Staphylococcal enterocolitis treatment. Intestinal infections of staphylococcal etiology in children

Staphylococcal infection is a group of diseases caused by bacteria of the genus Staphylococcus, characterized by diverse localization of the pathological process and clinical polymorphism.

From this article you will learn the main causes and symptoms of staphylococcus in children, how staphylococcus in children is treated and what preventive measures you can take to protect your child from this disease.

Treatment of staphylococcus in children

Treatment of staphylococcal diseases in children

The treatment is complex, aimed at neutralizing the pathogen and eliminating its toxic products, increasing the specific and nonspecific resistance of the macroorganism.

Children with generalized and severe forms of the disease, regardless of age, as well as newborns with any form of staphylococcal infection are subject to mandatory hospitalization. Patients are isolated in boxes (half-boxes), which helps prevent nosocomial infections.

The diet is prescribed depending on the child’s age, severity, form and period of the disease. Food should be high in calories with sufficient complete protein and limited carbohydrates, which promote the growth of staphylococci. Of particular importance in the treatment of staphylococcus is the use of lactic acid mixtures, which have a positive effect on intestinal eubiosis. For lesions of the gastrointestinal tract, accompanied by symptoms of toxicosis and exicosis, diet therapy is carried out according to the same principles as for other acute intestinal infections.

Treatments for staphylococcus in children

The basic rule of drug therapy for patients with various forms of staphylococcal infection is a rational combination of antibacterial drugs and specific agents. Sanitation of the primary focus is of great importance, and in case of generalized infection - secondary lesions. According to indications, detoxification and rehydration therapy is prescribed, emergency conditions are treated (infectious-toxic shock, cardiovascular, respiratory failure). The choice of antibacterial drugs depends on the form and period of the disease, the severity of the process, the age and premorbid background of the child.

How to treat staphylococcus in a child?

Antibacterial therapy for patients with mild and moderate localized forms of staphylococcus is carried out with semisynthetic penicillins (oxacillin, ampiox), macrolides (erythromycin, roxithromycin), and lincomycin. In severe forms of localized staphylococcal infection, aminoglycosides (gentamicin), rifampicin, and first generation cephalosporins (cefazolin) are prescribed; in generalized forms, cephalosporins of the second and third generations (cefotaxime, ceftazidime, ceftriaxone, cefuroxime), aminoglycosides of the third generation (netilmicin, tobramycin) are prescribed for the treatment of staphylococcus. Nitrofuran drugs (furazolidone, furadonin, furagin, nifuroxazide) can be used for various forms of staphylococcal diseases.

In the complex treatment of children with staphylococcal infection, specific therapy is important. If the course of the staphylococcal process is protracted (pneumonia, enterocolitis, furunculosis, staphyloderma), native staphylococcal toxoid is used for treatment, which is administered subcutaneously according to the following schemes:

scheme - 7 injections (0.1 ml - 0.2 ml - 0.3 ml - 0.4 ml - 0.6 ml - 0.8 ml - 1.0 ml; course dose 3.4 ml), treatment drug staphylococcus is administered at intervals of 2-3 days;

scheme - 5 injections (0.1 ml - 0.5 ml - 1.0 ml - 1.0 ml - 1.0 ml; course dose 3.6 ml), the drug is administered at intervals of 1 day.

Staphylococcal bacteriophage is used for treatment locally (for staphyloderma, furunculosis, osteomyelitis, infected wounds), orally (for acute enteritis, enterocolitis), subcutaneously or intramuscularly.

Hyperimmune antistaphylococcal immunoglobulin is indicated for patients with severe and generalized forms of staphylococcal infection, especially young children. The drug is administered intramuscularly at a dose of 5-8 AE/kg body weight per day daily or every other day; course of therapy - 5-7 injections. In severe cases, the dose is increased to 20-50 AE/kg.

Hyperimmune antistaphylococcal plasma is used from the first days of illness in the treatment of staphylococcal infections accompanied by toxicosis; administered intravenously, daily or at intervals of 1-3 days (5.0-8.0 ml/kg/day) for 3-5 days.

Along with etiotropic treatment, the administration of immunostimulating drugs (methyluracil, sodium nucleinate), probiotics (bifidumbacterin, lactobacterin, bactisubtil, etc.), enzymes (Creon, pancreatin, mezim-forte, abomin), vitamins (C, A, E, group B), symptomatic remedies.

Dispensary observation. Children who have suffered any form of staphylococcal infection are under clinical observation in the clinic or hospital where treatment was carried out. The period of medical examination is from 1 month. up to 1 year or more.

Treatment of staphylococcus in infants

The best method of combating staphylococcus is complex therapy aimed at increasing the body’s protective functions. The baby’s immune system is not perfect, it is still being “tuned”, so the baby’s tender age must be protected by all means. Try to protect your baby from potentially sick people, try to introduce more vitamins and nutrients into his food.

As for treating a baby who is currently suffering from a virus, the best thing you can come up with is a chamomile decoction. Chamomile can be given to drink, it can be used as an enema, as an inhalation or as nasal drops. Depending on the location and type of lesion, the place where the effort is applied is selected.

An excellent remedy for treating staphylococcus is camphor oil. It is not in vain that it is used as a personal hygiene product for babies. It has excellent antiseptic properties and does not dry out the baby’s skin at all.

Staphylococcus is a legacy for life. Once you catch a problem, you can fight it for the rest of your life. But this does not mean that knowing how and with what to treat staphylococcus in an infant is superfluous. Perhaps your treatment will be so effective that the baby will be able to forget about the problem for a long time.

Prevention of staphylococcus in children

Preventive work should be carried out in all medical institutions. The antenatal clinic organizes systematic observation and examination of pregnant women, with special attention paid to the diagnosis and treatment of “minor” forms of staphylococcal infection (rhinitis, conjunctivitis, staphyloderma).

Of particular importance is the early detection of pathogenic strains of staphylococcus and staphylococcal diseases among medical and service personnel of children's hospitals. Identified carriers of pathogenic staphylococcus (and patients) are subject to isolation and treatment; staff are removed from serving children. At the same time, sanitary and hygienic measures are carried out aimed at interrupting the spread of staphylococcus (disinfection of household items, high-quality cleaning of premises, strict implementation of the anti-epidemic regime, proper storage of infant formula, etc.). The rules of asepsis and antisepsis should be strictly observed when carrying out any medical procedures and surgical operations.

An important place in the prevention of staphylococcal infection is played by sanitary and educational work with pregnant women, as well as the proper organization and implementation of rational feeding of the child, compliance with the rules of the sanitary and hygienic regime at home and in child care institutions.

Symptoms of staphylococcus in children

The incubation period ranges from several hours (9-10) to 3-5 days.

Staphylococcal lesions of the skin and subcutaneous tissue are the most common localization of the pathological process in children.

Staphyloderma is one of the most common forms, observed at different ages. In newborns, vesiculopustulosis and neonatal pemphigus (pemphigus) are more often recorded, and Ritter's exfoliative dermatitis is less common.

Vesiculopustulosis is characterized by the appearance on the 5-6th day of a child’s life of pustules (2-3 mm in size), which are located on the scalp, torso and in skin folds. The bubbles burst after 2-3 days and crusts form. Sometimes infiltrates appear around the pustules; it is also possible to develop multiple abscesses and, less commonly, phlegmon.

Pemphigus of newborns is highly contagious. The general condition of children is disturbed, they become lethargic, body temperature rises, and appetite decreases. In the area of ​​the inguinal folds, armpits, on the skin of the abdomen and neck, blisters of various sizes appear, initially filled with serous, and after 2-3 days - with serous-purulent contents. When the blisters are opened, the erosive surface is exposed. Pemphigus in newborns can occur with complications (conjunctivitis, otitis, pneumonia) and be the primary focus of sepsis.

Ritter's foliative dermatitis is the most severe form of staphyloderma in newborns. The disease begins on the 5-6th day of a child’s life with the appearance of redness and maceration of the skin in the navel area or around the mouth. Soon blisters appear on the skin, which quickly increase in size and merge with each other. Detachment of the epidermis and formation of erosions occur. The disease occurs with symptoms of intoxication and high body temperature. By the 10-11th day of illness, exfoliative dermatitis takes on a pronounced character: the child’s skin turns red, extensive erosions appear on the torso and limbs. When rubbing areas of practically healthy skin, the epidermis wrinkles and peels off (Nikolsky's symptom).

Multiple skin abscesses, as a rule, occur at an early age in weakened children suffering from rickets, anemia, and malnutrition. Initially, nodules 0.5-2 cm in size of a purplish-red color appear on the skin, later a fluctuation is detected above them. The course of the disease is torpid, accompanied by a prolonged increase in body temperature and symptoms of intoxication.

Folliculosis is observed in older children. These include: folliculitis, furuncle, carbuncle, hidradenitis. The inflammatory process in these cases is localized at the mouth of the hair follicle. The most severe forms are boils and carbuncles, in which the deep layers of the dermis are involved in the process, and in the case of a carbuncle, the subcutaneous tissue is also involved. Folliculosis is most often localized on the back of the neck, in the lumbar region and armpits. Hidradenitis is observed mainly in children during puberty and is located in the area of ​​the apocrine sweat glands. It is characterized by a tendency to subacute and chronic course, often relapsing.

Staphylococcal infection with scarlet-like syndrome can develop at any location of the staphylococcal lesion (infected wound, burn surface, panaritium, phlegmon, boil, osteomyelitis). The onset is acute, body temperature rises to 38.5-39.5 ° C, and vomiting is sometimes observed. 3-4 days after the appearance of the primary staphylococcal lesion, a pinpoint rash appears, which is localized on the inner surface of the upper and lower extremities and lower abdomen. The rash is located on a hyperemic background of the skin, thickens around the primary lesion, and persists for 1-2 days. Moderate diffuse hyperemia may be observed in the pharynx; from the 4th day of illness - “papillary” tongue. Enlarged lymph nodes correspond to the location of the lesion.

Generalization of the process with the appearance of secondary purulent foci (otitis media, lymphadenitis, sinusitis) is possible.

During the period of convalescence, lamellar peeling of the skin may be observed.

Inflammation of the lymph nodes (lymphadenitis) and lymphatic vessels (lymphangitis) of staphylococcal etiology are more often observed in young children in the presence of staphylococcal skin lesions. The clinical picture includes an increase in body temperature and symptoms of intoxication (loss of appetite, headache, sleep disturbance). The affected regional lymph node is dense, enlarged, and sharply painful on palpation. Subsequently, catarrhal lymphadenitis turns into purulent with melting of the lymph node. With lymphangitis, pain and hyperemia of the skin with infiltration along the lymphatic vessels are noted.

Complications of staphylococcus in children

Damage to mucous membranes

Conjunctivitis of staphylococcal etiology is observed in both newborns and older children. Usually the lesion is bilateral, with purulent discharge from the eyes, swelling of the eyelids, conjunctival hyperemia and injection of scleral vessels. The inflammatory process can take a long time. In some cases, severe complications are observed in young children (purulent dacryocystitis, ethmoiditis, orbital phlegmon, sepsis). Aphthous-ulcerative stomatitis develops in young children with a burdened premorbid background, weakened by concomitant diseases. More often, stomatitis is preceded by a herpetic or respiratory infection. In severe cases, the disease begins with an increase in body temperature and symptoms of intoxication. Ulcers of the mucous membrane of the oral cavity and tongue are covered with yellow plaques, which often merge. The child experiences profuse salivation and severe pain during meals. As a rule, there is an increase in the submandibular and sublingual lymph nodes. Characteristic is the torpidity of the pathological process and the low effectiveness of the use of antibacterial agents.

Damage to ENT organs

Rhinitis and purulent nasopharyngitis of staphylococcal etiology are common forms of staphylococcal infection. Characterized by a gradual onset and protracted course. Rhinitis and nasopharyngitis are most severe in newborns and infants. The child becomes restless, refuses to eat, nasal breathing is difficult, and there is an increase in body temperature. There is copious, thick, purulent green discharge from the nose. Possible development of otitis, pneumonia, enteritis, sinusitis.

Staphylococcal sore throats occur in children of all ages. The onset of the disease is often gradual. In all patients, as a rule, body temperature rises to 37.5-39 ° C, symptoms of intoxication appear, increased salivation, vomiting, and sore throat are noted. In the pharynx there is diffuse hyperemia, swelling and infiltration of the mucous membranes. Sore throat can be lacunar, follicular, and more often has a purulent-necrotic character. Regional lymph nodes are enlarged, their palpation is sharply painful. The course of staphylococcal sore throat is torpid, the duration of fever is 7-8 days; Local changes in lacunar angina last 7-10 days.

Staphylococcal otitis occurs more often in young children. The inflammatory process in the middle ear is purulent in nature and tends to be protracted and chronic.

Damage to bones and joints

Osteomyelitis of staphylococcal etiology can occur primarily and secondarily, as a consequence of the septic process. The inflammatory process is localized mainly in the femur and humerus. Osteomyelitis is characterized by an acute onset, increased body temperature, severe intoxication, vomiting, anxiety, and the possible appearance of a pinpoint rash. In the first days of the disease, local changes are insignificantly expressed, but there is sharp pain when changing body position, and limited mobility of the affected limb. Later, local symptoms appear in the form of increased skin temperature, swelling, tension, and local pain on palpation.

