Streptococcal pathogenesis. Streptococcal infection: causes, signs, diagnosis, how to treat

Enzymatic properties. Streptococci have saccharolytic properties. They expand glucose, lactose, sucrose, beckon (not always) and maltose to form acid. Their proteolytic properties are poorly expressed. They curdle milk, do not thin gelatin.

Toxin formation. Streptococci form a number of exotoxins: 1) streptolysins - destroy erythrocytes (O-streptolysin has a cardiotoxic effect); 2) leukocidin - destroys leukocytes (formed by highly virulent strains);

3) erythrogenic (scarlet) toxin - determines the clinical picture of scarlet fever - intoxication, vascular reactions, rash, etc. The synthesis of erythrogenic toxin is determined by the prophage; 4) cytotoxins - have the ability to cause glomerulonephritis.

Antigenic structure and classification. Various antigens are found in streptococci. The cytoplasm of the cell contains a specific nucleoprotein antigen, which is the same for all AS streptococci. Protein type artigens are located on the surface of the cell wall. A polysaccharide group antigen is found in the cell wall of streptococci.

According to the composition of the polysaccharide group-specific fraction of the antigen, all streptococci are divided into

groups denoted by capital Latin letters A, B, C, D, etc. to S. In addition to groups, streptococci are divided into serological types, which are indicated by Arabic numerals.

Group A includes 70 types. This group includes most streptococci. Group B includes mainly streptococci, opportunistic for humans. Group C includes streptococci pathogenic to humans and animals. Group D consists of streptococci that are non-pathogenic for humans, but this group includes enterococci, which are inhabitants of the intestinal tract

humans and animals. Getting into other organs, they cause inflammatory processes: cholecystitis, pyelitis, etc. Thus, they can be attributed to opportunistic microbes.

The belonging of the isolated cultures to one of the serological groups is determined using the precipitation reaction with group sera. To determine serological types, an agglutination reaction with type-specific sera is used.

Resistant to environmental factors. Streptococci are fairly resistant in the environment. At a temperature of 60 ° C, they die after 30 minutes.

In dried pus and phlegm, they persist for months. The usual concentrations of disinfectants destroy them in 15-20 minutes. Enterococci are much more stable, disinfectant solutions kill them only after 50-60 minutes.

1. Describe the pathogenesis and diseases caused by streptococci. What is the prevention of streptococcal disease?

Sources of infection. People (sick and carriers), less often animals or infected foods.

Transmission routes. Airborne and airborne dust. Sometimes food, perhaps contact-household.

Diseases can occur as a result of exagenic infection, as well as endogenous, when conditionally pathogenic streptococci that live on the mucous membranes of the pharynx, nasopharynx, and vagina are activated. A decrease in the body's resistance (cooling, starvation, overwork, etc.) can lead to the occurrence of autoinfection.

Of great importance in the pathogenesis of streptococcal infections is preliminary sensitization, as a result of a previously transferred disease of streptococcal etiology.

When streptococci enter the bloodstream, they cause a difficult septic process.

Diseases in humans more often causes β-hemolytic streptococci of serological group A. They produce pathogenic enzymes: hyaluronidase, fibrinolysin (streptokinase), deoxyribonuclease, etc. In addition, streptococci have a capsule, M-protein, which have antiphagocytic properties.

Streptococci cause various acute and chronic infections in humans, both with the formation of pus and non-suppurative, differing in their clinical picture and pathogenesis. Suppurative phlegmon, abscesses, wound infections, non-suppurative acute infections upper respiratory tract. Erysipelas, scarlet fever, rheumatism, etc.

Streptococci often cause secondary infections with the flu. Measles, whooping cough, and other illnesses often complicate wound infections.

Prevention. It comes down to sanitary and hygienic measures, strengthening the general resistance of the body. Specific prevention not developed.

Streptococcal infection (A40) causes such diverse diseases as tonsillitis, scarlet fever, rheumatism, glomerulonephritis, erysipelas, pyoderma and others, and often generalized processes such as septicemia. Streptococci often play a leading role in the development of complications of other diseases. According to ICD-10, there are:

A40.0 - septicemia caused by group A streptococcus;

A40.1 - septicemia caused by group D streptococcus;

A40.3 - septicemia caused by streptococcus pnevmonine(pneumococcal septicemia);

A40.8 - other streptococcal septicemia;

A40.9 - unspecified streptococcal septicemia.

Streptococci are gram-positive bacteria of spherical or oval shape, 0.6-1 microns in diameter, located in pairs in the form of chains. When grown on blood agar, colonies with a diameter of 1-2 mm are formed. Streptococci are classified according to their ability to lyse erythrocytes in blood agar plates: colonies that form green breakdown products of hemoglobin within a narrow surrounding hemolysis zone are a-type, forming a wide light zone of hemolysis - to β-type, and colonies that do not give a hemolytic effect , - to the y-type. The ability to hemolysis varies widely and does not always indicate pathogenicity.

According to the carbohydrate antigens of the cell wall, streptococci are divided into groups. Currently, there are 21 groups from A to U, many of which are found in animals. Group A streptococci are β-hemolytic, they live mainly in the upper respiratory tract of humans. Disease in humans is caused primarily by group A streptococci (Str. Pyogenes).However, in children early age and newborns group B streptococci (Str. Agalactiae)and group C (Str. Equisimilis)often cause severe sepsis, as well as endocarditis, meningitis, osteomyelitis, and sometimes cause wound infections; group D streptococci (Str. Faecalis)sometimes play a leading role in the occurrence of urinary tract infections and intestinal infections; group F streptococci are responsible for deep inflammatory processes oral cavity and respiratory tract.

Streptococci produce various toxins and enzymes. There are more than 20 extracellular antigens secreted by β-hemolytic group A streptococci during growth in tissues. Of these, the most important are erythrogenic toxins (A, B, C), streptolysins O and S, streptokinases A and B, deoxyribonuclease, hyaluronidase, proteinase, etc. The main toxic component of streptococcus is exotoxin (erythrogenic toxin). In addition to erythrogenic activity, it is pyrogenic, capable of damaging tissues, suppressing the functions of the reticuloendothelial system, causing immunosuppression, affecting membrane permeability, etc. The erythrogenic toxin consists of thermolabile and thermostable fractions. The thermolabile fraction possesses toxic properties, while the thermostable fraction is a streptococcal allergen. Hemolysins and enzymes ensure the penetration of streptococcus into the tissues.

