

There is practically no provision for the introduction of N. In young children, there may be an increase in bowel movements without affecting the general condition.

Complications: urticaria-type rash, angioedema, vaccine-associated poliomyelitis.

Measles: Live measles vaccine strain L-16 is used for active immunization against measles. The vaccine is produced in a lyophilized state, has a yellowish-pink color, and before use it is diluted with the solvent that is included. Each dose = 0.5 ml, administered subcutaneously.

Vaccination at 12 months. and 6 years old. At the same time, the interval between the administration of measles vaccine and vaccination against polio, whooping cough, diphtheria and tetanus is not< 2 мес.

Ration for administration: B N (-). Some children have fever, mild hyperemia of the oropharynx, rhinitis, mild cough, conjunctivitis, and measles-type rash.

Complications:

1. Allergic: polymorphic rash, Quincke's edema, arthralgia; systemic like anaphylactic shock.

2. Encephalopathy: impaired brain function, intracerebral pressure, impaired consciousness, convulsions, encephalitis.

3. Toxic disorders: t?>38.6?C, manifestations of intoxication, catarrhal symptoms, rash, acute myocarditis.

Mumps: Live cultured mumps vaccine obtained by cultivating the attenuated mumps virus strain L-3. Available in the form of a lyophilized preparation of yellow-pink or pink color. It is administered subcutaneously in a dose of 0.5 ml. Routine immunization at 12 months of age.

Ration for administration: in N (-). Some children have t? r-tions, catarrhal manifestations from the nasopharynx. In rare cases - a slight increase in the parotid salivary glands in the absence of a violation of the general condition, slight hyperemia of the skin, mild swelling.

Complications:

1. Allergic: urticaria-type rash, Quincke's edema.

2. Encephalopathy: impaired consciousness, convulsions.

3. Toxic disorders: t?>38.6?C, vomiting, abdominal pain, serous meningitis against the background of increased t?.

Prevention of post-vaccination complications:

Strict adherence to the rules of vaccination provided for by current orders and instructions;

Individual approach to everyone who is vaccinated (familiarization with medical history, heredity, dynamics of physical and mental development, previous diseases, characteristics of reactions to previous vaccinations, the presence of sensitization to certain antigens);

Do not immunize immediately before admitting a child to a preschool institution;

Monitoring children in the post-vaccination period;

Protect children in the post-vaccination period (up to 1 month) from communicating with infected persons, hypothermia, overheating, heavy physical and mental stress.

Treatment of post-vaccination complications: depending on the manifestations.

Methods for examining children with tuberculosis

Tuberculin diagnostics plays a leading role in examining children.

Tuberculin diagnostics is a biological test based on the properties of tuberculin to cause delayed-type inflammatory reactions in the body of a sensitized person, which manifest themselves quantitatively and qualitatively. Tuberculin was proposed by Koch - it is a bioactive substance that contains MBT antigens, particles of destroyed MBT, endo and exogenous antigens, waste products of MBT. Test tube: Mantoux test (0.2 ml of tuberculin intracutaneously into the anterior surface of the forearm - 2 TO; carried out to study the infection of the population and select a contingent for vaccination; turn - a statistically significant change in the test, is recorded if: a hyperergic test appears for the first time, a positive test has passed into hyperergic, the size of the papule increased by 6 mm or more, the negative test turned positive).

If there is a bend or a hyperergic reaction, an X-ray examination of the chest organs is performed.

1. Laboratory: bacterioscopy, with flotation method, fluorescent microscopy, bacteriological (inoculation on Lowenstein-Jensen medium, growth after 24-30 days), biological

2. Other general clinical methods

Organization and conduct of tuberculin diagnostics

Children and adolescents undergo tuberculin diagnostics using the Mantoux test once a year. Technique: into the anterior surface of the forearm, 0.2 ml of tuberculin intracutaneously - 2 TO;

Conducted to study the infection rate of the population and select the population for vaccination; turn - a statistically significant change in the test, is recorded if: a hyperergic test appears for the first time, a positive test turns into a hyperergic test, the size of the papule increases by 6 mm, a negative test turns into a positive one).