Staphylococcal arthritis is characterized by severe pain, limited joint function, deformation, and local fever. In the absence of adequate treatment, destruction of cartilage and subchondral bone develops.

Damage to the respiratory system

Laryngitis and laryngotracheitis are the most common form of staphylococcal damage to the respiratory tract. They occur predominantly in young children against the background of respiratory viral infections (influenza, parainfluenza, adenoviral infection). In sick children, against the background of typical clinical manifestations of viral damage to the larynx (trachea), a new rise in body temperature to 39 - 40 ° C and a deterioration in general condition are observed. Symptoms of intoxication and signs of hypoxia are expressed (the child is restless, vomiting, petechial rash). Laryngoscopy reveals necrotic or ulcerative-necrotic changes in the larynx and trachea. The course of laryngo-tracheitis is long, with frequent development of laryngeal stenosis, obstructive bronchitis and pneumonia.

Staphylococcal pneumonia develops in young children as primary (infection occurs by airborne droplets) or as a result of secondary lung damage in various forms of staphylococcal infection. The clinical picture is characterized by polymorphism of symptoms. In typical cases, there is a rapid onset, accompanied by severe fever, intoxication and rapidly increasing changes in the lungs. The child is lethargic, adynamic, refuses to eat; there is a frequent painful cough, difficulty breathing. Shortness of breath appears up to 60-80 breaths per minute with the participation of auxiliary muscles. Percussion reveals shortening, in places a tympanic tint. On auscultation, against the background of bronchial or weakened breathing, localized sonorous fine-bubble rales are heard; on the 5-6th day of the disease, crepitations are heard. Signs of cardiovascular failure are detected (muffled heart sounds, tachycardia, small rapid pulse, acrocyanosis), bloating, hepatosplenomegaly, stool retention. The skin is pale, with a gray tint, and sometimes there is an ephemeral rash of a polymorphic nature.

One of the features of staphylococcal lung damage is the development of destructive pneumonia. Children often experience the formation of air cavities (bullae). Bullae can be either single or multiple. More often, air cavities appear during the period of convalescence and much less often at the height of the disease. With percussion over the lesion, tympanitis is determined, and auscultation reveals weakened or amphoric breathing. On X-ray examination of the lungs, bullae appear as ring-shaped formations with sharply defined contours. In most patients, the process of formation of bullae proceeds favorably, but in some cases the development of pneumothorax or emphysema is possible.

In the case of abscess formation, lung abscesses appear by the 5th - 6th day of the disease. Abscesses of staphylococcal etiology are characterized by a subpleural location, preferential localization in the right lung. The formation of an abscess proceeds rapidly, accompanied by a sharp deterioration in condition, hyperthermia, and an increase in respiratory and cardiovascular failure. When large purulent cavities form, amphoric breathing and wheezing with a metallic tint are detected by auscultation.

One of the severe manifestations of staphylococcal infection is purulent pleurisy. The development of purulent pleurisy is accompanied by a sharp deterioration in the patient’s condition: a pained expression appears, chest pain, painful cough; body temperature becomes hectic, shortness of breath increases, and cyanosis intensifies. In patients with a large amount of purulent effusion in the pleural cavity, there is asymmetry of the chest, smoothness of the intercostal spaces, a lag in the act of breathing of the diseased half of the chest from the healthy one, and possible displacement of the mediastinal organs. Percussion above the exudate zone reveals a distinct dullness, weakening of vocal tremors, and bronchophony. The severity of physical findings depends on the localization of pleurisy (parietal, basal, interlobar).

Gastrointestinal diseases

Gastrointestinal diseases of staphylococcal etiology in children are common and are characterized by various clinical variants.

Classification of acute intestinal infections of staphylococcal etiology:

By type:

Typical;

Gastrointestinal (food toxicoinfection):

  • gastritis;
  • gastroenteritis;
  • gastroenterocolitis.

Diarrhea (enteritis and enterocolitis) in young children:

  • primary;
  • secondary;
  • as a consequence of dysbiosis.

    Staphylococcal intestinal mixed infections.

    Atypical:

    • erased;
    • asymptomatic.

    By severity:

    Light form.

    Moderate form.

    Severe form.

    Severity criteria:

    • severity of local changes.

    Downstream:

    A. By duration:

    Acute (up to 1 month).

    Prolonged (up to 3 months).

    Chronic (more than 3 months).

    B. By nature:

    Unsmooth:

    • with complications;
    • with relapses and exacerbations;

    Typical forms

    The gastrointestinal form (gastritis, gastroenteritis, gastroenterocolitis) develops in older children.

    The incubation period is short (several hours). The disease begins acutely, with sharp pain in the epigastric region, repeated vomiting, weakness, dizziness, hyper- or hypothermia. At the same time, pronounced pathological changes in the nervous system (convulsions) and cardiovascular disorders (acrocyanosis, muffled heart sounds, threadlike pulse, decreased blood pressure) may be observed. Some patients develop a pinpoint or petechial rash. The disease can occur in a gastric variant (affecting only the stomach), but in most patients the small intestine (gastroenteritis) is involved in the pathological process, and less often the large intestine (gastroenterocolitis). Stools are usually frequent, loose, watery and mixed with mucus. In severe cases, along with toxicosis, exicosis develops. With timely, adequate therapy, after 6-8 hours, the symptoms of intoxication decrease and disappear by the end of the day. At the end of the first week of the disease, stool returns to normal and recovery occurs. Complications are rare.

    Causes of staphylococcus in children

    Historical data on staphylococcus

    Historical data. Purulent-inflammatory diseases of the skin, soft tissues and internal organs have been known since ancient times. In 1880, L. Paster first discovered pathogens in pus from a boil and called them “pyogenic vibrios.” In 1884, they were studied and described by F. Rosenbach under the name “staphylococci”. Much credit in the study of staphylococcal diseases belongs to domestic scientists: M. G. Danilevich, V. A. Tsinzerling, V. A. Khrushchova, O. I. Bazan, G. N. Vygodchikov, G. N. Chistovich, G. A. Timofeeva, A.K. Akatov, V.V. Smirnova, G.A. Samsygina.

    The causative agent of staphylococcus

    Etiology. The causative agents of staphylococcal diseases are bacteria of the genus Staphylococcus, which includes 19 species.

    Three types of staphylococcus are of greatest importance in human pathology: aureus (S. aureus), epidermal (S. epidermidis), saprophytic (S. saprophytics). The species of Staphylococcus aureus includes at least 6 biovars (A, B, C, D, E, F). The causative agent of human diseases is biovar A, other variants are pathogenic for various animals and birds.

    Staphylococci have a spherical shape, their diameter is 0.5-1.5 microns, and are gram-positive. In smears from a pure culture, microorganisms are located in clusters resembling bunches of grapes; in smears from pus, short chains, single and paired cocci are found. Staphylococci do not have flagella and do not form spores. Some strains form a capsule or microcapsule, mainly of a polysaccharide nature. Staphylococci grow well on ordinary nutrient media with a pH of 7.2-7.4 at a temperature of +37° C; form enzymes that break down many carbohydrates and proteins.

    In the pathogenesis of staphylococcal infection, plasmacoagulase, DNAase, hyaluronidase, lecithinase, fibrinolysin, and proteinase are of greatest importance.

    Plasmocoagulase causes plasma coagulation; hyaluronidase promotes the spread of staphylococci in tissues; lecithinase destroys lecithin, which is part of cell membranes; fibrinolysin dissolves fibrin, which delimits the local inflammatory focus, promoting the generalization of the pathological process.

    The pathogenicity of staphylococcus is primarily due to the ability to produce toxins: hemolysins - alpha (a), beta (p), gamma (y), delta (5), epsilon (e), leukocidin, exfoliative, entero-toxins (A, B, Cj , Сг, D, E, F), TOKCHH-1.

    The main one in the group of hemolysins is a-hemolysin, produced by Staphylococcus aureus. It causes tissue damage, dermonecrotic, neurotoxic and cardiotoxic effects.

    • α-hemolysin has a cytotoxic effect on human amnion cells and fibroblasts, monkey kidney cells, HeLa tissue cultures, platelets, and macrophages.
    • p-hemolysin lyses red blood cells of humans, rabbits, sheep, dogs, birds, and also has a lytic effect on leukocytes.
    • γ-hemolysin has a wide spectrum of cytotoxic activity; in low doses, like cholera enterotoxin, it causes an increase in the level of cAMP and an increase in the secretion of Na+ and C1+ ions into the intestinal lumen.

    Leukocidin has a detrimental effect on phagocytic cells, mainly polymorphonuclear leukocytes and macrophages, and has pronounced antigenic activity.

    Exfoliative toxins cause staphylococcal “burnt skin” syndrome in humans.

    Staphylococcal enterotoxins are heat-stable, resistant to proteolytic enzymes, and cause food poisoning in children. Enterotoxins cause the development of changes in the intestine similar to pseudomembranous enterocolitis, cause toxic shock syndrome, and affect immunocompetent cells and their precursors.

    Toxin-1 (TSST-1) is found only in certain strains of Staphylococcus aureus and is responsible for the development of toxic shock syndrome.

    The surface structures of staphylococcal microbial cells represent a complex system of antigens with diverse biological activities. The following have antigenic properties: peptidoglycan, teichoic acids, protein A, flocculent factor, type-specific agglutinogens, polysaccharide capsule.

    Peptidoglycan has an endotoxin-like effect (pyrogenicity, reproduction of the Schwartzmann phenomenon, complement activation, etc.).

    Teichoic acids cause activation of complement through the classical pathway, a delayed-type hypersensitivity reaction.

    Protein A is present in the cell wall of S. aureus and is capable of nonspecific combination with the Fc fragment of IgG, and has the properties of precipitinogen and agglutinogen.

    The flocculent factor prevents effective phagocytosis.

    The polysaccharide capsule is not a component of the staphylococcal cell wall, but is structurally associated with it and is considered a surface somatic antigen. The biological activity of capsular polysaccharides is expressed mainly in their antiphagocytic effect.

    Staphylococci have a number of plasmids that exhibit signs of resistance to antibiotics and the ability to synthesize coagulase, hemolytic toxins, fibrinolysin, and pigments. Resistance plasmids are easily transmitted from Staphylococcus aureus to epidermal, from staphylococci to Escherichia coli, Bacillus subtilis and other bacteria.

    During the infectious process, staphylococci can change their enzymatic, invasive and toxigenic properties.

    Staphylococcus aureus produces a golden-yellow pigment, capsule; synthesizes coagulase, a-toxin; Protein A and teichoic acids are present on the surface of the cell wall.

    Staphylococcus aureus is divided into three lytic (I, II, III) and three serological (A, B, F) groups, within which phagovars are distinguished.

    Staphylococcus epidermidis synthesizes a yellow or white pigment; protein A is absent in the cell wall; sensitive to novobiocin; does not produce coagulase and a-toxin.

    Saprophytic staphylococcus produces a lemon-yellow pigment, does not have protein A, and does not produce a-toxin or coagulase.

    Staphylococci are stable in the external environment: they tolerate drying well, and when exposed to direct sunlight they die only after a few hours. At room temperature, they remain viable on solid equipment for tens of days, and on patient care items for 35-50 days. They last especially long on food products, in particular fruits (up to 3-6 months). When boiled they die instantly, at a temperature of +80° C - after 20 minutes, under the influence of dry steam - after 2 hours. Less resistant to the action of chemical agents: 3% phenol solution and 0.1% mercuric solution kill them within 15-30 min, 1% aqueous solution of chloramine - 2-5 min.

    Source of staphylococcus infection

    Epidemiology. The main source of infection is a person - a patient or a bacteria carrier; pets are of secondary importance. The greatest danger is posed by persons with staphylococcal lesions of the upper respiratory tract (sore throat, pharyngitis, conjunctivitis, rhinitis), gastrointestinal tract (gastroenterocolitis, enterocolitis). The main reservoir of staphylococcus are bacteria carriers, in which the pathogen is localized on the nasal mucosa.

    Transmission mechanisms: droplet, contact, fecal-oral.

    Transmission routes: airborne droplets, airborne dust, household contact, food. Indoor air becomes infected when coughing, sneezing, or dry cleaning. The spread of the pathogen is facilitated by overcrowding of wards, poor lighting, insufficient ventilation, violation of the rules of disinfection, asepsis and antiseptics. Transmission of the pathogen is possible through consumption of infected food (milk and dairy products, creams, confectionery).

    Infection of children with staphylococcus

    Infection can occur antenatally and intranatally. In newborns and children in the first six months of life, the contact and household route of transmission predominates. Infection occurs through the hands of staff or the mother, through contact with contaminated care items, toys, as well as through consumption of infected formula and milk.

    Staphylococcal infection is recorded in the form of sporadic cases and group diseases. Epidemic outbreaks have been described in maternity hospitals, departments for newborns and premature babies, orphanages, children's surgical and infectious diseases hospitals.

    The highest incidence of staphylococcal infection is observed among newborns and children in the first six months of life. This is due to anatomical and physiological characteristics, the state of local immunity, specific and nonspecific protective factors. Children with a burdened premorbid background (early artificial feeding, exudative-catarrhal diathesis, rickets, malnutrition, dysbacteriosis, perinatal damage to the central nervous system) who receive antibacterial and corticosteroid therapy are especially often ill.

    Recently, there has been an increase in the incidence of staphylococcal infection in all countries. According to WHO, up to 50% of sepsis cases are caused by staphylococcus.