Streptococci persist for a long time at low temperatures, are resistant to drying, die in disinfectant solutions and when heated to 56 ° C for 30 minutes. In pus and sputum, on objects surrounding the patient, they persist for months. Group A streptococci are susceptible to antibiotics, especially penicillin.

Streptococcal diseases are recorded in all regions of the world. Skin diseases are more often observed in hot countries, while angina, scarlet fever - in countries with cold and temperate climates. Children of all ages are ill, starting from the neonatal period. Infection occurs through household contact and airborne droplets. Transmission through contaminated food is possible. The epidemic danger is posed by patients with angina, streptoderma, pneumonia, scarlet fever and other streptococcal diseases, as well as bacteria carriers.

In the pathogenesis of streptococcal diseases big role belongs to a toxic syndrome associated mainly with the action of an erythrogenic toxin, as well as an allergic syndrome caused by sensitization to the protein structures of streptococcus and tissues destroyed by it.

Clinical forms of streptococcal diseases reflect different directions of the pathological process. So, with pyoderma, the local septic effect of streptococcus is clearly manifested, with angina, scarlet fever - septic and toxic syndromes, and when myocarditis, glomerulonephritis occurs, the leading role belongs to allergy factors.

Formally, all clinical forms of diseases caused by streptococci can be classified as infectious diseases. However, in many clinical variants of streptococcal diseases (rheumatism, glomerulonephritis, osteomyelitis, etc.), the most important distinctive feature infectious disease - infectiousness. In this regard, the group of streptococcal infections should include only those that have all the signs of an infectious disease, namely infectiousness, incubation period, cyclic development clinical symptoms and the formation of specific immunity. These signs are fully consistent with diseases caused by group A β-hemolytic streptococcus (scarlet fever, tonsillitis, bronchitis, pneumonia, pharyngitis, erysipelas) and some purulent-inflammatory diseases of newborns caused by streptococci of other groups (streptoderma, phlegmon, abscess, etc.) ...

SCARLET FEVER

Scarlet fever (A38) is an acute infectious disease with symptoms of general intoxication, sore throat and skin rashes.

Etiology.Group A streptococci - the causative agents of scarlet fever - produce exotoxins, but the decisive role in the occurrence of scarlet fever belongs to the antitoxic immunity of the child's body. If at the time of infection there is no antitoxic immunity, then streptococcal infection proceeds as scarlet fever. In the presence of antitoxic immunity, angina, pharyngitis, asymptomatic infection occur, but not scarlet fever.

Epidemiology.Scarlet fever - anthroponous infection; the source of infection is a patient with an explicit or latent form of scarlet fever, as well as a patient with any other form of streptococcal infection.

Scarlet fever is distributed unevenly. The incidence is highest in countries with cold and temperate climates; scarlet fever is rare in hot countries.

The epidemic process in scarlet fever has periodic recessions and rises every 2-3 years and multi-year fluctuations with a period of 20-30 years. Seasonality is clearly revealed - an increase in the incidence in the autumn-winter months.

Children of preschool and early school age are more often ill. Children 1 year of life rarely get sick with scarlet fever, which is explained by transplacental immunity and physiological inactivity of infants to the effects of streptococcal toxin.

The main route of transmission is airborne. Overcrowding of children in the room contributes to the spread of the disease. The incidence also depends on the change in circulating strains of the pathogen in connection with the migration of people with different level antitoxic immunity.

The contagious index is approximate (since erased and inapparent forms of infection are not taken into account) is 40%.

A patient with scarlet fever is contagious from the very onset of the disease. Patients with an erased form of scarlet fever, as well as patients with other forms of streptococcal infection - angina, nasopharyngitis, pose a particularly great epidemiological danger.

In recent decades, there has been a clear trend towards a decrease in the overall incidence of scarlet fever, a decrease in periodic rises and severity. clinical manifestations... In more than 80% of cases, scarlet fever occurs in mild form.

Pathomorphology.Local changes are manifested by edema, hyperemia, leukocyte tissue infiltration. Catarrhal, purulent or necrotic inflammation is noted.

The initial fixation of the pathogen with the development of inflammation and regional lymphadenitis is called the primary scarlet fever complex.

The absorption of the toxin from the primary affect is accompanied by intoxication and the appearance of a typical scarlet fever.

The rash is small-point, occurs on a noticeably hyperemic skin. Microscopy reveals small lesions of the type of perivascular infiltration and moderate edema of the dermis. The epidermis is saturated with exudate, parakeratosis occurs, and later the stratum corneum is rejected by large plates (lamellar peeling of the palms and feet). In the internal organs (kidneys, myocardium, liver) are observed dystrophic changes and interstitial lymphohistiocytic infiltrates with an admixture of eosinophilic myelocytes, especially typical for scarlet fever. Disturbances in the microvasculature are noted. In the brain, autonomic ganglia, circulatory disorders and dystrophic changes in neurons are possible.

The depth of morphological disorders depends on the severity of the disease and its complications.

The most serious complication should be considered post-streptococcal glomerulonephritis with a possible outcome in nephrosclerosis.

With the development of septic complications, necrotic processes may prevail over purulent ones. In such cases, necrotizing otitis media, solid phlegmon of the neck, etc.

Pathogenesis.Development clinical picture scarlet fever is associated with the toxic, septic and allergic effects of streptococcus.

By penetrating into the mucous membrane or damaged skin, streptococcus causes inflammatory changes. The pathogen enters the regional lymph nodes along the lymphatic tracts and superficial vessels, toxic substances β- appear in the blood hemolytic streptococcusthat affect the cardiovascular, nervous and endocrine systems.

The toxic line includes symptoms of general intoxication with fever, rash, headache, and vomiting. In the most severe cases, hemodynamic disturbances with hemorrhages in the adrenal cortex, cerebral edema, dystrophic changes in the myocardium, damage to the vegetative nervous system up to sympathicoparesis.