Evaluation of Mantoux test results

Negative: if there is no reaction, a pinpoint injection;

Doubtful: hyperemia of any size, infiltrate up to 5 mm;

Positive: papule more than 5 mm (pronounced immunity);

Hyperergic: in adolescents more than 17 mm papule

Differential diagnostics of immune tubes

Signs

Post-vaccination

Infectious

Period of appearance of max (+) test after vaccination

1 year after Mantoux test with 2 TOs

Later dates

Infiltrate dimensions

12 or more, hyperergic reaction (17 or more)

Result of previous Mantoux tests

same or larger diameter

smaller diameter

Time of disappearance of the papule

1 month followed by pigmentation

Dynamics of sample tubes

weakening up to 4-5 years, at 6-7 years – negative

papules increase over time, turn

Nature of the infiltrate

fuzzy

clear, persistent

Symptoms of intoxication

Contact with a person with tuberculosis

Burdened heredity

Post-vaccination scar

weakly expressed

Tube intoxication in children and adolescents

TI is the only form of childhood tuberculosis with an unknown localization, characterized by the presence of a symptom complex of intoxication of the body without detecting local forms of tuberculosis in it during the period of change in tuberculin sensitivity and often paraspecific reactions. There are early (before 10 months) and chronic (after 10 months)

Clinic – changes in the child’s behavior (loss of cheerfulness and mobility - becomes capricious, irritable, gets tired quickly, loses the ability to concentrate), increased T to 37.1-37.5, poor appetite, micropolyadenopathy. Paraspecific reactions: general (febrile-septic syndrome) and local (syndromes: serositis, rheumatoid, neurological, cardiac, abdominal). There is erythema nodosum, moderate hyperemia of the mucous membranes of the pharynx and nose, runny nose, cough, arthralgia, phlyctenular keratoconjunctivitis, blepharitis

Differential diagnosis: helminthic infestation, chronic tonsillitis, chronic otitis, rheumatic carditis, chronic inflammation of the biliary tract.

Treatment: Gentle regimen. Hale-strengthening. Isoniazid 10-15 mg/kg once a day for 3-4 months. until the symptoms of intoxication disappear permanently.

Enterobiasis. Enterobiasis is a chronic invasion, accompanied by intestinal disorders and perianal itching. Etiology: pinworm (Enterobius vermicularis). Routes of infection: from humans (dirty hands, bed linen, and other objects contaminated with eggs) Clinic: itching of the anus for 1-2 days, then disappears and appears within 2-3 weeks, can be permanent. + possible dyspepsia. Diagnosis: scraping from the perianal folds followed by microscopy, three times with an interval of 3-5 days. Treatment: sanitary hygiene measures (washing at night with soap, boiling laundry, monitoring the cleanliness of hands and nails). Preparations - vermox 0.1 g 2 times / day. for 3-4 days with meals (children 2-10 years old, 0.05 g). Control every 3-4 weeks.

Ascariasis. Ascariasis is a chronic helminthiasis, characterized by the presence of an allergic syndrome in the initial stage of the disease and an abdominal syndrome in the later stage. The causative agent is Ascaris Lumbricoides. Ways of entry of roundworm eggs from the soil - with contaminated vegetables, hands, water, etc., seasonality from April to October. Phases of the pathogenesis of ascariasis: early migratory and late intestinal. Clinic: the early stage has a gradual course, lasting 2-3 days. after infection - weakness, low-grade fever, then - pulmonary syndrome (cough with sputum, over the lungs - shortening of the percussion tone, dry and moist rales, x-ray - migrating infiltrates). Chronic intestinal phase - gastrointestinal and neurological (headache, restless sleep, memory loss) syndromes. The full cycle of roundworm ripening is 75-90 days, lives in the intestines for about a year, then is removed on its own. Treatment: intestinal stage - decaris (50 mg for children from 10 to 20 kg, 75 mg - from 20 to 30, 1.5 hours after a light dinner), or pyrantel once 10 mg/kg, vermox (2.5-5 mg /kg 3 days h/h after meals). The effectiveness of treatment is 2-3 weeks. 3-time stool examination.