    Staphylococcal infection does not have a pronounced seasonality; cases of the disease are recorded throughout the year.

    Pathogenesis. The entrance gates (for exogenous infection) are damaged skin, mucous membranes of the oral cavity, respiratory tract and gastrointestinal tract, conjunctiva, and umbilical wound. At the site of pathogen penetration, a primary purulent-inflammatory focus appears. In the mechanism of limiting the focus, the reaction of regional lymph nodes is of great importance. In young children, due to a decrease in the content of granulocytes in the blood and the ability to digest microbes, phagocytosis of virulent strains of staphylococcus is incomplete; persistent and long-term bacteremia occurs. Enzymes secreted by staphylococci promote the proliferation of microbes in the inflammatory focus and spread into the tissue (lymphogenous and hematogenous routes).

    Bacteremia is promoted by nutritional disorders, vitamin deficiency, and irrational use of antibiotics. As a result of the reproduction and death of staphylococci, a significant amount of toxin accumulates in the macroorganism, which leads to the development of general intoxication. Clinical manifestations of staphylococcal infection are varied and are caused by different types of staphylococcal toxins. With the predominance of hemolysins, damage to organs and tissues with hemorrhagic syndrome develops, with the production of toxin-1 - toxic shock syndrome, with exposure to enterotoxins - damage to the gastrointestinal tract.

    In the pathogenesis of staphylococcal diseases, the age of patients and the state of specific and nonspecific resistance are of great importance.

    Pathomorphology. At the site of entry of the pathogen, an inflammatory focus appears, which is characterized by serous hemorrhagic exudate, a zone of necrosis, surrounded by leukocyte infiltration and accumulation of staphylococci. The formation of microabscesses with their subsequent fusion into large lesions is possible.

    Staphylococcal pneumonia is characterized by multiple foci of inflammation and destruction.

    With staphylococcal lesions of the gastrointestinal tract, which occur as a foodborne toxic infection, there is a predominant damage to the stomach and small intestine. These organs are somewhat dilated; their lumen contains greenish-yellow fluid. The mucous membrane is full-blooded, swollen, gray pityriasis-like deposits are noted, and occasionally massive fibrinous-purulent filmy deposits are noted. Lymphatic follicles (Peyer's patches) are enlarged and swollen. In the colon, only plethora is most often determined.

    With primary and secondary staphylococcal enteritis and enterocolitis, maximum changes are detected in the colon. Intestinal mucosa with pronounced focal hyperemia and hemorrhages. The folds are thickened, covered with mucus, and in some places with yellowish-gray, grayish-brown or dirty green filmy deposits that easily separate to form ulcers.

    Pathological findings in sepsis are varied. Often, with very violent clinical manifestations, morphological changes are very scarce. Characterized by icteric discoloration of the skin and sclera, hemorrhages on the skin and in internal organs, especially in the kidneys, and vein thrombosis. The spleen is significantly increased in volume, flabby, with copious scrapings on the incision. In all parenchymal organs and cardiac muscle there are signs of degeneration and fatty infiltration.

    Classification of staphylococci in children

    By prevalence:

    Localized forms with lesions:

    • skin, subcutaneous tissue (staphyloderma, multiple skin abscesses, folliculosis, staphylococcal infection with scarlet-like syndrome);
    • lymphatic system (lymphadenitis, lymphangitis);
    • mucous membranes (conjunctivitis, stomatitis);
    • ENT organs (rhinitis, pharyngitis, tonsillitis, adenoiditis, sinusitis, otitis);
    • bones, joints (osteomyelitis, arthritis);
    • respiratory system (laryngitis, tracheitis, bronchitis, pneumonia, pleurisy);
    • digestive system (esophagitis, gastritis, duodenitis, enteritis, colitis, cholecystitis);
    • nervous system (meningitis, meningoencephalitis, brain abscess);
    • genitourinary system (urethritis, cystitis, adnexitis, prostatitis, pyelonephritis, kidney abscesses).

    Generalized forms:

    • septicemia;
    • Septicopyemia.

    By severity:

    Light form.

    Moderate form.

    Severe form.

    Severity criteria:

    • severity of intoxication syndrome;
    • severity of local changes;

    Downstream:

    A. By duration:

    Acute (up to 1 month).

    Prolonged (up to 3 months).

    Chronic (more than 3 months). B. By nature:

    Unsmooth:

    • with complications;
    • with a layer of secondary infection;
    • with exacerbation of chronic diseases.

    Staphylococcal diseases in children

    Staphylococcal enteritis and enterocolitis

    Primary staphylococcal enteritis and enterocolitis arise as a result of food or household contact infection, which often occurs already in the maternity hospital (from mothers, medical personnel, etc.). The disease most often affects weakened children, mainly in the first year of life, who are on artificial or mixed feeding, with manifestations of rickets, anemia, malnutrition, and exudative-catarrhal diathesis.

    The disease begins acutely or gradually. Regurgitation, anxiety, increased body temperature (low-grade, less often febrile), and pale skin are noted. The stool gradually becomes more frequent, retains a fecal character, and contains a large amount of mucus; By the end of the week, streaks of blood may appear. The abdomen is swollen, the liver is often enlarged, and less often the spleen. The frequency of stool in mild forms does not exceed 5-6 times, in moderate forms - 10-15 times a day. Intestinal dysfunction is often long-term; stools return to normal no earlier than the 3-4th week of illness. Low-grade fever persists for 1-2 weeks; exacerbations are often observed.

    Secondary enteritis and enterocolitis are a manifestation of a generalized staphylococcal infection. In these cases, damage to the gastrointestinal tract joins other foci of staphylococcal infection (otitis media, pneumonia, staphyloderma). The leading clinical symptoms are: low-grade (or febrile) body temperature, persistent regurgitation or vomiting, persistent anorexia, intestinal dysfunction, weight loss, anemia. In such patients, intestinal damage begins gradually; enterocolitis, including ulcerative necrotizing, is characteristic. The disease is severe with severe symptoms of toxicosis and, often, toxicosis. With the development of necrotizing ulcerative colitis, there is a sharp deterioration in the child’s general condition, an increase in dyspeptic disorders, bloating, and the appearance of mucus, blood, and sometimes pus in the stool. Intestinal perforation with the development of peritonitis is possible. There is a high mortality rate.

    In these cases, damage to the gastrointestinal tract is caused by antibiotic-resistant strains of staphylococcus, which rapidly multiply in the absence or with a decrease in obligate intestinal microflora (high-grade Escherichia coli, bifidumbacteria, lactobacilli, etc.). The most common are staphylococcal enteritis and pseudomembranous staphylococcal enterocolitis (the course is severe, cholera-like syndrome is characteristic, intestinal ulcers may develop).

    Staphylococcal intestinal mixed infections arise as a result of exposure to the body of both pathogenic staphylococcus and other microbes (Shigella, Escherichia, Salmonella) and viruses. In most cases, mixed infections are exogenous and have a severe course.

    Forms of staphylococcal enteritis and enterocolitis

    Atypical forms

    The erased form is characterized by the absence of symptoms of intoxication with mild and short-lived intestinal dysfunction.

    Asymptomatic form: no clinical manifestations; there is a repeated seeding of pathogenic staphylococcus in diagnostic concentrations and/or an increase in the titer of specific antibodies over the course of the study.

    Complications of staphylococcal enteritis and enterocolitis

    Lesions of the nervous system of staphylococcal etiology (purulent meningitis, meningoencephalitis). They are more common in young children, especially newborns, and are one of the manifestations of staphylococcal sepsis. Primary damage to the meninges is rarely observed. The occurrence of meningitis and meningoencephalitis is facilitated by cranial injuries of various origins.

    In infants, meningoencephalitis is more often observed, which begins with rapidly expressed cerebral symptoms. Anxiety appears, followed by drowsiness, vomiting, body temperature rises to 39-40 ° C, tremor of the chin and hands, convulsive readiness, and skin hyperesthesia are noted. Tension and bulging of the large fontanelle, clonic-tonic convulsions are detected; focal neurological symptoms are observed. Meningeal symptoms are usually mild.

    In older children, the pathological process is often more limited. The clinical picture is dominated by symptoms of damage to the meninges (meningitis). In patients, along with severe fever, repeated vomiting, chills, adynamia, and photophobia are observed. Meningeal syndrome is determined from the first days of the disease. Focal neurological symptoms are unstable and disappear by the end of the first week of the disease.

    A feature of staphylococcal meningitis and meningoencephalitis is a tendency to a protracted wave-like course, abscess formation and frequent involvement of the brain substance in the inflammatory process. The formation of severe residual changes in the central nervous system (hydrocephalus, epilepsy, etc.) is characteristic.

    Lesions of the genitourinary system of staphylococcal etiology manifest themselves in the form of urethritis, cystitis, pyelitis, pyelonephritis, and nephritis. Clinical symptoms indicating involvement of the urinary tract and kidneys in the pathological process do not differ from similar manifestations caused by other bacterial flora. When examining urine, leukocyturia, hematuria, cylindruria, and proteinuria are detected.

    Staphylococcal diseases - sepsis in children

    Generalized forms of staphylococcal infection (septicemia, septicopyemia) are more common in young children. The risk group for the development of sepsis includes premature infants, children with perinatal dystrophy and hypoxia. Depending on the entrance gate, the following forms of sepsis are distinguished: umbilical, cutaneous, pulmonary, enteral, tonsillogenic, otogenic.

    Based on clinical and anatomical signs and symptoms, two types of sepsis are distinguished: septicemia (sepsis without metastases) and septicopyemia (sepsis with metastases).

    The course of sepsis can be acute (fulminant), acute, subacute and chronic.

    With fulminant sepsis, the onset is violent. Body temperature rises to 39.5-40° C, intoxication appears, hemodynamic disturbances and acidosis increase. At the end of the first day of the disease, a clinical picture of infectious-toxic shock may develop (earthy-gray skin color, acrocyanosis, pointed facial features, tachycardia, thread-like pulse, expansion of the boundaries and weakening of heart sounds, decreased blood pressure, toxic shortness of breath, anuria). The cause of death is acute adrenal insufficiency caused by hemorrhages in the adrenal glands.

    In acute sepsis, fever up to 39-40° C is typical, chills are possible. During the 1st week. of illness, body temperature remains at febrile levels, only at a later stage (from the 2nd week) it takes on a typical septic character (with a daily range of 1-1.5 ° C). In the early period of the disease, a pinpoint, small-spotted or hemorrhagic rash may be observed. Symptoms characteristic of a septic condition are noted: agitation or lethargy, yellowness of the skin, dry mucous membranes, tachypnea, tachycardia, intestinal paresis, hepatosplenomegaly, delayed or frequent bowel movements, decreased diuresis. Subsequently, secondary septic lesions appear (abscess pneumonia, meningitis, osteomyelitis, arthritis, endomyocarditis). Mortality is high.

    Subacute course of sepsis: characterized by a gradual onset at normal or subfebrile body temperature, anxiety or lethargy, loss of appetite; There is periodic vomiting, stopping weight gain, bloating, and intestinal dysfunction. Subsequently, malnutrition and anemia increase, the liver and spleen enlarge, and subicteric skin appears. The disease is often accompanied by sluggish secondary lesions (pneumonia, otitis media, enterocolitis).

    Staphylococcal sepsis can take a chronic course, which is associated with the formation of metastatic foci and the development of an immunodeficiency state.

    Based on severity, staphylococcal diseases are divided into mild, moderate and severe.

    In a mild form, the body temperature rises to 38.5 ° C, the symptoms of intoxication are moderate. Local changes and functional impairments are minor.

    In the moderate form, body temperature is increased to 38.6-39.5 ° C. Symptoms of intoxication and local changes are significantly expressed.

    The severe form is characterized by fever above 39.5 °C, pronounced changes in the nervous and cardiovascular systems, severe metabolic disorders and local manifestations.

    Current (by duration).

    In most patients, the course of staphylococcal diseases is acute (up to 1 month). However, in newborns and infants with a burdened premorbid background, as well as in older children with an immunodeficiency state, the pathological process can take a protracted (up to 3 months) or chronic course (more than 3 months).

    Flow (by nature).

    It can be smooth or non-smooth (with complications, exacerbations of chronic diseases, etc.).

    Features of staphylococcal infection in young children

    In newborns and infants, staphylococcal diseases occupy a leading place in infectious pathology. They are especially common in newborns and premature babies suffering from malnutrition, exudative-catarrhal diathesis, and weakened by concomitant diseases. In newborns, the pathogens are St. aureus, St. epidermidis and St. saprophyticus; in infants - mainly St. aureus. Risk factors for the development of purulent-inflammatory diseases of staphylococcal etiology are: complicated pregnancy and childbirth, perinatal pathology of the child, etc.

    Forms of staphylococcal infection

    Among the localized forms, the following are often found: omphalitis, vesiculopustulosis, pemphigus of newborns, exfoliative dermatitis of Ritter, pyoderma, pemphigus, panaritium, paronychia, lymphadenitis, otitis, mastitis, conjunctivitis, enteritis and enterocolitis.

    A severe manifestation of staphylococcal infection is phlegmon of newborns, in which extensive purulent-necrotic processes develop in the subcutaneous fatty tissue, most often on the back and neck. The disease is accompanied by severe fever, severe intoxication, a sharp disturbance in the general condition, and vomiting.