The septic line of the pathogenesis of scarlet fever is due to the effect of a microbial cell in -hemolytic streptococcus. It is manifested by purulent and necrotic changes at the site of the entrance gate and purulent complications. Septic manifestations can occur at different periods of the disease. In some cases, the septic component plays a leading role in the clinical picture from the first days of the disease. This is manifested by damage to the paranasal sinuses, purulent otitis media, lymphadenitis, adenophlegmon. With necrotizing otitis media, the process can go to bone tissue, hard meninges, venous sinuses.

The allergic line of pathogenesis is caused by the body's sensitization to β-hemolytic streptococcus and antigens of destroyed tissues. Allergy sometimes occurs from the first days of the disease, but it is most pronounced in the 2nd and 3rd weeks from the onset of scarlet fever. Clinically, allergic syndrome is manifested by various skin rashes, acute lymphadenitis, glomerulonephritis, myocarditis, synovitis. "Allergic waves" with unmotivated rises in body temperature and various skin rashes are also caused by allergies.

The manifestations of all 3 lines of scarlet fever pathogenesis are interrelated.

Immunity.As a result of the transferred scarlet fever, persistent antitoxic immunity to the entire A-group of β-hemolytic streptococci is developed. It lasts for life. Antimicrobial immunity is less stable and type-specific, that is, it is effective only against the streptococcus serotype that caused the disease.

Children of the first 6 months of life have transplacental antitoxic immunity, obtained from a mother who previously had scarlet fever, therefore, children of this age practically do not get scarlet fever. Antitoxic immunity to β-hemolytic streptococcus also appears as a result of "silent" immunization after other transferred forms of streptococcal infections. In the absence of antitoxic immunity to streptococcus in the child's blood, any type of it can cause scarlet fever. At the same time, antitoxic immunity when infected with β-hemolytic streptococcus protects a child from scarlet fever, but not from another clinical form of streptococcal infection (tonsillitis, erysipelas, etc.).

The early use of penicillin for the treatment of patients with scarlet fever contributes to the rapid elimination of streptococcus from the body and thereby prevents the formation of tense antitoxic immunity, in connection with which a recurrence of scarlet fever is possible.

Clinical manifestations.The incubation period for scarlet fever is 2-7 days. It can be shortened up to several hours and lengthened up to 12 days. The disease begins acutely, with a rise in body temperature. The child complains of a sore throat when swallowing, a headache, and there is a single vomiting. A few hours after the onset of the disease, a pink dotted rash appears on the face, trunk, limbs on the hyperemic background of the skin (see Fig. 111 on the color insert). On the face, the rash is located on the cheeks, but the nasolabial triangle is free from the rash (see Fig. 112 in the color insert). The patient's appearance is characteristic: the eyes are shiny, the face is bright, slightly swollen, the flaming cheeks contrast sharply with the pale nasolabial triangle (Filatov's triangle). In the natural folds of the skin, on the lateral surfaces of the trunk, the rash is more saturated, especially in the lower abdomen, on the flexor surface of the limbs, in the armpits, elbows and groin (see Fig. 113, 114, 115, 116 in the color insert). There are often dark red stripes here as a result of the concentration of the rash and hemorrhagic soaking (Pastia symptom) (see fig. 117 on the color insert). White dermographism is characteristic (see fig. 118 on the color insert).

Separate elements of the rash can be miliary, in the form of small, pinhead, bubbles with a clear or turbid liquid. In more severe cases, the rash takes on a cyanotic hue, and dermographism is intermittent and mild. With scarlet fever, capillary permeability is increased, which is easily detected by the imposition of a tourniquet. The rash usually lasts 3-7 days and, disappearing, does not leave pigmentation.

After the disappearance of the rash at the end of the 1st - the beginning of the 2nd week of the disease, peeling begins: on the face - in the form of delicate scales, on the trunk, neck, auricles - pityriasis. It is more profuse after miliary rash. For scarlet fever, lamellar peeling on the palms and soles is typical, manifested first in the form of cracks in the skin at the free edge of the nail and then spreading from the fingertips to the palm and sole (see Fig. 119 on the color insert). The skin on the limbs flakes off in layers. Currently, with scarlet fever, peeling is less pronounced.

One of the permanent and cardinal signs of scarlet fever are changes in the oropharynx (see Fig. 120 on the color insert). There is a bright delimited hyperemia of the tonsils, arches, uvula, but it does not affect the mucous membrane of the hard palate. On the 1st day of illness, it is often possible to see a point enanthema, which can become hemorrhagic. Changes in the oropharynx are so pronounced that they are called, in the words of NF Filatov, "fire in the throat", "flaming sore throat."

Angina with scarlet fever is catarrhal, follicular, lacunar, but necrotizing angina is especially characteristic of this disease (see fig. 121 on the color insert). Depending on its severity, necrosis is either superficial, in the form of separate islets, or deep, completely covering the surface of the tonsils. They can also spread beyond the tonsils: to the arches, uvula, to the mucous membrane of the nose and throat.

Necrosis often has a dirty gray or greenish color. They disappear slowly, within 7-10 days. Catarrhal and follicular sore throats disappear in 4-5 days.

According to its severity, the defeat of the oropharynx affects the regional lymph nodes. They become dense, painful on palpation. First of all, the tonsillar and anterior cervical ones increase. In cases accompanied by necrosis, the process may involve the cervical tissue surrounding the lymph nodes, and there is a clinical picture of periadenitis and even adenophlegmon.

At the beginning of the disease, the tongue is dryish, densely coated with a grayish-brown bloom, from the 2-3rd day it begins to clear from the tip and sides, becomes bright red, with prominently protruding swollen papillae, similar to raspberries ("raspberry", "papillary", "Scarlet" tongue). This symptom is clearly detected between the 3rd and 5th day, then the brightness of the tongue decreases, but for a long time (2-3 weeks) it is possible to see enlarged papillae (see Fig. 122, 123 on the color insert).