Trichocephalosis in children. Chronic helminthiasis with extensive damage to the function of the digestive tract. The causative agent is the whipworm (Trichocephalus trichiuris) - a geohelminth. The source of infection is a person who excretes eggs in feces. Infection through the mouth through consumption of contaminated vegetables, fruits, and water. Pathogenesis: in the intestine, larvae are formed from eggs, which are fixed to the intestinal mucosa, especially in the ileocecal corner. Tumor-like formations are formed, erosions of the mucous membrane, viscero-visceral reflexes from the mucous membrane of the ileocecal angle contribute to the disruption of the secretory and motor functions of the gastrointestinal tract. Clinic: nausea, loss of appetite, drooling, periodic abdominal pain. Possible appendicular colic or hemocolitis with frequent bloody bowel movements, anemia, eosinophilia. Treatment: Vermox (2.5-5 mg/kg 3 days 1 hour after meals). Control ovoscopy every 3-4 weeks, three times.

Primary tuberculosis complex

PTCL is one of the local forms of primary tuberculosis. Characterized by specific inflammation in the lung tissue (pulmonary component - pneumonitis), regional intrathoracic lymph nodes (lymphoglandular component - lymphadenitis), blood vessels (lymphovascular component - lymphangitis), usually during the period of the turn of tuberculin and paraspecific reactions.

Clinic: localization of the pulmonary component - most often in 1, 2, 4, 5 and rarely 6,7 segments of the lungs. X-ray (4 stages):

1. pneumonia - intense lesions in the lungs, merging with the shadow of the root. The latter is expanded, it contains the contours of enlarged lymph nodes. Max wedge symptoms

2. resorption - the size of the shading begins to decrease, a symptom of bipolarity appears (the pulmonary and glandular components of PTCL and the linear shadow of lymphangitis are clearly defined, which combines them - Redeker's symptom)

3. Inlay, organization and sealing

4. petrification – wedge, there are no symptoms of tuberculosis

Differential diagnosis: pneumonia, eosinophilic infiltrate, primary lung cancer

Treatment: 3 or more drugs (isoniazid + rifampicin + streptomycin (ethambutol) and/or pyrazinamide). After signs of intoxication disappear, streptomycin is discontinued.

Tuberculosis of the intrathoracic lymph nodes.

TVGLU is one of the most common clinical forms of primary tuberculosis with damage to the intrathoracic lymph nodes, which is localized in the mediastinum, the root of the lung and parietal.

Clinic (options):

1. inoperceptively (asymptomatic) – the diagnosis is determined after identifying the variation of the mAntu reaction and after an x-ray examination.

2. if there are signs of intoxication and an X-ray (tomo)gram reveals enlarged lymph nodes of the root of the lung and/or mediastinum.

3. when intoxication and bronchopulmonary syndrome are combined, the cat manifests itself with a cough. Also divided depending on the severity of inflammatory and necrotic changes

Infiltrative

Tumor-like

Differential diagnosis: sarcoidosis, lymphagranulomatosis, central lung cancer, lymphosarcoma, lymphocytic leukemia

Treatment: 3 drugs for 3-6 months, then 2 drugs for 12 months + nonspecific therapy. For tumor-like variants, chemotherapy is less effective; surgical treatment

Myloliary tuberculosis

MT is a bilaterally symmetrical total lesion of the lungs and other organs by small foci with a sharply reduced body resistance.

Clinics (syndromes)

1. Pulmonary dissemination

2. Intoxication syndrome

3. Breathing failure

Main symptoms: intoxication, shortness of breath, bronchopulmonary, signs of damage to other organs. Conventionally divided according to the wedge flow: pulmonary, typhoid, meningeal, septic.

Diff. diagnostics: heart disease, pulmonary carcinomatosis, focal pneumonia, Goodpasture's syndrome, idiopathic fibrosing alveolitis, lung damage in cystic fibrosis, pulmonary toxoplasmosis.

Treatment: 3 drugs for 3-6 months, then 2 drugs for 12 months + nonspecific therapy.

Tuberculous meningitis

TM – damage to the meninges tuba. infection, more often with milliary tuberculosis.

Clinical and morphological:

Basilar diffuse meningitis

Cerebral meningoencephalitis

Serous meningitis

Clinic: severe headache, nausea, vomiting, hyperesthesia, may be intestinal paresis, urinary retention or involuntary urination. Consciousness gradually darkens. A typical pose is that the knees are brought to the stomach, the head is thrown back. (+) meningeal signs. An altered vascular reaction is characteristic - the temporary appearance of large red spots on the face and torso (Trousseau spots), red persistent dermographism. Confirmation of the diagnosis - lumbar puncture (increased pressure, during the study - pleocytosis, increased protein to 1-2 g/l, cell-protein dissociation, decreased glucose to 0.6-1.1 mmol/l, decreased chlorides).