    Generalized forms are characterized by severe severity. The following symptoms are noted: agitation or lethargy of the child, anorexia; Possible regurgitation, vomiting, hypothermia. The skin is pale gray in color, cyanosis increases, and icterus of the sclera appears; edematous and hemorrhagic syndromes develop. Due to metabolic and circulatory disorders, shortness of breath, bloating of the chest, tachycardia, intestinal paresis, hepatosplenomegaly, and enterocolitis occur. Sepsis in newborns is often fatal.

    Diagnosis of staphylococcal infection

    Supportive diagnostic signs of staphylococcal infection:

    • characteristic medical history;
    • local focus of staphylococcal infection;
    • fever;
    • intoxication syndrome;
    • multiple organ lesions;
    • tendency to protracted flow.

    Laboratory diagnosis of staphylococcal infection

    The bacteriological method is decisive for the etiological confirmation of the diagnosis. Depending on the severity of the disease and the localization of the pathological process, material is taken from the mucous membrane of the pharynx, oral cavity, nose, and larynx; skin, wounds, purulent foci. In generalized forms, bacteriological examination involves culture of blood, urine, bile, bone marrow punctate, pleural, cerebrospinal and synovial fluid. In the intestinal form of the disease, cultures of feces, vomit, gastric lavage, food debris, and breast milk are carried out.

    In the case of examining sectional material, blood from the heart, palatine tonsils, lungs, liver, spleen, small and large intestines, mesenteric lymph nodes, contents of the stomach, intestines, and gall bladder are subjected to bacteriological study. Inoculations are carried out on solid nutrient media - yolk-salt agar, blood agar, milk-salt agar. Isolation of staphylococcus is of diagnostic significance only in the first days of the disease in monoculture and in a diagnostically significant concentration (> 105-106 CFU per 1 g of material). Laboratory study, in addition to quantitative assessment of contamination, includes determination of the potential pathogenicity of staphylococcus: plasma coagulation reaction, fermentation of mannitol under anaerobic conditions, DNase activity, hemolyzing ability, lecithinase test, hyaluronidase activity, toxigenicity. Of great importance is the establishment of the phagotype, genotype of pathogenic staphylococci, as well as sensitivity to antibiotics.

    The serological research method is used to detect antibodies in blood serum: agglutinins and α-anti-toxins. For this purpose, an agglutination reaction is used with the museum strain of staphylococcus “505” or an autostrain in the dynamics of the disease. A titer of agglutinins in RA of 1:100 or an increase in the titer of specific antibodies by 4 times or more is considered diagnostic.

    The staphylococcal etiology of the disease is also confirmed by an increase in the titer of antistaphylolysin in the neutralization reaction.

    Express diagnostic methods: radioimmune, enzyme immunoassay and latex agglutination.

    Differential diagnosis of staphylococcal infection

    Differential diagnosis of staphylococcal infection is carried out with localized and generalized forms of purulent-inflammatory diseases of other etiologies. Clinical diagnosis without laboratory confirmation is almost impossible. Differential diagnosis of primary lesions of the gastrointestinal tract of staphylococcal etiology with other acute intestinal infections is presented in Table.

Contents of the article

Among the wide variety of clinical forms of staphylococcal infection, the most common is damage to the digestive tract. With this localization, it is customary to isolate a toxic infection, known since the last century. In the second half of this century, other forms were identified, mainly in the form of enterocolitis, enteritis, occurring mainly in young children.

Etiology of intestinal infection in children

The etiological origin is staphylococci, whose cultural and biochemical properties are approximately the same as those of staphylococcal diseases of other localizations. Some differences, even inconsistent ones, are noted in strains isolated during foodborne toxic infections (frequent formation of enterotoxin and greater stability in the external environment).
The epidemiological patterns are the same as for other intestinal infections, with some originality.

Pathogenesis and pathological anatomy of intestinal infection in children

In the pathogenesis of staphylococcal infection, which occurs in the form of foodborne toxic infection, the main role is played by a massive dose of infection. A huge number of staphylococci and their metabolic products immediately enter the body.
Enteritis and enterocolitis are observed mainly in young children. They may be primary. The entry gate is the gastrointestinal tract, where pathological processes develop. Along with this, secondary processes are distinguished that arise as a result of the penetration of staphylococcus into the intestines from other foci in the body. As a rule, children of early age, especially the first year of life, who are weakened by previous diseases, become ill. The anatomical and physiological characteristics of the gastrointestinal tract (slight vulnerability of the mucous membrane, insufficient motor, enzymatic activity and bactericidal activity of gastric juice, pancreatic secretions, bile, etc.), imperfection of the reticuloendothelial system, immaturity of the cerebral cortex, etc. are important.
In case of food toxic infection under the influence of staphylococci and their toxins, acute inflammatory changes occur, mainly in the small intestine. Necrosis of the epithelium occurs, sometimes of the deeper layers of the mucous membrane, infiltration of the mucous and submucosal membranes, mainly by lymphocytes, with severe circulatory disorders (plethora, stasis, minor hemorrhages). Lymph node hyperplasia usually occurs; in the parenchymal organs there is plethora, there may be protein and fatty degeneration. Despite the rapid course of the disease, changes usually reverse quickly, clinical manifestations last for several days, and deaths are rare.
In other forms of staphylococcal intestinal infection, changes occur less rapidly and last longer. Staphylococci multiply on the mucous membranes of the intestines and in the lymph nodes.
Enzymes secreted by staphylococcus (coagulase, fibrinolysin, hyaluronidase) contribute to the penetration of the pathogen into tissues and generalization of the process, especially in weakened children; Bacteremia is often detected, and septic thrombi appear in the capillaries.
Serous-desquamative, fibrinous-purulent necrotic changes in the mucous and submucosal membranes appear in the intestines, followed by the formation of ulcers. There is some parallelism between the prevalence and severity of morphological changes and the severity of clinical manifestations. With milder lesions, the process may be limited to catarrhal changes; as severity increases, fibrinous-necrotic ulcerative lesions appear, and there may be diphtheritic inflammation with fibrinous filmy overlays. Morphological changes are more frequent and more pronounced in the small intestine (enteritis), but they can also spread to the large intestine (enterocolitis). Ulcerative enteritis and enterocolitis can lead to perforation. In other organs, plethora, protein and fatty degeneration are determined.
From the local focus, a complex of toxins, enzymes and other waste products of staphylococcus enters the blood and central nervous system, resulting in intoxication phenomena. The latter is facilitated by the influence of pathological products of impaired metabolism.
Recovery occurs due to an increase in the level of specific antibodies, neurohumoral and tissue protective reactions with the direct participation of phagocytes. Of the specific antibodies, an increase in the titer of antihemolysin, antitoxin, agglutinins, antistaphylolysin, and antihyaluronidase was detected.
intestinal infection in children to staphylococcal infection is weak, short-lived, it is determined by antimicrobial antibodies; “antitoxic protection” is of some importance.

Clinic of intestinal infection in children

The clinic distinguishes forms that occur in the form of food toxic infection (gastroenteritis, gastroenterocolitis), enteritis, enterocolitis.
Food poisoning(acute gastroenteritis, gastroenterocolitis) occurs mainly in older children after a very short incubation period (3 - 5 hours or less).
Sharp pain in the epigastric region, repeated and even uncontrollable vomiting appear. The temperature is mostly high (39-40° C). In the very first hours, in the most severe cases, there may be convulsions, impaired consciousness, changes in cardiovascular activity - cyanosis, muffled, and then dull heart sounds, decreased blood pressure (maximum and minimum); Hemorrhages and various rashes may appear on the skin. The stool is usually copious, liquid, watery, may be cloudy, foul-smelling, sometimes mixed with mucus and isolated streaks of blood. Diarrhea may appear several hours after the onset of the disease and is usually preceded by vomiting. It is often possible to establish the simultaneous illness of several family members or even a group of people from the same group after eating the same food, which helps in diagnosis.
The further course with proper therapy is, as a rule, favorable, the symptoms of intoxication quickly pass, the temperature drops, vomiting stops, and after a day or two the patient’s well-being becomes satisfactory; Muffled heart sounds and diarrhea last for a long time. The stool returns to normal by the end of the first, less often the second, week.
Diseases that occur as foodborne toxic infections can be observed in young children. In extreme cases, the course is less favorable, a syndrome of toxic dyspepsia or acute enteritis occurs, when the stool becomes very profuse, foul-smelling, cloudy, and gray in color. Intestinal changes and elevated temperature last a long time (up to 2 weeks or more).
Staphylococcal enteritis, enterocolitis in young children both begin and proceed differently. It is possible either a primary staphylococcal process isolated primarily in the intestine, or a combined lesion of the intestine and inflammatory staphylococcal processes of another localization.
Diseases of the first group (isolated processes) are relatively benign. The onset can be either acute or gradual, often with preceding or simultaneous catarrhal symptoms of the upper respiratory tract. The temperature is moderately elevated; it can be normal or subfebrile. The stool is increased up to 3-4 times, less often up to 8-10, mainly with changes characteristic of enterocolitis. The stool is light, sometimes semi-thick, sometimes more liquid, with mucus, admixed with pus, and sometimes streaked with blood. The tongue is often coated, the abdomen is moderately swollen or unchanged; sometimes palpable
spleen. The symptoms of intoxication are insignificant: slightly decreased appetite, regurgitation, and sometimes vomiting. The process is lengthy, dragging on for weeks and even months, especially without appropriate treatment. There may be periods of improvement. Children become capricious, anemic, pale, lose weight, but usually there is no significant weight loss.
Staphylococcal enteritis, enterocolitis of the second group, which are part of a general generalized staphylococcal infection, are much more severe. They are characterized by severe and usually widespread morphological changes in the intestine (necrotic, ulcerative, fibrinous). The onset can be acute, with the occurrence of pneumonia, otitis media, and diarrhea. At the same time or 1-2 days earlier, catarrhal symptoms from the upper respiratory tract may be observed, most likely due to ARRI.
The onset of the disease may be more gradual, and in addition, in the form of an exacerbation, as if an “explosion”, with the addition of pneumonia, against the background of previous mild staphylococcal diarrhea.
The stool is increased up to 6-8-10 times, with mucus, and maybe some blood. In the most severe cases, symptoms of enteritis are expressed, indicating a widespread process involving the small intestine (loose, watery, foul-smelling stools). The abdomen is swollen, the tongue is coated; The size of the liver often increases slightly, and the spleen is often palpable. Intoxication is manifested by high fever, vomiting, cardiac dysfunction and other symptoms.
Recovery is slow, after the elimination of inflammatory foci. For 2-3 weeks, both constant and periodic low-grade fever is often observed. An admixture of mucus remains in the stool for a long time. The process often involves the bile ducts, where inflammatory changes are persistent.
In the peripheral blood, leukocytosis and neutrophilia with a shift to the left are noted. Elevated ESR is observed especially often and for a longer period of time. The criterion for recovery is the elimination of all these changes; the development of anemia is almost natural.
Staphylococcal intestinal processes as a result of exogenous infection often overlap with other diseases: measles, whooping cough, acute respiratory viral infection, as well as dysentery, coli infection, and sometimes dysbacteriosis.
The latter occurs in connection with the use of antibiotics for the underlying disease, which disrupts and destroys the “competitive” flora and creates favorable conditions for the growth and reproduction of staphylococci.

Diagnosis of intestinal infection in children

Diagnosis of intestinal infection of staphylococcal etiology, especially in patients of the first group, i.e. with isolated intestinal processes, is difficult. Severe colitis syndrome is similar to dysentery, but the presence of cloudy mucus and pus is more characteristic of staphylococcal lesions. Cultivation of pathogenic staphylococcus from feces is of decisive importance. Isolation of staphylococcus can be prolonged, which usually serves as evidence of an incomplete process. Bacteremia is often detected. It can be long-lasting - up to several weeks. A positive agglutination reaction with staphylococcus with an increasing titer of serum dilution is often noted. When breastfed children become ill, staphylococcus is often cultured from the breast milk of their mothers, often in high concentrations.
In case of death, all existing inflammatory foci and intestinal contents are subject to bacteriological examination.

Prognosis of intestinal infection in children

The outcome of intestinal infections of staphylococcal etiology depends on many factors. The age and condition of the patient are of primary importance. The highest mortality rate is observed in early infancy, in weakened children. The most unfavorable outcomes are with secondary, combined lesions and with delayed insufficient treatment. Correct, timely treatment using general restoratives and a sufficient amount of appropriate antibiotics significantly improves the prognosis.