The severity of symptoms of intoxication with scarlet fever depends on the severity of the disease. Usually, intoxication is manifested by a rise in body temperature, lethargy, headache, repeated vomiting. In severe cases, the body temperature rises to 40 ° C, there is a strong headache, repeated vomiting, lethargy, sometimes agitation, delirium, convulsions, meningeal symptoms. Modern scarlet fever is often not accompanied by intoxication at normal body temperature.

Changes in the vascular system at the onset of the disease are manifested by the predominance of the tone of sympathetic innervation (tachycardia, increased blood pressure, which is designated by the term "sympathicus phase"). After 4-5 days, the tone of the parasympathetic system begins to prevail, which manifests itself (bradycardia, muffling of heart sounds, lowering blood pressure - vagus phase). In this period of the disease, there is often a slight expansion of the boundaries of relative cardiac dullness, impurity of the I tone or systolic murmur. The ECG usually shows sinus bradycardia and arrhythmias. These changes are interpreted as "infectious heart", they are based on extracardiac influences and only in rare cases - myocardial damage.

Changes of cardio-vascular system usually persist for 2-4 weeks, after which they disappear without a trace.

White dermographism with scarlet fever at the onset of the disease has an elongated latent (10-12 minutes) and shortened (1-1.5 minutes) overt period (in a healthy person, the latent period is 7-8 minutes, and the overt period is 2.5-3 minutes) ... In the future, the latent period is shortened, the explicit one becomes more persistent.

In peripheral blood, neutrophilic leukocytosis with a shift to the left is noted; ESR is increased.

Classification.According to A.A. Koltypin, scarlet fever is divided by type, severity and course. By type, they distinguish between typical and atypical scarlet fever.

The typical forms are those with all the symptoms characteristic of scarlet fever: intoxication, sore throat and rash.

The atypical ones include the erased lightest forms with mild clinical manifestations, as well as the extrapharyngeal form (burn, wound and postpartum) with a primary focus outside the oropharynx. With extrapharyngeal scarlet fever, a rash appears and is more intense at the entrance gate, there are symptoms of intoxication: fever, vomiting. Angina is absent, but there may be a mild hyperemia of the mucous membrane of the oropharynx. Regional lymphadenitis occurs in the area of \u200b\u200bthe entrance gate and is less pronounced than with typical scarlet fever.

The most severe forms - hemorrhagic and hypertoxic - can be classified as atypical.

Typical forms are classified as mild, moderate, and severe. The severity is determined by the severity of symptoms of intoxication and local inflammatory changes in the oropharynx.

In recent years, scarlet fever in most cases proceeds in a mild form, less often in a moderate form (see Fig. 124 in the color insert). Severe forms practically never occur.

Flow.The course of scarlet fever can be smooth, without allergic waves and complications, as well as uneven, with allergic or septic complications.

With a smooth course, the pathological process ends in 2-3 weeks.

With scarlet fever, there are relapses, usually they appear on the 2nd or 3rd week and, as a rule, are associated with reinfection and superinfection with a new type of streptococcus when the convalescent comes into contact with newly admitted patients.

Complications.Most frequent complications scarlet fever are lymphadenitis, otitis media, sinusitis, nephritis, synovitis, purulent arthritis, mastoiditis. They occur both in the early and late stages of the disease and are explained by allergies, reinfection and superinfection.

Infectious and allergic complications(nephritis, synovitis and simple lymphadenitis) are usually observed in the second period of the disease, more often on the 2-3rd week. Purulent complications can join both early and late, more often in young children, weakened by previous diseases.

Now, due to the early use of antibiotics for the treatment of patients with scarlet fever, which contributes to the rapid reorganization of the body, and the exclusion of reinfection during hospitalization, relapses and purulent complications are rare.

Scarlet fever in young children.Children under the age of 1 year suffer from scarlet fever very rarely. The clinical picture in infants has features. In children with residual transplacental immunity, scarlet fever proceeds as a rudimentary erased infection. In these cases initial symptoms expressed slightly, cardiovascular syndrome is not very noticeable, body temperature is low. The rash is weak, sometimes almost invisible, and quickly disappears. Little or no peeling. Diagnostics can be very difficult. In infants who are not immune to scarlet fever, the disease sometimes proceeds according to the septic type with severe necrotizing sore throat, pharyngitis and numerous purulent-necrotic complications.

At an early age, with scarlet fever, manifestations of allergies and complications of an infectious-allergic nature are rarely observed - nephritis, synovitis.

Diagnostics.In typical cases, the diagnosis is not difficult. Sudden acute onset of the disease, fever, vomiting, sore throat when swallowing, delimited hyperemia of the arches, tonsils, uvula, pink small-point rash on a hyperemic skin background, pale nasolabial triangle, enlargement of regional lymph nodes in the neck give grounds for clinical diagnosis scarlet fever. An auxiliary method can be a picture of peripheral blood: neutrophilic leukocytosis with a slight shift to the left and increased ESR.

Difficulties in diagnosis arise with erased forms and late admission of the patient to the hospital.

With erased forms, delimited hyperemia of the oropharynx, lymphadenitis phenomena, white dermographism and a picture of peripheral blood are of diagnostic value.

With late admission of the patient, long-lasting symptoms are diagnostically important: a raspberry tongue with hypertrophied papillae, petechiae, dryness and peeling of the skin. In such cases, epidemiological data are very important - on the contact of a child with a patient with other forms of streptococcal infection.

For laboratory confirmation of the diagnosis, it is important to isolate β-hemolytic streptococcus in cultures of mucus from the oropharynx, determine the titer of antistreptolysin-O, other enzymes and antitoxins of streptococcus. Scarlet fever is differentiated from pseudotuberculosis, yersiniosis, staphylococcal infection, accompanied by a scarlet fever-like syndrome, toxic-allergic condition, measles, meningococcemia, enterovirus exanthema, etc.

Treatment.Patients with scarlet fever are hospitalized for clinical and epidemiological indications. Patients with mild and moderate forms are treated at home. Hospitalization is mandatory for severe forms of scarlet fever and when it is impossible to isolate the patient at home and create conditions for his treatment. Patients are placed in boxes or wards for 2-4 people, filling them simultaneously. Contact should not be allowed between newly arriving patients and convalescents. Discharge from the hospital is made according to clinical indications after the end of the course of antibiotic therapy, usually on the 7-10th day from the onset of the disease. When treating at home, it is necessary to isolate the patient in a separate room and comply with sanitary and hygienic rules when caring for him (current disinfection, individual dishes, household items, etc.). It is necessary to monitor compliance with bed rest during the acute period of the disease. The diet should be complete, with a sufficient amount of vitamins, mechanically sparing, especially in the first days of illness.