Diff. diagnosis: with meningitis of another etiology.

Treatment: isoniazid, rifampicin, ethambutol, streptomycin. If the patient is unconscious or the condition worsens, then + daily subarachnoid 0.1 calcium chloride streptomycin, with a sluggish course - prednisolone. To reduce headaches - chloral hydrate in enemas (0.5 per 20 ml of water) or analgin 0.3.

Tuberculous pleurisy.

Damage to the pleura, developing as a form itself or as a complication or as a manifestation of polyserositis and characterized by a wedge picture caused by exudation into the chest cavity (or lack thereof)

1. Fibrinous: pain in the chest, dry cough, low-grade fever, slight weakness, pleural friction noise

2. Exudative – pain in the chest, shortness of breath, which increases with the accumulation of exudate; physically – dullness of percussion sound over the lower parts of the lung, weakening of breathing; Elissa – Damoise – Sokolov line – upper limit of effusion

Confirmation of the diagnosis - detection of MBT in sputum or pleural exudate + histologically by pleural biopsy.

Differential diagnosis: pleurisy of other etiology

Treatment: 3 drugs - for 3-6 months, then 2 drugs for 12 months + nonspecific therapy, surgical - pleural puncture, according to indications - pleurectomy, decortication

Complications of tuberculosis in children that require emergency medical care.

Hemoptysis and pulmonary hemorrhages: occur mainly in destructive forms of tuberculosis, bronchiectasis, and hilar sclerosis. Especially common in patients with pulmonary cirrhosis. They arise due to the rupture of a vessel in the cavern wall (with cavernous TBC), the sweating of red blood cells through the vessel wall, and damage to the granulation tissue. The main cause is pathological changes in the wall of blood vessels or their rupture.

They are divided according to intensity:

Hemoptysis - blood is coughed up in separate spits or mixed with sputum; there may be streaks of blood in the sputum and blood clots.

Bleeding - the patient coughs up 40-60 ml of blood at a time.

Hemorrhage – due to the rupture of a large vessel, there may be large bleeding.

Pulmonary hemorrhages often result in death from asphyxia due to the filling of the bronchi and trachea with blood clots.

The main sign of pulmonary bleeding or hemoptysis, in contrast to nasal, laryngeal, gastric or esophageal, are pathological destructive changes in the lungs. Blood from the lungs is released during coughing, foamy, bright red.

The localization of the bleeding site is established on the basis of anamnesis, auscultation, percussion, and Ro examination data.

Treatment: max physical. and psycho. calmness, semi-sitting position in bed; decrease in pressure in the pulmonary circulation - intravenous euphilin (10 ml of 2.4% solution), papaverine (1-2 ml of 2% solution), atropine (1 ml of 0.1% solution); hemostatic therapy - vikasol, aminocaproic acid, contrical (10,000-20,000 units), fibrinogen (1-4 g in the form of 0.3% solution), calcium gluconate (10 ml of 10% solution) or chloride intravenous calcium (10 ml of 10% solution); ascorbic acid (0.1 3-5 r/day).

If conservative treatment is ineffective, artificial pneumothorax is used; if it is ineffective, surgical treatment is required.

Spontaneous pneumothorax: most often occurs due to rupture of a bullous-emphysematous lung in cases of fibrous focal, chronic hematogenously disseminated TBC or lung cyst; rarely occurs due to a breakthrough of the cavity into the pleural cavity. The clinical picture depends on the size of the free pleural cavity, the nature of the pneumothorax (closed, open, valvular), characterized by the development of acute respiratory failure - pain in the affected half of the chest, shortness of breath, coughing; objectively – significant cyanosis, tachycardia, tympanitis, decreased breathing on the side of spontaneous pneumothorax. Confirmation of diagnosis – Ro.

Treatment: Half-sitting position, administration of morphine or omnopon to reduce pain and suppress the cough reflex; Prescribe 2 ml of 10% sulfocamphocaine solution subcutaneously, oxygen therapy. In severe cases, puncture of the pleural cavity followed by aspiration of gas until negative pressure is established (Bülau drainage).