Intestinal disorders due to viral infections

The question of the role of viruses in the etiology of acute intestinal diseases was raised back in the 20s of this century, but it has not yet been sufficiently studied. In the etiology of intestinal diseases, both enteroviruses Coxsackie, ECHO, and viruses of the respiratory group (adenoviruses, parainfluenza viruses) play a role. Diarrhea is most often observed with enteroviral and adenoviral infections.
Epidemiological patterns have not been sufficiently studied. It is known that the source of infection is patients and carriers. Many viruses (enteroviruses, adenoviruses) can be released into the external environment with feces; infection via the enteral route is very likely. The duration of virus isolation characterizes adenoviral infection, in which the virus is detected in feces for 3 weeks or more.
The frequency of acute intestinal diarrhea of ​​a viral nature has not been sufficiently studied. It is only known that otsi arise mainly at an early age, especially in the first months of life. Intestinal diarrhea can occur in sporadic cases or small epidemic outbreaks.
The pathogenesis is unclear. It is possible for enteroviruses and adenoviruses to multiply in the intestine, in the epithelium of the mucous membranes of the small intestine. In most children, diarrhea is part of a complex of pathological changes. The upper respiratory tract is most commonly affected. This is evidenced by catarrh of the upper respiratory tract due to viral diarrhea. Changes in the intestine are a consequence of direct damage to the mucous membrane.
Anatomical changes usually occur in the small intestine. They are characterized by degenerative damage to the epithelium of the mucous membrane, local mild circulatory disorders, increased permeability of the intestinal wall, as a result of which enzymatic and motor functions are impaired. The most common is enteritis or enterocolitis, usually of a focal nature, with similar changes in the intestinal lymphatic system. Macroscopically, only slight hyperemia of the mucous membrane and watery contents in the intestinal lumen are determined. Pathogenesis includes a general toxic effect on the body, a decrease in general and local immunity. All this, together with anatomical changes, contributes to the layering of microbial flora; a high frequency of virus-microbial associations in diarrhea is known. Along with this, associations of different viruses or different types of the same virus are identified.

Clinic of intestinal disorders of viral etiology

In the clinic of intestinal disorders due to viral infections, there is a wide variety. As a rule, the general features of the corresponding viral infection appear, to which diarrhea is added.
The latter can occur from the onset of the disease simultaneously with other changes, precede them, or be delayed by 1-2 days. The stool becomes more frequent, but usually not abruptly, becomes liquid, sometimes with an admixture of greenery, and not abundant.
With enterovirus infections, a small amount of mucus is often observed, and abdominal pain is not uncommon. Intestinal disorders usually progress favorably. In some cases, short-term relapses are observed. More pronounced changes in stool in the form of pus and a large amount of mucus, the duration of the changes indicate a microbial infection.
The phenomena of intoxication and other various changes during illness are determined by the characteristics of the corresponding viral infection, the characteristics of which are given in special chapters.

Diagnosis of intestinal disorders of viral etiology

The diagnosis is difficult and is established mainly on the basis of moderate and short-term intestinal disorders, mainly without colitis syndrome, in combination with catarrh of the upper respiratory tract. In all cases, in the dynamics of the disease, feces are cultured for a pathogenic microbial group to exclude the microbial etiology of intestinal infection - dysentery, coli infection, staphylococcal infection. Clarification of the viral nature of the disease is achieved using virological research methods.
The prognosis is usually favorable.
Treatment and preventive measures come down to general measures taken for intestinal infections.
Treatment is symptomatic and pathogenetic, depending on the entire complex of manifestations of the disease. There are no specific drugs. In more severe forms, it is necessary to promptly use antibiotics, keeping in mind the possibility of bacterial flora involvement.

Modern features of intestinal infections

All bacterial infections - dysentery, coli infection, salmonellosis, staphylococcal diarrhea - in the past were characterized by a high frequency of severe forms and significant mortality.
The cause of death in older children was severe forms of dysentery, in young children - complications and exacerbations with secondary metabolic toxicoses, progressive dystrophy due to a protracted course, against which pneumonia often developed. The share of severe forms among the causes of death accounted for about 20%, the share of exacerbations and secondary toxicoses accounted for approximately the same amount, and about 30% of patients died in the later stages of the disease from progressive dystrophy with a protracted course of the disease. Sometimes the cause of death was a mixed infection (Officerov V.N., 1946).
Dysentery in the past was caused by dysentery bacilli Grigoriev - Shiga. In the 30s they were supplanted by Flexner sticks, and now by Sonne sticks. The isolation of dysentery bacilli that cannot be typed has become more frequent. The most severe forms were caused by the Grigoriev-Shiga bacillus. Currently, the bulk of the disease is caused by mild forms of the disease. Clinical symptoms have changed. For example, in the past, in severe cases, bowel movements were very frequent - 20-60 times a day, and the duration of intestinal changes was 4-5 weeks (M. G. Danilevich). Now the stool is much less frequent, the amount of pathological impurities has decreased and the duration of dysfunction is often reduced to several days. Many erased forms with mild colitis syndrome and short-term dysfunction have appeared. There are almost no exacerbations of the process with secondary toxicosis, and chronic forms are rare; deaths in Leningrad have not been recorded for many years.
In recent years, in chronic forms of dysentery, prolonged bacterial excretion has been observed with scant clinical changes, mainly in the form of some lethargy, pallor, loss of appetite and loss of body weight. The stool is also slightly disturbed. It is often mushy or even shaped, with an inconsistent presence of mucus. During sigmoidoscopy, disturbances may be limited to only mild catarrhal changes in the mucous membrane of the colon; Disorders in the form of agrophic catarrhal-erosive processes are observed less frequently.
The clinical manifestations of coli infections have changed. The identification of enteropathogenic Escherichia coli became possible only after Kaufman developed a method for their serological typing.
With toxic dyspepsia, according to M. S. Maslov, mortality ranged from 49-73%. with subtoxic - within 25-33% (data for 1946). One might think that the staggeringly high mortality rate reported was largely due to coli infection. After the introduction of the EPKP typing method, already with an accurately established diagnosis of coli-infection caused by EPKP.
0-111, mortality in the 50s was much lower than the figures given, but still significant. In the 60s it decreased noticeably, but still persisted. In recent years, rare deaths in Leningrad are practically due to the presence of severe congenital defects due to layered coli infection.
Mild forms predominate, while severe forms are rare and are usually caused by mixed infection.
A similar situation can be stated with regard to salionellosis. An illustration is the decrease in mortality from 30-40% and even 50% in the 30-40s among infants to zero in recent years.
A high frequency of severe forms with high mortality was observed in patients with staphylococcal diarrhea even in the 50s. Recently, measures have been developed to combat them, but in a number of regions of the country the mortality rate is still 3-4%.
The reasons for the mitigation of historically extremely severe intestinal microbial infections are not entirely clear. Obvious reasons include the use of new treatment methods, the introduction of etiotropic therapy and the improvement of the hospitalization system.
In the past, in the case of dysentery, an important role was played by antitoxic antidysentery serum, which was prepared by immunizing horses with toxins of dysentery bacilli. This serum helped cope with toxic forms. A radical fracture occurred after the introduction of etiotropic. therapy, first in the form of sulfonamide drugs, and subsequently antibiotics, which made it possible to act directly on the pathogen. With timely use of etiotropic therapy, the local process, as a rule, quickly undergoes reverse development, and intoxication is also eliminated. Taking this into account, serum is not currently used in practice.
It is suggested that the use of etiotropic drugs over the past three decades has led to the loss or weakening of the pathogenic properties of dysentery bacilli (they even talk about their saprophytization), which was one of the reasons for changes in the clinical manifestations of dysentery. The development and widespread use in practice of nonspecific means of detoxification and increasing nonspecific reactivity were important.
Changes in the course of dysentery after the acute period, in addition to early exposure to dysentery bacilli with etiotropic drugs, were facilitated by the developed hospitalization system aimed at preventing new infections in hospitals. As a result, exacerbations, especially secondary toxicoses, are almost completely absent. All this taken together helped eliminate dystrophies in dysentery, as well as the formation of chronic forms.
There are no specific antitoxic drugs for the treatment of patients with coliform infection, salmonellosis, or staphylococcal diarrhea. The remaining provisions given in relation to dysentery remain relevant.