With scarlet fever, antibiotic treatment is indicated. In the absence of contraindications, the antibiotic of choice is still penicillin. The duration of the course of antibiotic therapy is 5-7 days.

When treating at home, phenoxymethylpenicillin is given orally at the rate of 50,000 ME / (kg. Day) in 4 doses. In a hospital, it is more advisable to inject penicillin intramuscularly in 2 doses. In severe forms, the daily dose of penicillin is increased to 100 mg / kg or more or switched to treatment with 3rd generation cephalosporins.

Forecastfavorable. With rationally conducted therapy (early penicillin therapy in conditions excluding reinfection), the course of the disease is smooth, complications rarely occur.

Prevention.Specific prevention of scarlet fever has not been developed. Preventive measures include early identification and isolation of patients with scarlet fever and any other streptococcal infection. According to the instructions, the sick are isolated for 7-10 days immediately after the onset of the clinical manifestations of scarlet fever, but in children's institution those who have recovered are allowed to be sent after 22 days from the onset of the disease due to the possibility of various complications. Patients with other forms of streptococcal infection (tonsillitis, pharyngitis, streptoderma, etc.) in the focus of scarlet fever are also isolated for 22 days.

Since scarlet fever is currently almost exclusively mild and does not cause complications, especially when treated with antibacterial drugs and adherence to the regimen, these decreed periods of isolation need to be reduced. In our opinion, patients with scarlet fever should be isolated for no more than 10-12 days from the onset of the disease, after which they can be admitted to an organized group.

ANGINA

Angina is one of the forms of streptococcal infection with the localization of the inflammatory process in the lymphoid tissue of the oropharynx, mainly in the tonsils. It is accompanied by intoxication, fever, sore throat and a reaction of regional lymph nodes.

Angina is a very common disease in childhood. In practical work, one should distinguish between angina as an independent disease and angina that occurs against the background of another infectious disease.

Streptococcal sore throat is isolated in an independent nosological form, but in children it usually develops as a complication of ARVI or as a result of exacerbation of chronic tonsillitis.

Epidemiology.The source of the pathogen is patients with streptococcal infection and healthy carriers in- hemolytic streptococcus. The infection is transmitted by airborne droplets and by household contact, as well as through food.

The entrance gate and the place of reproduction of the pathogen is the lymphadenoid tissue of the pharynx.

Streptococcal tonsillitis is more often observed in children over 3 years old, primarily in those suffering from chronic tonsillitis. At the age of 1 year, such angina is rare due to the presence of antitoxic and antimicrobial immunity obtained transplacentally, as well as due to insufficient differentiation of the lymphoid tissue of the oropharynx.

There are rises in the incidence of angina in autumn and winter, associated with closer contact of children. Hypothermia seems to play a secondary role.

Pathogenesis.The ability of group A β-hemolytic streptococcus to affect mainly the epithelial cover of the lymphoid tissue of the pharynx is associated with the direct local effect of one of the antigenic structures of the microorganism - lipoteichoic acid associated with the M-protein, which ensures the fixation of the pathogen on the tonsils. M-protein reduces the phagocytic activity of leukocytes at the site of the entrance gate and thereby contributes to the increased susceptibility of the child to streptococcus.

Pathomorphology.Morphological changes in streptococcal angina are manifested by purulent fusion of lymphoid follicles, accumulation of purulent masses in lacunae, necrosis of the superficial epithelium and, possibly, tonsil tissue.

Depending on the morphological changes, follicular, lacunar and necrotic sore throat are distinguished.

When follicular sore throatpurulent fusion of the tonsil tissue is noted in the area of \u200b\u200bsingle follicles located on the free surface of the tonsils.

When lacunar sore throatlymphoid follicles located along the palatine tonsils undergo purulent fusion.

When necrotic sore throatin connection with necrosogenic activity in β-hemolytic streptococcus, not only lymphoid follicles, but also areas of the tonsil stroma undergo necrotic changes.

Clinical manifestations.Streptococcal sore throat begins acutely with an increase in body temperature to 38-39 ° C, chills, headache and pain when swallowing. Clinical symptoms reach their maximum severity as early as the 1st day from the onset of the disease. Patients complain of general weakness, decreased appetite, sore throat, sometimes radiating to the ear and lateral parts of the neck. In more severe cases, repeated vomiting, delirium, agitation, convulsions are possible. The patient's appearance is characteristic: the skin is dry, the face is hyperemic, the cheeks are flushed, the lips are bright, red, dry, in the corners of the mouth there are seizures.

Changes in the oropharynx usually include bright diffuse hyperemia, covering the soft and hard palate, tonsils, posterior pharyngeal wall, but sometimes delimited hyperemia of the tonsils and palatine arches is observed. The tonsils are enlarged mainly as a result of infiltration and swelling. With lacunar angina, the overlays are located in the lacunae. Sometimes the overlays strictly repeat the convoluted gaps, but often they are mosaic, i.e. they are located not only in the gaps, but also in the form of islets on the amygdala or completely cover its part. Usually these overlays are yellowish-white in color, can be easily removed with a spatula and rubbed between the slides, that is, they consist of pus and detritus.

When follicular sore throaton the amygdala, whitish follicles with a diameter of 2-3 mm appear, slightly rising above its surface. They are not removed with a swab or spatula, as they are subepithelially located purulent masses formed as a result of the destruction of the lymphoid follicles of the tonsils. Usually microabscesses ripen and open, which is accompanied by a new rise in body temperature and the appearance on the tonsils of superficially located purulent overlays in the form of islands.

When necrotic sore throatthe affected areas of the tonsil tissue are covered with a plaque with an uneven, pitted, dull surface of greenish-yellow or gray color, extending into the depths of the mucous membrane. Often the plaque is saturated with fibrin and becomes dense. When you try to remove them, a bleeding surface is left. After rejection of the overlays, a tissue defect is formed that has a whitish color, irregular shape, and an uneven, bumpy bottom. Necrosis with streptococcal infection can spread beyond the tonsils - to the arches, uvula, back wall of the pharynx.