Respiratory tuberculosis in adolescents.

Primary tbc complex. Includes the primary focus of specific inflammation in the lung tissue (Gon's focus) and inflammation in the regional lymph node, interconnected by lymphangitis ("path"). It forms in childhood and adolescence in 98% of people, sometimes completely asymptomatic. In the center of the inflammation in the lung, as well as in the corresponding lymph node, tissue caseosis is formed and, as an allergic reaction, perifocal nonspecific inflammation is formed.

Clinic: severe symptoms of intoxication (febrile t?, alternating with low-grade fever), paraspecific allergic reactions (erythema nodosum, usually accompanying the appearance of infiltration in the area of ​​the primary complex). Damage to the lungs in the form of shortness of breath, dry cough, local shortening of percussion sound according to the site of infiltration of the lung tissue, weakened breathing. With a poor clinical picture, there are clear Ro changes. In the blood - leukocytosis, lymphopenia, eosinophilia, ?ESR up to 35-40 mm/hour. Tuberculin tests are always (+).

Pulmonary tuberculoma. Encapsulated caseous lesions of round or oval shape with a diameter of 1-1.5 cm. In half of the cases it is combined with damage to the bronchi and the formation of a fistula. The reaction of the root of the lung is almost always moderate, intoxication is rare. The course is torpid, and in more than half it is detected by chance during medical examinations.

Tbc intrathoracic lymph nodes (tbc bronchoadenitis). The most common local form of primary tuberculosis in children. Pat. the process involves the lymph nodes not only of the root of the lung, but also of the mediastinum. At the same time, despite the presence of signs of clinical-Ro activity, changes in the lung tissue are not detected. A special place is occupied by small forms of tbc bronchoadenitis, which occurs with simultaneous damage to several lymph nodes, not extending beyond the capsule. Characterized by a gradual onset of obstruction, minor clinical and erased Ro manifestations in the form of deformation of the pulmonary pattern in the hilar zone, slight expansion and infiltration of the root. Infiltrative and caseous forms of bronchoadenitis, torpid, usually develop with massive infection, mainly in children who had contact with a TBC patient in the family at an early age, especially with late diagnosis and inadequate treatment. These forms are characterized by a wavy ridge. flow. Often complicated by the formation of bronchial fistulas. Clinical manifestations: cough, often paroxysmal, bitonal (due to bronchial compression); attacks of suffocation reminiscent of asthma; persistent pain in the interscapular space, an expanded venous network on the chest and dilated capillaries in the area of ​​the VII cervical vertebra (Sm Frank), shortening of percussion sound along the spine below the third thoracic vertebra (Sm Koranyi), and in addition, in the interscapular space, parasternally (Sm Filatov). In the same area - ? bronchophony and whispered speech (Sm D'Espina), bronchial breathing. Ro - an increase in the size of the root with convex external contours, infiltration in the hilar pulmonary tissue. Complicated by pleurisy, atelectasis, bronchial tbc.

Disseminated pulmonary tbc. Associated with an active process in the lymph nodes of the mediastinum. By wedge. The flow is divided into acute (miliary), subacute and chronic. In children and adolescents, the first two predominate. A distinctive feature is TBC-damage not only to the lungs, but also to other organs (kidneys, larynx, pleura, peritoneum, pericardium) with the formation of small tubercles in each of them as a result of hematogenous introduction of MBT.

Focal TBC of the lungs. Characterized by the development of inflammatory foci not > 1 cm in 1-2 segments of the lungs. In children and adolescents, this form of TBC is usually associated with the period of primary infection and active changes in the mediastinal lymph nodes. The course is asymptomatic. Revealed during FG.

Infiltrative TBC of the lungs. Pneumonic process with a predominance of the exudative component of inflammation. The onset is acute (similar to pneumonia). Confirmation of the diagnosis - isolation of MBT. Ro is a heterogeneous shadow with areas of clearing caused by the disintegration of lung tissue and foci of contamination around the shadow.

Cavernous tbc of the lungs. The most dangerous form. Rarely observed in children and adolescents. Ro – a cavity with foci of contamination around. With inadequate treatment - pulmonary fibrosis, emphysema, bronchiectasis.

Bronchial Tbc. It is observed infrequently (15-20% of cases). Specific changes in the bronchi are asymptomatic and have limited productive characteristics.