Differential diagnosis, treatment and prevention of acute intestinal infections

Differential diagnosis. Among acute intestinal infections, differential diagnosis must be made between dysentery, coli infection, salmonellosis, staphylococcal infection, and diarrhea due to viral infections. Their clinical differentiation is possible with the most pronounced manifestations of the disease. With mild forms, difficulties increase, and erased, atypical forms are often indistinguishable.
The main clinical and morphological syndromes of the listed intestinal infections are dyspepsia, enteritis, colitis, enterocolitis, gastroenteritis, gastroenterocolitis. When they occur, it should be taken into account that in the vast majority of cases they are of infectious origin. Along with this, it is necessary to resolve the question of whether they are the result of nutritional disorders.
Nutritional disorders in infants are predominantly simple dyspepsia syndrome. Typically, such disorders arise gradually, at normal temperatures, often as a result of improper feeding (overfeeding, violation of intervals, quality composition of food). Correction in nutrition in most cases quickly leads to improvement. In contrast, infections usually occur acutely and often occur with fever; Dietary restrictions do not provide immediate results. Epidemiological data can help in making a diagnosis: having contacts with relevant patients makes it easier to resolve the issue in favor of infections.
Parenteral disorders (in particular, parenteral dyspepsia in young children) resulting from functional disorders are extremely rare. Intestinal disorders with pneumonia, otitis, sepsis and other diseases are a consequence of direct damage to the intestines. Often they are staphylococcal or mixed microbial, microbial-viral in nature. Nutritional and parenteral disorders in older children are even more rare and, as a rule, are manifested by a short-term increase in frequency and dilution of stools.
Differential diagnosis within the group of intestinal infections between diseases of different etiologies is especially difficult at an early age, in the first year of life, in children with malnutrition. The difficulty increases with early etiotropic treatment: it can quickly smooth out the typical manifestations of infection. Dyspepsia syndrome is often caused by EPKP, so-called parenteral dyspepsia - mainly by staphylococcus. Enteritis, enterocolitis in young children can be caused by salmonella, staphylococcus, colitis is predominantly of a dysenteric nature. The clinical syndrome of the so-called foodborne toxic infection can be caused by dysentery bacilli, salmonella, and staphylococcus. In resolving the issue of its etiology, not only intestinal disorders, but also the whole complex of changes help.
In the differential diagnosis, dysentery must first be excluded. The basis for the diagnosis of dysentery is colitis syndrome. In typical forms of dysentery, stool is scanty, contains cloudy mucus, and streaks of blood may be observed. Defecation is painful, tenesmus is noted, and a spastically contracted sigmoid colon can be felt. Symptoms of intoxication - fever, vomiting - are observed at the very beginning of the disease. Stool disorders may be delayed and occur at the end of the first day or on the 2nd day. Pathological impurities in the stool may also be absent at first and appear later. Subsequently, on the 2nd, 3rd day of the disease, there is predominantly parallelism in the degree of intoxication and intestinal dysfunction. The higher the temperature, the more frequent the stool and the more pronounced the colitic, hemocolytic changes in it. In infants, colitis syndrome due to dysentery may be less pronounced than in older children. The stool is often fecal in nature and is quite copious; individual portions may be watery, but along with this there is mucus. Sometimes there are streaks of blood. In children, equivalents of tenesmus are observed in the form of restlessness, crying, redness of the face before and during bowel movements, and pliability or gaping of the anus. At this age, the abdomen is often swollen, and spasm of the sigmoid colon is not detected.
Coli infection, characterized by the syndrome of simple or toxic dyspepsia, is manifested by increased bowel movements. It is plentiful, watery, sometimes bright yellow, with undigested residues, often in the form of a chopped egg. There may be an admixture of mucus, but it is transparent and rather scanty. Blood streaks are observed in rare cases in one or two portions, in small quantities. Tenesmus and their equivalents, changes in the sigmoid colon are absent, the stomach is swollen. Fever with symptoms of toxicosis can last for several days; vomiting is persistent and prolonged.
Lethargy, adynamia, and severe pallor of the skin quickly develop. Coli infection caused by EPKP 0-124 does not differ in clinical symptoms from dysentery.
Salmonellosis is the most difficult for differential diagnosis due to the variety of clinical forms. Most children have a dysentery-like (colitis) form. The less severe severity of colitis syndrome and the symptoms of enteritis that often coexist with it help. In these cases, the stools contain an admixture of mucus, but they are abundant, do not lose their fecal character, are often foamy, sometimes green in the form of swamp mud, in contrast to the scanty mucous (muco-bloody) stools in dysentery. There are no other symptoms of colitis (tenesmus, spasm of the sigmoid colon). There are natural differences in the relationship between temperature and clinical changes. In salmonellosis, stool may be relatively infrequent at high temperatures, while in dysentery there is initially a parallelism between the frequency of stool and the degree of temperature rise. Both elevated temperature and other symptoms of intoxication with salmonellosis last longer (a week or more), while with dysentery the temperature drops to normal or becomes low-grade after 2-3 days from the onset of the disease. In approximately a quarter of patients with salmonellosis, the size of the liver and sometimes the spleen are enlarged, the abdomen is usually swollen, and the tongue is coated.
Dyspeptic forms of salmonellosis have to be differentiated mainly from coli infection, which is clinically difficult. Often present symptoms of enteritis help, sometimes an admixture of greenery (swamp mud) instead of the bright yellow color of stool during coli infection. TN forms occur predominantly in older children. They are easier to differentiate from dysentery, but are similar to typhoid paratyphoid diseases.
Staphylococcal enterocolitis often give rise to an erroneous diagnosis of dysentery. However, they often have symptoms of enteritis, indicating simultaneous damage to the small intestine. Feces, unlike dysentery, are more abundant and retain a fecal character; no tenesmus; the admixture of mucus is more scanty, the streaks of blood are rare and scanty. The temperature may become septic, and prolonged low-grade fever is noted. In more severe forms, there are often inflammatory foci outside the intestine (pneumonia, otitis media, etc.). With staphylococcal infection, changes in the peripheral blood are more pronounced (leukocytosis, neutrophilia with a shift to the left, and especially increased ESR), which are usually observed in mild forms of the disease.
Viral diarrhea occur with less severe colitis; with them there is no hemocolitis and other changes (tenesmus, gaping of the anus, etc.), and this distinguishes viral diarrhea from dysentery. In contrast to coli infection, stools are not as watery and less frequent. The color of stool mostly does not change, intestinal dysfunction is not pronounced. Characterized by an acute onset, fever and catarrh of the upper respiratory tract, against which intestinal dysfunction fades into the background. Vomiting is observed only with more severe intoxication, as well as loss of appetite and loss of body weight. There are no changes in the tongue or abdomen.
Dysentery, salmonellosis and staphylococcal infections that occur as a food poisoning in the first day, especially in the first hours, may “have many common symptoms that are extremely difficult to differentiate. Later, after 1-2 days, they acquire their characteristic differences. For dysentery, the greatest Symptoms of colitis are important. Rare pathogens of food poisoning can be representatives of enteropathogenic Escherichia coli and Proteus. Laboratory data play a decisive role in diagnosis in these cases.
Clinical differential diagnosis of erased forms, which are inherent in all intestinal infections, is difficult and often impossible. For all intestinal infections, epidemiological data must be taken into account. The occurrence of a disease in the focus of any infection known by etiology resolves the issue in its favor.
Mixed forms, i.e., diseases caused by different pathogens, present extreme difficulties for differential diagnosis. These diseases occur in a variety of combinations; each of the participants can cause changes inherent in it: nia. A frequent companion to coli infections and salmonellosis is staphylococcus. This contributes to the formation of more protracted forms, the occurrence of septic changes, prolonged elevated temperature, and the intensification or appearance of symptoms of enteritis. In patients with dysentery, suspicion of staphylococcal infection is caused by prolonged elevated temperature, low-grade fever, admixture of pus in feces, pronounced changes in white blood, significantly increased ESR, etc. Dysentery can occur in combination with salmonellosis. A wave of similar mixed infections was observed in the Soviet Union in the second half of the 40s - early 50s (M. G. Danilevich, V. M. Berman, E. M. Novgorodskaya, V. N. Chernikova, etc.). Such diseases are characterized by the spread of the pathological process to the upper parts of the intestine (the development of ileitis) and, as a consequence, the addition of enteritis symptoms to the dysentery colitis syndrome.
Mixed infections can occur from the onset of the disease as a result of simultaneous infection with different pathogens. Along with this, an additional infection may occur during illness as a result of subsequent infection. In the latter cases, diagnosis becomes easier. Acute changes develop against the background of improvement of the “first” infection and may have more defined clinical manifestations in accordance with the layered flora.
Mixed infections can be of a viral-microbial or mixed viral nature. The presence of ARRI is manifested by the characteristic clinical symptoms of catarrh of the upper respiratory tract, against the background of which severe complications often arise, especially from the lungs.
Amoebiasis found mainly in southern latitudes (the etiological role of amoebas was first established in 1875 by Lesh, St. Petersburg). Infection occurs as a result of ingestion of amoeba cysts in water or food. The main source of infection is humans. The disease is characterized by a protracted, fever-free course with symptoms of colitis, with typical features of stool in the form of raspberry jelly. Sigmoidoscopy reveals deep ulcers with overhanging edges. Eosinophilia is often detected in peripheral blood. The diagnosis is made laboratory - the presence of Entamoeba histolytica or its cysts.
Giardiasis. Giardia infestation among children is widespread, but their pathological significance has not been sufficiently studied. With giardiasis, the bile ducts are most often affected. Its etiological significance in the origin of intestinal dysfunctions, dysfunctions of a protracted, chronic nature has been questioned in recent years.
Nonspecific ulcerative colitis It usually begins gradually with vague symptoms such as weakness, bloating, and discomfort in the abdomen. The stool initially remains formed, but an admixture of fresh blood appears; subsequently, the stool becomes unstable, mushy, mixed with blood, pus, and sometimes mucus. The disease becomes persistent.
The therapeutic effect of antibiotics is completely absent. The patient has a fever, the size of the liver and spleen increases, anemia develops, and weight loss is noted. Sigmoidoscopy reveals pronounced vulnerability of the intestinal mucosa and erosive and ulcerative changes.
Secondary colitis, arising from measles, malaria and other diseases, in most cases of an infectious, mainly dysenteric nature, mainly of exogenous origin. Dyspepsia, developing against the background of pneumonia, sepsis, as a rule, is also of an infectious nature. It can be a manifestation of the main process (as, for example, in sepsis, pneumonia) due to the spread of inflammation to the intestinal tract, as well as an additional process caused by another etiological factor.
Symptoms similar to those of acute intestinal infection can be observed with intussusception, so such patients are often sent to infectious diseases hospitals. The cause of the error is frequent stools with mucus and blood. Intussusception is characterized by the sudden onset of acute, cramping pain in the abdomen, which is manifested by a sharp anxiety of the child, sometimes followed by calmness. In this case, the child, tired of the attack of pain, quickly falls asleep. At normal temperatures, the child secretes mucus, mostly glassy in nature, with drops of fresh blood, sometimes with a small amount of feces, which simulates diarrhea. On examination, some abdominal bloating is detected, sometimes the contours of a swollen intestine with reverse peristalsis and asymmetry of the abdomen are outlined. On palpation, in some cases a sausage-shaped tumor is determined. A digital examination of the rectum, if it is low, may reveal intussusception, and blood may be found on the finger after examination. In case of intussusception, urgent surgical intervention is indicated.
In some cases, based on vomiting and abdominal pain, an erroneous diagnosis of appendicitis is made and the patient is hospitalized in the surgical department, where it can become a source of infections. It is even more dangerous when, on the contrary, acute appendicitis is mistaken for dysentery, and surgical assistance is not provided and perforation and peritonitis can occur. The reason for the incorrect diagnosis is the presence in some cases of appendicitis of loose stools, sometimes with pathological impurities. For differentiation, the entire complex of symptoms characteristic of dysentery and the localization of pain in appendicitis, which is uncharacteristic of dysentery, are important.
In the diagnosis and differential diagnosis of intestinal infections, auxiliary methods are used: scatology, sigmoidoscopy, etc. The results of laboratory examination are of greatest importance.
Examination of patients using laboratory methods is necessary for any intestinal disease, regardless of the clinical diagnosis. In case of atypical, erased forms, it is used to establish a diagnosis, and in case of classical manifestations - to confirm it and to accurately identify the pathogen (species, serotype). Due to the diversity of etiology and the frequent presence of mixed forms, laboratory examination cannot be limited to the search for any one pathogen (only Shigella, only EPKP, etc.). Such an examination should be comprehensive, with the most frequent possible examination of not only stool, but also blood (cultures on appropriate media, immunological reactions).

Auxiliary methods for diagnosing intestinal infections

Sigmoidoscopy allows you to determine the condition of the distal colon: the nature of the pathological process, its dynamics. In healthy children, the mucous membrane of the colon is shiny, elastic, and pink. In infants, it is juicy, more brightly colored, and the vascular pattern and follicles are clearly visible on it. With colitis, the mucous membrane is hyperemic, bleeds easily, sometimes with hemorrhages and erosions; - there may be mucus deposits on the surface, and in more severe cases - ulcerations, swelling of the follicles. The changes are focal or diffuse in nature. Since the phenomena of colitis are most characteristic of dysentery, such changes indicate in favor of this infection. However, mild hyperemia of a diffuse or focal nature can be observed in colitic forms of intestinal infections and other etiologies.
Sigmoidoscopy is used not only for diagnostic purposes, but in some cases also to judge the dynamics of the process. Sigmoidoscopy is not performed on infants. In the acute period of the disease, it is contraindicated at all ages.
Scatological method, like sigmoidoscopy, is not specific, but as an auxiliary one it is of great value. It allows us to judge changes in the intestines, as well as the inflammatory process and motor and enzymatic activity. The study is carried out after processing several microscopic preparations of feces on a glass slide with different solutions and paints. Use Lugol's solution to identify starch and Giemsa stain. to differentiate neutrophils from lymphocytes. Methylene blue detects fatty acids, and sulfuric acid detects soaps. More often, coproscopy is used, in which native stool preparations are examined on a glass slide without any processing. In this case, mucus, leukocytes, red blood cells, and epithelial cells can be detected as evidence of inflammation in the colon. Pronounced changes indicate dysentery. At the same time, a small amount of mucus, leukocytes and even red blood cells can be observed in other etiological forms. A significant amount of neutral fat is a sign of changes mainly in the small intestine and, as a consequence, dysfunction of the digestive system “associated with pancreatic insufficiency, characteristic of dyspepsia syndrome, therefore, mainly coli-infection. There may be undigested food remains, a large amount of detritus as a manifestation of enteritis, increased secretory function of the small intestine. Using coproscopy, in addition, you can identify protozoa (giardia, balantidia), yeast cells, fungal mycelium, worm eggs, etc.
Skin test(Tsuverkalov test) can only help in diagnosing dysentery. It is carried out with dysenterin (allergen), prepared by hydrolysis of the dysentery microbes Flexner and Sonne. 0.1 ml of dysenterine is injected intradermally. The reaction is taken into account after 24 hours. It is considered positive when not only hyperemia, but also papules with a diameter of at least 1 cm2 appear at the site of dysenterin administration. A positive reaction, depending on the size of the papule, is assessed as weak (papule diameter from 1 to 1.9 cm), medium (diameter from 2 to 2.9 cm) and strong (diameter more than 3 cm). If the results are positive, the reaction appears from the 4-6th day of illness. It reaches its maximum intensity in the 2-3rd week and, upon recovery, subsides on the 30-40th day of illness. With dysentery in children over one year of age, it is positive in 80% of cases or more, but in 20% of cases the reaction becomes positive in other intestinal infections (E.I. Kopkova). The diagnosis of dysentery cannot be made on the basis of a skin test alone, and if the diagnosis is confirmed using other methods, the need for it disappears, so the skin test is not very important.
Hematological changes in diagnosis are of very relative importance. With salmonellosis and coli infections in the acute period, a tendency to leukopenia, neutrophilia with a shift to the left, and aneosinophilia with a slight increase in ESR are more often detected. However, leukocytosis is often observed, as with dysentery.

Specific diagnosis of intestinal infections in children

Bacteriological research. For all intestinal diseases, feces are examined, and for diseases that occur as foodborne toxic infections, vomit, gastric lavage, and blood are examined.
When examining stool, the best results are obtained in the early stages of the disease, before chemotherapy. With repeated multiple studies for 2 - 3 days in a row, trotting ability increases. For research, the most altered particles of fresh feces (mucus, streaks of blood, pus) are selected. Stool can be collected directly from the rectum with a cotton swab or glass tube. There is a Ziemann tube with a diameter of 5 mm specially proposed for this with a sealed end and two side holes. Sowing is done immediately. If this is not possible, the material is placed in a 30% glycerin mixture with an isotonic sodium chloride solution and delivered to the laboratory as quickly as possible.
For all intestinal infections (dysentery, coli infection, salmonellosis) solid media are used. To isolate E. coli, Endo and Levin media are used; for dysentery bacilli, the best is Ploskirev's medium (baktoagar Zh), which inhibits the growth of E. coli, thereby increasing the inoculation rate of dysentery bacilli. For targeted testing for the presence of Salmonella, Muller and Kaufman enrichment media containing tetrathione sodium are used. They inhibit the growth of E. coli, which promotes better growth of salmonella. Staphylococci grow best on blood agar. Further clarification of the type, serological type of dysentery bacilli, E. coli, and salmonella is carried out in an agglutination reaction of the isolated culture with monoreceptor, specially prepared sera, on a glass slide. It can also be carried out by biochemical characterization according to the Hiss color series using a number of sugars - lactose, sucrose, mannitol, etc. This method is more cumbersome and is almost never used in practice; Phagotyping is also used for Salmonella.
The use of special media for the most complete detection of dysentery, E. coli, salmonella, and staphylococci during a comprehensive examination of patients is quite cumbersome and must be performed by qualified specialists in a sufficiently equipped laboratory.