In addition to the characteristic changes in the oropharynx, all patients with streptococcal angina have an increase in regional lymph nodes. On palpation, they are painful and dense. The involvement of lymph nodes in the process is proportional to the severity of changes in the oropharynx.

The severity of angina is determined taking into account the severity of general and local disorders, and general toxic disorders are of decisive importance: the height of fever, changes in the central nervous system, cardiovascular and endocrine systems.

Flow.Usually streptococcal sore throats are acute, the outcome is favorable. With timely treatment, the symptoms of intoxication and local changes in the oropharynx disappear within a week and a period of convalescence begins. Complications are mainly due to the spread of the process to nearby organs (purulent lymphadenitis, sinusitis, otitis media), infectious and allergic complications rarely occur (glomerulonephritis, myocarditis, etc.).

Features of angina in young children.In children of the first 3 years of life, streptococcal angina usually occurs against the background of ARVI. The clinical picture in these cases consists of the symptoms of acute respiratory viral infections and lesions of the oropharynx, severe catarrhal phenomena (cough, runny nose) persist for a long time. Changes in the oropharynx correspond to the form of angina, but there is a slow cleansing of the tonsils from overlaps, persistent hyperemia and swelling of the mucous membranes of the oropharynx, as well as an increase in the tonsils and regional lymph nodes, persist. These patients are more likely to develop complications.

Diagnostics.Streptococcal sore throat is diagnosed on the basis of clinical data (severe intoxication, bright hyperemia of the mucous membrane of the oropharynx, necrotic changes in the tonsils), epidemiological history (contact with a patient with streptococcal infection) and positive results laboratory research... In crops of mucus from the oropharynx, β-hemolytic streptococcus is detected, titers of antibodies to streptococcus antigens (antistreptolysins, antihyaluronidase, etc.) increase.

Treatment.Patients with streptococcal angina are usually treated at home. Only children with severe forms of illness or complications, as well as children in whom it is difficult to exclude diphtheria of the oropharynx, are subject to hospitalization. The patients are placed in a box. Bed rest for 5-6 days, mechanically sparing food, multivitamins are recommended. To rinse the oropharynx, decoctions are used: chamomile, eucalyptus, sage, St. John's wort, as well as solutions of liniment 5% cycloferon, furacilin, potassium permanganate, etc. Antibiotic therapy is required. In mild and moderate forms, you can limit yourself to the appointment of phenoxymethylpenicillin, erythromycin, amoxiclav, azithromycin in an age-specific dose. In case of intolerance to antibiotics, sulfa drugs are given (bactrim, lidaprim, etc.).

PHARYNGITIS

With a steptococcal infection, in a significant part of cases, the pharynx is involved in the process, there is acute pharyngitis.

The term "pharyngitis" is usually used to refer to changes in the oropharynx in various infectious diseases (ARVI, diphtheria, measles, meningococcal infection, etc.). Pharyngitis is often combined with damage to the tonsils, nasopharynx, and respiratory tract. However, the diagnosis of acute pharyngitis is established when the main process is localized on the back of the throat.

The disease begins acutely, with complaints of pain when swallowing, headache, abdominal pain, vomiting and may be accompanied by a rise in body temperature from subfebrile to febrile. Painful sensations in the oropharynx vary from mild to quite pronounced, leading to difficulty in swallowing. Dryness, irritation and other discomfort occur in the back of the throat. The pharyngoscopic picture shows a sharp increase, hyperemia, swelling of the posterior pharyngeal wall with frequent suppuration of follicles, superficial necrosis, sometimes with ulceration. Changes in the palatine tonsils are weak or absent. Soreness and enlargement of the anterior and posterior cervical lymph nodes are noted with great constancy.

Features of pharyngitis in young children.In children of the 1st year of life, streptococcal pharyngitis is difficult, a runny nose appears early, mucopurulent nasal discharge flows down the hyperemic and edematous posterior pharyngeal wall, body temperature rises to 39 ° C, vomiting begins, appetite deteriorates sharply. The disease is often accompanied by complications - otitis media, sinusitis, meningitis, etc. Against the background of streptococcal pharyngitis, a pharyngeal abscess sometimes forms.

Parapharyngeal, or retropharyngeal, abscessoccurs in the periopharyngeal space due to inflammation and suppuration of the prevertebral lymph nodes. Inflammation occurs against the background of pharyngitis, as the lymphatic ducts of the nodes drain the nasopharynx and the posterior nasal passages. A pharyngeal abscess can develop as an independent disease, but more often it occurs against the background of pharyngitis or nasopharyngitis. The body temperature rises, swallowing is difficult, sharp pains in the throat bother, difficulty breathing, salivation appear; the child refuses food.

With pharyngoscopy on the posterior wall of the pharynx, lateral to the midline, one can see swelling of a rounded shape and elastic consistency (or with fluctuations). Sometimes the abscess is localized in the nasopharyngeal region, causing difficulty in nasal breathing and swelling of the soft palate.

The inflammatory process sometimes spreads to the esophagus, the lateral surface of the neck, to the mediastinum, sometimes causing destruction of the large vessels of the neck.

Diagnostics.Streptococcal pharyngitis is diagnosed on the basis of the clinical picture, the isolation of a culture of streptococcus in the mucus crops from the lesion focus and an increase in the titer of antibodies to streptococcal antigens in the dynamics of the disease. With a retropharyngeal abscess in difficult-to-diagnose cases, an x-ray of the neck or nasopharynx is performed.

Treatment.With streptococcal pharyngitis, antibiotics, desensitizing agents, vitamins, rinsing the oropharynx with disinfectants and saline solutions, herbal infusions. If a retropharyngeal abscess develops, surgical treatment is indicated.

PNEUMONIA

Pneumonia caused by β-hemolytic streptococcus occurs as bronchopneumonia or interstitial pneumonia as a complication of ARVI or other infectious diseases. Children aged 2-7 years get sick more often.