Principles and methods of treating children with tuberculosis.

Therapy should be carried out taking into account the child’s age, his anatomical and physiological characteristics, the form and activity of the tbc process.

The main methods of drug administration are the usual, single daily dose of the drug, intermittent, intravenous, inhalation.

Chemotherapy. The main method of treatment. Start immediately upon diagnosis, continue for a long time, continuously, with drugs in various combinations. Drugs of group A (isoniazid, rifampicin), group B (streptomycin, pyrazinamide, ethambutol, kanamycin, cycloserine, viomycin) and group C (PAS sodium) are used.

Treatment for acute limited forms of TBC should begin with three main drugs (isoniazid, rifampicin, streptomycin) and after 3-4 months. continue isoniazid with pyrazinamide, ethambutol or prothionamide. In cases of early TBC intoxication in preschool children, treatment can be carried out with isoniazid alone. The total duration of treatment for closed forms of TBC is 6 months, of which 1-3 months. in the hospital. Patients with destructive forms are also treated with isoniazid, rifampicin, and streptomycin. Other drugs are kept in reserve and prescribed in case of side effects, intolerance or drug resistance. Combining antitube. drugs, take into account the sensitivity of MBT to them according to bacteriological examination.

Surgery. Radical (lung resection), collapsosurgical (artificial pneumothorax, pneumoperitoneum, thoracoplasty), intermediate (cavernotomy, cavernoplasty, cavity drainage, ligation of the bronchus, pulmonary artery).

Nonspecific treatment. Hygienic and dietary regime (work, rest, nutrition, treatment with air, water, sun). At the same time, vitamin preparations are also prescribed and symptomatic treatment is carried out. San-kur treatment is widely used.

Work in the focus of tuberculosis infection to prevent tuberculosis in children and adolescents.

In children, infection prevention is carried out, which is important at an early age, and disease prevention (specific).

Prevention of infection consists in the improvement of foci of infection, carrying out sanitary education work, and regular (2 times a year) examination of employees of children's institutions for tuberculosis. dispensaries, organizing recreational activities among the entire child population.

The main methods of specific prevention of TBC in children are vaccination (re-vaccination) with BCG and chemoprophylaxis, the organization of specialized sanatorium-type children's institutions (sanatorium nurseries, schools) for infected children.

Anti-tuberculosis vaccination and revaccination with BCG.

BCG vaccination and revaccination is carried out according to the vaccination schedule for newborns (on the 3rd-5th day of life) and at the age of 7 and 14 years. Vaccination and revaccination are carried out once. Revaccination is carried out for healthy children in whom the Mantoux test with 2 TE PPD-L gave a (-) result (complete absence of infiltration and hyperemia or hyperemia with a solution of 1 mm).

Vaccination and revaccination help reduce infection and morbidity in children and prevent the development of acute and generalized forms of TBC.

Chemoprevention of tuberculosis among children and adolescents.

Chemoprophylaxis is carried out in children of the following groups:

1. Those in contact with patients secreting MBT (2 2-month courses per year, in spring and autumn, for 1-3 years).

2. Having a bend of tuberculin tests without signs of intoxication (once within 3 months).

3. Tuberculin-positive convalescents after measles and whooping cough (once within 2 months).

4. Providing hyperergic reactions for the administration of tuberculin, in the development of which TBC infection plays a major role (once for 3 months).

For this purpose, isoniazid is used at a dose of 5-8 mg/kg/day. Children with a positive reaction to tuberculin are sent to the anti-tuberculin clinic for chemoprophylaxis. sanatorium institutions.

Sanitary prevention is the improvement of foci of tbc infection, sanitary and veterinary control, carrying out sanitary education work, early detection and treatment of first-time cases of tbc. It is carried out mainly in the focus of TBC infection (the home where a patient with an active form of TBC lives, secreting MBT. In this case, maintaining a sanitary culture, disinfection, and control of contacts are important.

When a child gets sick, you think it would be better if you got sick yourself. When rushing to help your children, do not self-medicate. Some diseases have the ability to “disguise” themselves as completely different diseases, and here you cannot do without the help of a specialist.

What are childhood diseases?