The presence of the pathogen in feces, vomit, and gastric lavage for all microbial intestinal infections is crucial for the diagnosis. Negative results are considered taking into account the conditions in which the examination was carried out. The worst results of bacteriological examination are obtained when there is a long interval from the collection of stools to their inoculation on the medium, especially if they were in a warm room, when using poor-quality media, when examining the patient 2 - 3 days after the start of chemotherapy treatment. The patient must be examined many times.
Blood cultures necessary when a disease occurs that occurs as a foodborne toxic infection. With salmonellosis and staphylococcal infections, bacteremia is often observed. It is often found in other clinical forms of these infections. Blood taken from a vein is simultaneously inoculated into 10-20% bile broth and sugar broth. The broth is placed in a thermostat; with the growth of microbes, after 2 - 3 days it becomes cloudy. It is used to inoculate on solid media for subsequent identification of the pathogen using conventional methods for determining their type and serotype.
Bacteriological examination of stool takes about 3-4 days, and blood - about a week, so the desire to create accelerated methods is natural. In recent decades, for all intestinal infections, the immunofluorescence method, based on the use of specific sera treated with fluorescent dyes, has been successfully used to study stool. In the presence of microbes corresponding to the serum, an antigen-antibody complex is formed, which gives a glow visible under fluorescent microscopy. This rapid diagnostic method is highly sensitive and allows you to get an answer within 2-3 hours.
In case of death, to make an accurate diagnosis, cultures of blood, bile, contents of all parts of the intestine, material from inflammatory foci, as well as from lymph nodes, spleen, and liver are done. In recent years, organ examination using the fluorescence method has been added to this.
Specific methods are not limited to those listed. For diagnosis, an accelerated method is proposed based on the reaction of increasing phage titer in feces (dysentery, salmonellosis), isolation of dysentery bacilli in the carbon agglutination reaction (CAA), etc.
Serological study carried out mainly in an agglutination reaction according to the Widal reaction type. An appropriate microbial culture is used as an antigen.
Antibodies are determined in the patient's blood serum. There are ready-made diagnostics from killed cultures, but the best results are obtained when using live cultures. In some cases, autostrains are used. Agglutinins appear at the end of the 1st week or 2nd week of illness. They reach maximum titers by the end of the 2nd or 3rd week of illness. The presence of agglutination in the reaction at the serum dilution titer is considered diagnostic
1:100 or more. The most reliable increase in serum dilution titer is observed over the course of the disease. It can be quite significant - up to 1:800 or more. The value of the agglutination reaction for the diagnosis of salmonellosis is undeniable; it is also quite widely used in the diagnosis of dysentery. Positive results for dysentery are noted in 60 - 80% of cases, which provides very significant help. However, E.M. Novgorodskaya points out that in dysentery this reaction is nonspecific and its suitability is limited.
The assessment of the agglutination reaction in patients with coli-infection is controversial. This reaction has very limited use, mainly in specialized laboratories for the scientific study of this infection. In case of coli infection, an agglutination reaction is performed with museum culture and with autostrains. Some authors observed positive results in 60-85% of cases (N.I. Nisevich, B.G. Shirvindt, V.P. Davydov, etc.), others - in a very small percentage of cases and in low titers (G.A. Timofeeva, N. A. Yanshina, etc.). The agglutination reaction gives better results with a heated culture of EPPC, and is more often positive in more severe forms. The increase in titer in the dynamics of the disease, in most cases after the 10th day of illness, is of diagnostic importance.
In recent years, RNGA has increasingly come into practice, which is based on the fact that erythrocytes adsorb bacterial antigens and at the same time acquire the ability to agglutinate with serum containing the corresponding antibodies. RNGA is more sensitive than the agglutination reaction. It becomes positive in the earlier stages of the disease (from the first week of the disease), its intensity increases in the 2nd week, and in the 2nd month it begins to gradually decrease. The value of RNGA for dysentery is confirmed by M. E. Sukhareva et al. They consider the titer starting at 1:40 to be a diagnostic titer. For coli infection N.I. Nisevich determines the diagnostic titer to be 1:80 or more.
The use of antimicrobial therapy (antibiotics) in children can lead to a later and less intense increase in agglutinin levels.
Specific diagnostic methods for viral infections include virus isolation and detection of immunological reactions.
The most correct is a comprehensive examination of patients using bacteriological and serological examination. Such examination should be continued when any pathogen is isolated to identify the possible presence of mixed infections, which are very common, especially in severe forms of the disease. Accurate establishment of the etiology of intestinal infections is necessary for choosing a treatment method, proper placement of patients in a hospital, carrying out anti-epidemic measures and, finally, for their scientific study.
The diagnosis of salmonellosis, coli infection, staphylococcal intestinal infection, viral infection in sporadic diseases is allowed only in case of laboratory confirmation (seeding of the pathogen or the presence of specific immune bodies). The diagnosis of dysentery can be made on the basis of clinical data and a negative laboratory test result.

Treatment of intestinal infections in children

Treatment of patients with intestinal infections of different etiologies is based on general principles. The differences relate mainly to etiotropic drugs, which are used to directly influence the pathogen. The most important conditions for successful treatment are the correct regimen, care, and diet.
Hospitalization. Patients with acute gastrointestinal infections are subject to hospitalization. Treatment at home is allowed as an exception only for mild forms, subject to the provision of full medical care and isolation in strict compliance with the sanitary-epidemiological regime with systematic ongoing disinfection under the supervision of an epidemiologist.
The main causes of nosocomial infections are:
1) polymorphism in the etiological structure;
2) the prevalence of clinically similar forms in infections of different etiologies;
3) weakness, late formation and strict specificity of immunity in relation to the type, type of pathogen that caused the disease;
4) frequent combination of forms mixed in etiology;
5) pronounced contagiousness. Therefore, the system of hospitalization of patients with intestinal infections includes a differentiated distribution of patients and strict adherence to anti-epidemic rules. In hospitals, a diagnostic department (wards) is organized to accommodate patients with an unclear diagnosis and departments of different profiles (for patients with dysentery, patients with coli-infection, etc.) with separate services.
The diagnostic department (wards) should be served by the most qualified personnel who observe preventive measures. It is necessary to provide sufficient space for the patient, separation with the help of screens, half-boxes, and assign care items to the child. It is more correct to place infants in boxes until the diagnosis is clarified.
The distribution of patients begins from the emergency department. All children with an unclear diagnosis are placed in the diagnostic department, and with clinically pronounced symptoms of dysentery - in the emergency room of the dysentery department. From the diagnostic department (ward), as the diagnosis is clarified, patients are transferred to the appropriate departments, depending on the causative agent of the infection. From the reception ward of the dysentery department, from the diagnostic department, when sowing dysentery bacilli, enteropathogenic E. coli, etc., patients are grouped according to the type of pathogen; patients in whom the pathogen cannot be identified are placed in a special ward separately. In addition, bacteria carriers without clinical manifestations of the disease are placed separately. All these patients, placed in departments and wards, are served by qualified personnel.
Hospitals also organize convalescent departments, where children who have had dysentery are placed for a period of 2 weeks to 1 month to determine the stability of their recovery and confirm epidemiological safety through additional bacteriological examinations.
In addition to protecting the patient from contracting intestinal infections, CVD is prevented by isolating children when symptoms of these diseases appear.
Diet are prescribed taking into account the form of the disease and age. In case of intoxication in infants, nutrition is based on a scheme developed in the past for patients with toxic dyspepsia.
A water diet is prescribed for a period of 12 to 24 hours, depending on the degree of intoxication (the amount of liquid is about 150 ml per 1 kg of body weight). Subsequently, dosed feeding of expressed breast milk is prescribed, 10 ml 10 times a day every 2 hours. The amount of food that is missing due to age is compensated for with liquid. Drinks are prescribed in the form of tea, Ringer's solutions, and glucose. A carrot mixture rich in potassium and calcium salts and vitamins is very useful. In subsequent days, as detoxification progresses, the amount of milk is increased to 500-1000 ml per day. By the end of the 4-5th day, the baby can be attached to the breast for 5 minutes 1-2 times a day and in the following days gradually transferred to regular breastfeeding 6-7 times a day. In the absence of breast milk, it is replaced with kefir of age-appropriate dilution.
This scheme may change depending on the patient’s condition, and with the rapid elimination of intoxication, the amount of milk before transferring to normal feeding is increased more quickly. In case of mild intoxication, the duration of the water diet is reduced to 6 hours; complementary foods are stopped for 1-2 days and then normal food is introduced.
In older children with toxic forms, the same water break is carried out, usually for 6-12 hours, rarely for 24 hours. After it, a predominantly milk-based diet is introduced, but with the exception of whole milk: porridge, soups, jelly, kefir, yogurt, vegetable purees, pureed meat, cottage cheese, etc. After a few days, the child is transferred to normal food.
In mild forms of intestinal infections and mild intestinal dysfunction, normal nutrition is prescribed according to the patient’s age, with only some restrictions in the first few days. Milk is replaced with kefir, yogurt, and dishes containing large amounts of fiber and fat are excluded. At any age, it is important to introduce foods rich in protein (cottage cheese, cheeses, meat, eggs) and vitamins into the diet.
During exacerbations of the process, the diet is the same as at the beginning of the disease, depending on the nature of the exacerbation and the presence of intoxication.
In prolonged, chronic forms, the patient is given food that is complete in terms of calories and quality composition with an increased amount of protein (up to 3.5 - 4 g per 1 kg of body weight) and vitamins (vegetables, fruits, berry juices, yeast). In these cases, it is especially important to individualize nutrition based on the child’s appetite and body weight.
Measures to influence the pathogen. For all microbial intestinal infections - dysentery, coli infections, salmonellosis, staphylococcal diarrhea - etiotropic drugs are used - chemotherapy drugs. They are necessary for almost every patient for two reasons:
1) to more quickly eliminate the pathological process in the patient;
2) in the interests of others to more quickly eliminate the source of infection.
Sulfonamides, used since 1940 to treat dysentery, have played a major role in reducing mortality from this disease. Gradually, the effectiveness of these drugs decreased due to the emergence of resistance to dysentery bacilli. Currently, sulfonamide drugs (norsulfazole, phthalazole, sulgin, etazol, etc.) are prescribed mainly to older children and for mild forms of the disease, and for more severe forms, only in combination with antibiotics, at the rate of 0.2 g per 1 kg of body weight (daily dose), and for older children - 0.5-1 g.
The daily dose is divided into 4 doses. The drug is given at the indicated dose for 7-8 days. If there is no effect, sulfonamides are replaced with antibiotics.
Antibiotics are necessary for all patients of early age, and at an older age with severe clinical phenomena at the earliest possible date. The first antibiotic used for dysentery was syntomycin, then it was replaced by chloramphenicol, which remains effective in many patients to this day (0.01 mg/kg body weight). Streptomycin was widely used. Subsequently, tetracycline drugs gained recognition, but they are gradually losing their importance due to the frequent resistance of dysentery bacilli to them.
Currently, preference is given to monomycin, to which dysentery bacilli remain sensitive (50 - 75 mg/kg per day orally in 4 divided doses). Ampicillin is used: for children under 1 year - 100 mg/kg; from 1 year to 4 years - 100-150 mg/kg, over 4 years - 1-2 g per day, nitrofuran preparations. If vomiting is frequent, antibiotics can be administered rectally in the first days through a thin catheter in one and a half to double doses in the form of an emulsion in warm fish oil. Antibiotics usually quickly have a therapeutic effect; if there is no improvement, a change in drug is necessary after 1-2 days. The course of treatment is 5-7 days. Repeated courses are carried out during exacerbations of the process.
Mild and many moderate forms are often treated with diet and one course of antibiotics. Concomitant diseases and exacerbations delay recovery and require appropriate treatment. For more severe moderate forms, especially for severe forms, a combination of antibiotics and appropriate anti-intoxication measures are required (given below).
For coli infection a more pronounced therapeutic effect is exerted by drugs of the neomycin series: neomycin, kanamycin (50 mg/kg per day), monomycin (10-25 mg/kg per day).
The course of treatment is also 5-7 days. If there is no effect, ampicillin can be used.
With mild forms of coli infection, as well as with dysentery, you can limit yourself only to diet and a course of antibiotics.
Patients with moderate and severe forms, especially with septic symptoms, in addition to the indicated antibiotics, are prescribed oletethrin, oleandomycin, gentamicin sulfate, ampicillin are administered intramuscularly; use nitrafuran drugs (furazolidone, furadonin).
For salmonellosis the most effective are chloramphenicol, then ampicillin, polymyxins, gentamicin, and nevigramon. The course of treatment is 5-7 days, but for salmonellosis it is often not enough; in the absence of clinical improvement or a protracted process, repeated 2-3 courses with a change in antibiotic are necessary. For more severe moderate and severe forms, a combination of two antibiotics and the use of detoxification measures according to appropriate indications are necessary.
For the treatment of staphylococcal intestinal infections, broad-spectrum tetracycline antibiotics are recommended: tetraolean, oletethrin. Penicillin is used only in large doses - from 100,000 to 300,000 units or more per 1 kg of body weight. In severe forms, when intestinal damage is one of the signs of a generalized staphylococcal infection, a combination of two, sometimes three antibiotics is necessary. The use of semi-synthetic penicillin preparations is very useful: oxacillin, ampicillin, etc. Similar tactics should be used in the event of inflammatory processes (pneumonia, otitis and other septic processes) in children suffering from any intestinal infection.
To specific means refers to staphylococcal toxoid, used to activate immunological processes - subcutaneously in a gradually increasing dose (0.1; 0.2; 0.4 ml), but its positive effect is not entirely convincing. Immune drugs include specific -γ-globulin and plasma.
Phages that were used for dysentery also have an effect on the pathogen. However, the effectiveness of phage therapy is low, and gradually, as sulfonamides and then antibiotics were introduced into practice, phages were no longer used. In recent years, work has been carried out to improve phages. The main reason was the search for means to influence the long-term bacterial release of pathogens resistant to existing chemotherapy drugs, which are often observed in children after dysentery.
There are no measures to control the causative agent of viral intestinal infections. With more pronounced lesions, microbial flora is usually involved, so it is necessary to additionally prescribe antimicrobial drugs.
Antibiotics Providing a bacteriostatic effect on pathogens of intestinal infections, it also promotes detoxification. However, in some cases other means are required.
Detoxification measures for different intestinal infections are almost the same. In these cases, a 20% glucose solution (20-30 ml), a 10% calcium gluconate solution (2-5 ml) is injected intravenously. In more severe cases, plasma (50-100 ml), blood-substituting synthetic colloidal low-molecular drugs: neocompensan, polyvinylpyrrolidone, etc. (10 - 15 ml/kg per day) are administered. Corticosteroids are indicated (prednisolone 1-3 mg/kg per day) with a rapid reduction in the initial dose and a total course duration of 5-7 days; potassium salts are prescribed at the same time. Sufficient urine separation is important, so Lasix and mannitol are used.
If there is a tendency to hyperthermia, lytic mixtures are administered (4% amidopyrine solution 0.5 ml/kg, 50% analgin solution 0.1 ml per year of life), for convulsions - aminazine and pipolfen (2.5% solution 1 ml), sulfate magnesium (25% 1 ml per year of life), a lumbar puncture is performed. An ice pack is placed over the child's head and humidified oxygen is given.
The tactics are similar for intestinal infections that occur in the form of foodborne toxic infections. In these cases, gastric lavage with a 2% sodium bicarbonate solution is also very useful.
In young children, metabolic disorders with the development of exicosis become of great importance in the pathogenesis of intoxication. In such cases, it is necessary to administer large amounts of fluid. Depending on the degree of intoxication and the degree of exicosis, intravenous infusions are continued from several hours to 2-3 days. Infants are administered up to 150 ml/kg of liquid, older children = 60-80 ml/kg. Use 5% glucose solution, Ringer's solution. For children in the first months of life, their ratio should not exceed 1:1. at older ages, with water-deficient exicosis, glucose should predominate (in a ratio of 2:1 or 3:1), and with salt-deficient exicosis, these ratios should be inverse (1:2 and 1:3). For intravenous drip infusions, Darrow liquid, isotonic sodium chloride solution and the same low-molecular drugs are used: neocompensan, polyvinylpyrrolidone, etc. They are administered at the rate of 10-15 ml/kg per day. To this add 50-100 ml of plasma. During drip infusions, antibiotics are added to the mixture. When vomiting, gastric lavage is useful. For children with severe intestinal infections, a 10-20% solution of serum albumin is indicated; One or two intravenous drips of 1-2% serum polyglobulin are used. In all cases, according to indications, cardiac drugs (strophanthin, korglykon) are used.
Patients with intestinal infections need vitamins, especially when treated with antibiotics; prescribe ascorbic acid, B vitamins, primarily B, and B;. In more severe forms, vitamins are administered parenterally; ascorbic acid is administered intravenously along with solutions.
To reduce pain and tenesmus, heating pads, ozokerite and paraffin applications are used on the abdominal area.
In case of a protracted process, enzymes are indicated: gastric juice, pepsin, pancreatin, festal, panzinorm, etc. In addition, it is necessary to identify concomitant pathological conditions for appropriate treatment; aimed at eliminating them (rickets, anemia, etc.). In case of infestation by helminths and protozoa, it is also necessary to carry out treatment, but after the elimination of acute manifestations of the underlying disease. The cause of a protracted process, especially at an early age, may be dysbacteriosis. To eliminate it, biological products are used: bifidum-bacterin, lactobacterin, bificol, etc.
For protracted chronic forms of dysentery, V. L. Troitsky’s vaccine was proposed to stimulate specific body defenses