In the morphological picture, there are small foci with areas of necrosis. Subsequently, the areas of inflammation increase, merge with each other and capture whole lobes of the lung.

Often the pleura is involved in the process, pleurisy and empyema develop.

The disease begins violently, with severe intoxication, fever, chills. Body temperature rises to 39-40 ° C, chest pains, cough with phlegm appear. Physical data with streptococcal pneumonia are often scarce, percussion changes are not typical, wheezing is heard inconsistently. When pleurisy occurs, changes in percussion sound and weakened breathing on the affected side appear.

The X-ray picture includes pronounced interstitial changes with multiple rounded foci in different phases resorption. Sometimes a massive infiltration can be seen. For streptococcal pneumonia, enlargement of the lymph nodes of the root of the lung is typical. In the blood there is neutrophilic leukocytosis with a shift to the left, ESR is increased.

Diagnostics.Streptococcal pneumonia is diagnosed on the basis of cumulative clinical, radiological and laboratory data

Treatment.For the treatment of streptococcal pneumonia, penicillin or its semi-synthetic derivatives is used at the rate of 100-200 mg / (kg. Day) intramuscularly in 2 doses. Other antibiotics (protected penicillins, cephalosporins) can also be used. With empyema, thoracocentesis is performed.

ROZHA

Erysipelas (A46) is a form of streptococcal infections. Called in- hemolytic streptococcus, manifested by focal serous-exudative or serous-hemorrhagic inflammation of the skin and subcutaneous fat and general toxic reactions.

Etiology.The causative agent of erysipelas - in- hemolytic streptococcus of group A. Poor sowing of streptococcus from the erysipelas, its extremely rare isolation from the blood of patients prompted the search for other pathogens. However, the assumption of the existence of a dermatogenic streptococcus serotype has not been confirmed. It was also found that staphylococcus and other pyogenic bacteria play an etiological role in complications of erysipelas. It is assumed that L-forms of streptococcus are involved in the etiology of recurrent erysipelas.

Epidemiology.The source of infection is a patient with streptococcal infection or a carrier of bacteria. It is often impossible to establish the source.

Transmission mechanismairborne and contact through infected objects, more often in violation of the integrity of the skin.

The individual predisposition of the child plays a role in the occurrence of erysipelas. More often young children suffering from dermatitis and other skin diseases are ill.

Erysipelas occurs as an exogenous and endogenous infection... Endogenous develops in the presence of chronic lesions. The penetration of the pathogen by contact is facilitated by microtraumas of the skin and the wound surface.

Activation of the process in recurrent erysipelas is facilitated by a decrease in factors immune defense, auto- and heterosensitization. Intercurrent diseases, bruises, insect bites should be considered an unfavorable background.

The highest incidence of erysipelas is observed in late summer and autumn, more often in the form of sporadic cases.

Children get sick much less often than adults. Infection of newborns can occur during childbirth from the mother or medical staff, as well as through infected dressings.

The incidence of erysipelas in recent years has significantly decreased, the mortality rate is practically zero.

Pathogenesis and pathomorphology.β-Hemolytic streptococcus, penetrating exo or endogenously, multiplies in the lymphatic vessels of the dermis. The local process is formed under the condition of initial skin sensitization to hemolytic streptococcus. In the origin of inflammatory changes in erysipelas, along with streptococcal toxins, tissue biologically plays a huge role. active substancessuch as histamine, serotonin and other mediators of allergic inflammation.

In the absence of allergies, the introduction of streptococcus leads to the development of a banal purulent process.

Plasma impregnation of the dermis, serous or serous-hemorrhagic exudate with fibrin loss, necrobiosis of cells, lysis of elastic and collagen fibers of the skin, pronounced vascular changes in the form of fibrinous lesions of the vascular walls, swelling of the endothelium from the perivascular lymphoid, plasmacytic and reticulo-histiocytic elements.

It has been shown that lymphocytes proliferating and differentiating in the skin are capable of an immune response without further migration to peripheral lymphoid organs. In patients with erysipelas, the main process is localized in the dermis, in its papillary and reticular layers. Here, vascular lesions, hemorrhages and necrosis occur, in the development of which immunopathological processes play an undoubted role. With recurrent forms of the disease, disorders of hemostasis, regulation of capillary circulation and lymph circulation are detected.

It should be noted that the pathogenesis of various clinical forms of erysipelas is not the same. Primary and repeated erysipelas refers to acute streptococcal infection and occurs as a result of exogenous infection. Recurrent erysipelas refers to a chronic endogenous streptococcal infection and often occurs during treatment with hormones and cytostatics. In children, recurrent erysipelas is extremely rare.

Clinical manifestations.The incubation period for erysipelas lasts from several hours to 3-5 days. The disease, as a rule, begins acutely, but in some cases there is a prodrome in the form of malaise, a feeling of heaviness in the affected limb, paresthesia, pain in the region of regional lymph nodes.

Acute onset of the disease is accompanied by headache, chills, fever up to 38-40 ° C; weakness, nausea, vomiting are noted. In severe forms, delirium, the phenomena of meningism are possible.

A few hours after the onset of symptoms of intoxication on the skin of the affected area, erythema and pronounced edema develop, accompanied by sharp pains (Fig. 5). The inflammatory process can be found on any part of the body, but more often it is localized on the skin of the face and on the legs, and very rarely affects the mucous membranes.

As a rule, in the lesion, the skin is hot to the touch, painful and tense. Erythema rapidly increases, erythematous spots merge with newly appearing ones, the skin becomes glossy, sometimes acquiring a cyanotic hue. The affected area protrudes above the level of healthy skin, delimited from it by an inflammatory roller with scalloped edges. Regional lymph nodes are enlarged and painful. In some cases, against the background of erythema and edema, detachment of the epidermis occurs, as a result of which bubbles (bullae) of an oval or round shape and of various sizes, filled with serous hemorrhagic fluid, appear in the focus.

There is a parallelism between general intoxication and local manifestations - bullous elements are more often observed in severe forms of the disease.

Classification.By the nature of local manifestations, erythematous, erythematous-bullous, erythematous-hemorrhagic and bullous-hemorrhagic forms of erysipelas are distinguished.