One of the main places is occupied by the most common childhood diseases. Immediately after birth, the baby’s gastrointestinal tract begins to work in a “new mode,” and the first problems begin with the well-known crying from “gas in the tummy.” Pediatricians recommend placing the baby on his stomach more often, dry heat, dill drops, and feeding by the hour. By three months, the pain usually goes away and is safely forgotten.

If at the beginning of life we ​​teach children a routine, then over time, often, everything changes. Irregular nutrition, an abundance of poor quality foods, stuffed with all sorts of “E”, are reflected in the child’s gastrointestinal tract by developing gastritis.

Reflux

When a child complains of abdominal pain or suffers from belching with an unpleasant odor, reflux, an inflammation in the esophagus, can be suspected. The reason is the throwing of stomach contents back into the esophagus, the entry of bile into the stomach.

Constipation and diarrhea

Constipation and intestinal disorders associated with poor diet and stress. There is even such a concept - “nervous stomach”. They can also be a consequence of an infectious disease. The main thing is to find the cause and prescribe appropriate treatment. If the cause is an infection, antimicrobial medications will be required.

Autoimmune diseases occur due to a malfunction in the child's immune system. The body “fights” with itself. You need advice and help from an immunologist.

Obesity in children

Childhood obesity can truly be called the disease of the century. Unfortunately, a side effect of computerization is that children spend more time in front of a monitor screen than outside. The lack of outdoor games, the abundance of fatty and unhealthy foods, consisting of many preservatives, is a provoking factor. It is fraught with diabetes, liver diseases, coronary heart disease and even early heart attack and stroke.

Digestive organs such as the stomach, large and small intestines, as well as the duodenum have a number of interrelated diseases - gastroenteritis, enterocolitis, duodenitis, peptic ulcer.

The listed diseases have common symptoms and causes.

Infectious diseases in children

Quite varied and contagious. With the spread of vaccination, the risk of contracting some diseases has been reduced to almost zero. But despite this, it is necessary to know about these diseases.

Viral mumps (mumps), scarlet fever, polio, diphtheria. Quite an impressive list. The source of disease is a virus transmitted from a sick person. All diseases have a certain incubation period - the time the disease develops in the body. Infectious diseases are not at all harmless; they are dangerous due to complications. Treatment is carried out strictly under the supervision of a doctor! Vaccinations are given against all these diseases, and they should not be neglected.

Flu

If a person gets sick with the diseases described above once, then the infection haunts us throughout our lives. Strengthen your child’s immunity, strengthen his body, enroll him in a sports section, and take your child to the sea once a year. Dysentery is a disease of dirty hands. Do not allow children to eat unwashed vegetables and fruits, teach them the rules of personal hygiene, and do not buy food from suspicious goods.

Diseases of the urinary system

Children, like adults, are susceptible. It is not uncommon for parents to bring their child with complaints of pain in the kidneys, pain when urinating, and spotting. As a rule, these are symptoms of diseases such as urethritis and others. Timely treatment will help avoid complications, such as stones in the urinary system.

Respiratory diseases in children

Pneumonia is bacterial with signs of acute respiratory infections. Timely treatment is the key to a quick recovery. Do not start, always seek medical help.

Occurs due to the spread of a cold to the bronchi. It can occur in a mild form, or maybe in a severe form, with high temperature. Accompanied by a strong dry cough with or without sputum, depending on the degree of the disease. Modern medications cope well with this disease. Traditional medicine also has effective recipes in its arsenal.

Dental diseases

Dental diseases of children are diseases of the oral mucosa. Low resistance to infections, various injuries, viruses, are the cause of the development of seizures. Oral diseases can be easily treated by rinsing with traditional medicine and using medications at home.

ENT diseases in a child

ENT diseases in children can occur from the first days of life. Inflammatory diseases can occur as complications of infection. Often, which are expressed, so and . Such diseases must be promptly examined and measures taken for treatment.

We have reviewed a list of the most common childhood diseases that can arise from the first year of life and bring worries to parents.

And finally. In order for children to get sick less, you need to start taking care of this from the first day of life - do not neglect breastfeeding. Only with mother's milk does the child receive all the necessary vitamins, strong immunity, and disease resistance.

Temper your child, let him run barefoot, don’t wrap him up too warmly, and don’t rush to give antibiotics for any illness. Children is our future. May they be healthy and beautiful!