Staphylococcal enterocolitis The disease mainly affects young children, especially premature babies and children with an unfavorable premorbid background, who have reduced specific immunological protection against staphylococcus and at the same time protective barriers (skin, mucous membranes) are easily permeable to infection. Children with hereditary immunodeficiency conditions are especially susceptible to the disease.
The onset of the disease is gradual. The course is long. There are primary and secondary staphylococcal enterocolitis.

Primary enterocolitis develops against the background of complete health after contact with patients with purulent diseases or food poisoning. Secondary enterocolitis develops much more often against the background of various diseases (acute respiratory infections, pneumonia, dysentery) as a result of exogenous or endogenous staphylococcal infection, as a result of dysbacteriosis (with a long course of the underlying disease and the use of antibiotics), as well as with generalized forms of staphylococcal infection (sepsis , pyoderma, staphylococcal pneumonia).
In the mechanism of development of secondary staphylococcal enterocolitis, importance is attached to allergic conditions of the body.

Pathoanatomical changes in enterocolitis may be widespread or limited. The inflammation is serous-desquamative, fibrinous-purulent or necrotic in nature. Necrosis of the mucous membrane can spread to the serous layer, with the formation of deep ulcers with purulent infiltration. bottom and edges with a large number of microbial colonies. Blood clots may be found in the vessels of the mesentery against the background of circulatory disorders.
In some cases inflammation has a widespread hemorrhagic-necrotic character with massive leukocyte infiltration.

Rare cases have been observed staphylococcal pseudomembranous enterocolitis. Its pathogenesis is not clear: it is characterized by the development of superficial necrosis of the mucous membrane and the formation of a membrane from the dead part of the mucous membrane, permeated with fibrin, mucus, leukocytes and bacteria.

For staphylococcal enterocolitis complications are possible in the form of perforation of the intestinal wall, the development of fibrinous-purulent-fecal peritonitis, and the development of staphylococcal sepsis. Death occurs from complications or toxicosis.

Intestinal coli infection

In the etiology and epidemiology of intestinal coli infections, pathogenic strains of Escherichia coli 0III-B4, 055-B5, 026-B6, 0145 are important. They differ from non-pathogenic strains of Escherichia coli in their antigenic structure (somatic antigen O, surface antigen K with subgroups A and B, and flagellar antigen B ).

Intestinal coli infection- a disease predominantly in children of the 1st year of life, especially newborns and premature infants, who have a high susceptibility to this infection. Changed protective properties of the child’s body and a decrease in its resistance are of primary importance for the development and severity of intestinal coli infection.
Infection occurs from patients and convalescents through contact, through water and milk.

Possible autoinfection autoinfection. The pathogenesis of intestinal coli infection has not been sufficiently studied. It is believed that the main condition for the development of the disease is the migration of E. coli to the upper parts of the gastrointestinal tract, where it does not normally live. In newborns, especially premature ones, this is favored by age-related features - reduced acidity and bactericidal properties of gastric juice, high permeability of the intestinal epithelial barrier and the endothelial barrier of capillaries.

As a rule, in sick babies with this disease, against the background of pronounced intoxication, the body temperature rises, and the number of bowel movements increases to 10-15 times a day. The stool in children with staphylococcal enterocolitis is liquid and contains blood and mucus.

Causes and signs of enterocolitis in newborns

Diseases of the digestive tract in children in the first months of life caused by pathogenic staphylococci, unfortunately, tend to spread.

This is facilitated by the high adaptability of staphylococci to environmental conditions, their rapid adaptation to widely used antibiotics, as well as their increasing toxicity.

Staphylococcal enterocolitis in infants can be primary when the pathogen enters the child’s digestive tract with the milk of a mother suffering from mastitis, with contaminated milk formula, from family members or staff of the maternity hospital or hospital with pustular diseases.

In other cases, an intestinal disorder develops in a child suffering from pneumonia, otitis media, purulent inflammation of the umbilical wound, or pyoderma as a complication of the underlying disease. In older adults, the cause of enterocolitis may be dysbacteriosis, which requires long-term treatment with antibiotics.

The most common cause of enterocolitis in newborns is Staphylococcus aureus, which owes its beautiful name to the golden pigment secreted by the pathogen.

Staphylococci affect children with weakened immune systems, with allergies to staphylococcal antigens, and with disturbed intestinal flora. By multiplying in the digestive tract, microorganisms release a toxin that leads to intestinal disorders. Symptoms of enterocolitis in children are vomiting, bloating, loose stools up to 15 times a day - yellow, watery, with mucus, greens, sometimes streaked with blood.

The disease can occur in a mild form, when the baby’s condition practically does not suffer, only loose stools with greens and mucus 5-6 times a day remind of trouble.

In severe cases, there is an increase in temperature to 38 ° C, and repeated vomiting and frequent loose stools quickly lead to dehydration.

Children of the first half of the year who are on early mixed or artificial feeding are most often exposed to staphylococcal aggression, with accompanying malnutrition.

There are often indications of intrauterine infection and a long anhydrous period during childbirth. A significant proportion of infants upon discharge from the maternity hospital experience pustules on the skin and purulent discharge from the umbilical wound. In this case, signs of enterocolitis in children may appear already in the first month of life.

In some families, both the first and subsequent children suffer from staphylococcal infection. Along with the above reasons, it is worth thinking about the carriage of pathogenic staphylococci among family members and close relatives, as well as compliance with the sanitary and hygienic regime in the family.

Treatment and diet for enterocolitis in children

Having identified the symptoms of staphylococcal enterocolitis in children, treatment is carried out in a specialized department, since the deterioration of the sick child’s condition can occur catastrophically quickly and require intensive care. Only there the child will receive comprehensive treatment, taking into account the severity and phase of the infectious process, condition and the presence of concomitant diseases.

Modern medicine has drugs that can fight toxicosis, dehydration, impaired metabolic processes, and also directly influence staphylococci with specific drugs - antistaphylococcal gamma globulin and plasma, staphylococcal bacteriophage. Toxoid and antifagin are also recommended for the treatment of enterocolitis in children.

Of great importance in the treatment of children with enterocolitis is the diet, which is prescribed taking into account age, severity of the condition, stage of the disease and the nature of feeding before the disease. Food number one is breast milk, which is given on the first day in expressed form, 10-20 ml every 2 hours, 10 times a day. The rest of the food is replenished with glucose-salt solutions, tea, and drinking water. The amount of food administered is increased carefully, by 100-150 ml every next day. You can apply the baby to the breast on the 3-4th day for 5-7 minutes, continuing to give a sufficient amount of liquid.

In the absence of breast milk, preference is given to fermented milk mixtures fermented with bifidobacteria, which displace pathogenic flora from the intestines.

In case of intestinal disorders, the absorption and synthesis of vitamins (groups B, K, PP) is impaired, therefore, from the first days of the disease, the child should receive various vitamins

A decrease in the activity of one’s own digestive enzymes requires outside help in the form of taking enzymatic preparations: festal, enzistal, pancreatin, panzinorm, etc.

In the prevention of staphylococcal diseases in young children, maintaining breastfeeding, rational use of antibiotics, increasing immunity, preventing and early treatment of dysbacteriosis, as well as strict adherence to a hygienic regime are of great importance.

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Staphylococcal enterocolitis can be primary when the pathogen enters the child’s digestive tract with the milk of a mother suffering from mastitis, with contaminated milk formula, from family members or staff of a maternity hospital or hospital with pustular diseases.

Intrauterine infection is not uncommon. A significant proportion of these children, upon discharge from the maternity hospital, have pustules on the skin, purulent discharge from the umbilical wound, and staphylococcal enterocolitis occurs already in the first month of life.

Intestinal disorder as a complication of the underlying disease can occur in a child suffering from pneumonia, otitis media, purulent inflammation of the umbilical wound, or pyoderma. In older children, long-term antibiotic treatment may contribute to the development of the disease.

In some families, both the first and subsequent children suffer from staphylococcal infections. That's why

It is worth thinking about family members and close relatives who are carriers of pathogenic staphylococci and tightening the sanitary and hygienic regime in the family.

Most often, the cause of the disease is Staphylococcus aureus, which owes its beautiful name to the golden pigment secreted by the pathogen. Staphylococci affect children with weakened immune systems, with allergies to staphylococcal antigens, and with disturbed intestinal flora.

By multiplying in the digestive tract, microorganisms secrete a toxin that leads to intestinal disorders: regurgitation, vomiting, bloating, loose stools up to 15 times a day - yellow, watery, with mucus, greens, sometimes streaked with blood. The disease can also occur in a mild form, when the child’s general condition is satisfactory, and only loose stools with greens and mucus 5-6 times a day indicate trouble. In severe cases, the temperature rises to 38 o C, and repeated vomiting and frequent loose stools quickly lead to dehydration.

Children most often exposed to staphylococcal aggression in the first six months of life are on early mixed or artificial feeding with accompanying rickets, anemia, and malnutrition.

Staphylococcal enterocolitis in a newborn and a child in the first months of life is treated in a specialized department of the hospital, since the deterioration of the condition can occur catastrophically quickly and require intensive care.

Modern medicine has drugs that can fight toxicosis, dehydration, and metabolic disorders; there are specific drugs that directly affect staphylococci: antistaphylococcal gamma globulin and plasma, staphylococcal bacteriophage, toxoid, antiphagin.

Particular attention should be paid to the child’s nutrition, which the doctor recommends, taking into account the age, severity of the condition, stage of the disease and the nature of feeding before the disease. The most important and necessary food is breast milk, which is given in expressed form on the first day, 10-20 ml every two hours, 10 times a day. The rest of the food is replenished with glucose-salt solutions, tea, and drinking water. The amount of food is increased carefully, by 100-150 ml every next day. You can put the baby to the breast on the 3rd-4th day for 5-7 minutes, continuing to give liquid in addition to milk. In the absence of breast milk, give preference to fermented milk mixtures fermented with bifidobacteria, which will displace pathogenic flora from the intestines.

In case of intestinal disorders, the absorption and synthesis of vitamins (groups B, K, PP) is impaired; therefore, from the very first days of the disease, the child should receive various vitamins.

A decrease in the activity of one’s own digestive enzymes requires outside help in the form of taking enzymatic preparations: festal, enzistal, pancreatin, panzinorm.

To prevent staphylococcal diseases, it is important to breastfeed the child for as long as possible, use antibiotics rationally and only after consultation with a pediatrician, promptly treat dysbacteriosis, and strictly observe a hygienic regime.

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