According to the severity of intoxication, mild, moderate and severe forms of the disease are distinguished.

According to the frequency of the disease, primary, repeated and recurrent erysipelas are distinguished, according to the prevalence of the local process - localized, widespread, wandering, metastatic.

There are also local (phlegmon, abscess, necrosis) and general (sepsis, pneumonia, etc.) complications of erysipelas.

Erythematous form- the most common form of erysipelas (50-60% of cases).

In the erythematous form, there is a sharply delimited skin hyperemia with zigzag outlines in the form of teeth, arcs, tongues.

Erythema can be from barely noticeable to bluish-purple, always accompanied by edema that extends beyond the erythema and captures the underlying adipose tissue. Sometimes the swelling leads to compression blood vessels, then edema predominates, and erythema fades into the background. In the lesion focus, the patient feels a burning sensation, tension, soreness.

Regional lymphadenitis is sometimes complicated by periadenitis and lymphangitis.

When erythematous-bullous formagainst the background of edema and hyperemia, bullous elements containing a clear liquid are formed (Fig. 6).

Items appear in different terms, range from small vesicles to large blisters. Subsequently, the bubbles burst, their contents dries up, crusts of gray or gray-yellow color are formed, less often - erosion and ulcers with the development of granulations.

Erythematous-hemorrhagic formaccompanied by the appearance of hemorrhages against the background of edema and hyperemia in the area of \u200b\u200binflammation. Their sizes vary from petechiae to extensive ecchymosis. There is a deep lesion of blood vessels and lymphatic capillaries with the development of complications in the form of necrosis and ulcers.

When bullous hemorrhagic formblisters soaked in hemorrhagic contents appear. This is the most severe form of erysipelas, it almost never occurs in children (see Fig. 125 on the color insert).

Expressiveness common symptoms intoxication and local inflammatory changes in the skin determines the severity of the clinical form of the disease.

Flow.The average duration of erythematous erysipelas usually does not exceed 7-10 days with timely and adequate treatment. After disappearing acute manifestations peeling begins at the site of erythema.

In bullous hemorrhagic forms, after opening the blisters, crusts of brown or black color are formed, sometimes - erosion and ulcers.

After the transferred erysipelas, the pastiness and pigmentation of the skin, peeling, and sometimes elephantiasis develop for a long time.

Features of the disease in newborns and children 1 year of life.Erysipelas in newborns is extremely rare. The process is more often localized in the navel area and within 1 day spreads along the anterior abdominal wall, goes down to the genitals, goes to the back and trunk. In infants, skin hyperemia is less pronounced than in older children, the limiting roller is indistinct. Newborns often have a widespread or wandering form of erysipelas. Intoxication can grow rapidly, hyperthermia, anxiety occur; the child refuses to breast, convulsions, septicopyemia are possible.

Erysipelas in children 1 year of life is also difficult, the inflammation is localized at the site of intertrigo or on the face. The process spreads quickly, sepsis, meningitis may develop.

Diagnostics.Erysipelas is diagnosed mainly on the basis of the clinical picture. Laboratory data are of secondary importance: in peripheral blood - leukocytosis with neutrophilic shift, eosinophilia, toxic granularity of neutrophils, ESR increased.

In more severe cases, the amount of fibrinogen in the blood increases, the indicators of the blood coagulation system and fibrinolytic activity are changed. C-reactive protein is positive.

Bacteriological research is inappropriate. Serological studies reveal antibodies to streptococcus antigens.

Treatment.The most effective antibiotics in the treatment of erysipelas are cephalosporins of the 3-4th generation in usual doses for 5-7 days. If necessary, you can use macrolides - erythromycin, azithromycin or metacyclin. Relapses after treatment with aminopenicillins occur in 10-12% of cases during the year. The main cause of recurrence is considered to be intracellular localization of group A beta-hemolytic streptococcus. Perhaps the appointment of sulfonamides, it is advisable - ascorbic acid, rutin, B vitamins, nicotinic acid.

In cases of bullous erysipelas and with severe symptoms of intoxication, it is allowed to use corticosteroid drugs at a dose of 1-2 mg / (kg. Day) for 3-5 days.

It was found that the administration of interferon inducers to patients with erysipelas (cycloferon, Gepon, etc.) causes a positive clinical effect, manifested in a reduction in the treatment time of patients, an acceleration of their recovery, as well as a 3-fold decrease in the number of relapses of the disease.

LABORATORY DIAGNOSTICS OF STRETOCOCCUS DISEASES

The variety of clinical forms of streptococcal infections and their similarity with other pyoinflammatory diseases bring laboratory diagnostics to the fore in many cases.

For express diagnostics, test systems are currently used to determine the presence of streptococci in flushes within a few minutes, as well as their group affiliation. These systems are based on RLA, RCA or various modifications of ELISA.

Microbiological methods have not lost their importance, which include inoculation of the test material on blood agar, selection of colonies with hemolysis and characteristic morphology with their subsequent group serological identification. Until now, serological reactions based on the determination of antibodies to the extracellular products of streptococcus are widespread: streptolysin-O, hyaluronidase, streptokinase, etc.

Clinical and microbiological diagnostics of streptococcal infections includes identification of streptococci using culture methods and standard biotyping systems, determination of M-, Ti-OF-types of isolated strains and antibiotic sensitivity.

Recently, the development of an immunodiagnostic system based on the detection of antibodies to the components of the cell wall: group polysaccharide A, nontype-specific proteins, M-associated protein, peptidoglycan, cytoplasmic membrane, etc.

The systems of enzyme immunoassay for the determination of circulating A-polysaccharide and protein-ribosomal antigens have been tested.

The agglutination reactions are used to determine the antigens of L-forms of streptococcus in patients with erysipelas.

To assess immunopathological processes in secondary forms of streptococcal infections, the test for the determination of anti-tissue antibodies, the determination of the CEC level, the level of complement, the quantitative content of IgM, IgG and IgA are highly informative.

The phenomenon of phage conversion is also determined, since in a number of streptococcus strains there are specific bacteriophages with an erythrogenic toxin gene.

The set of tests should be selected depending on the specific research objectives.

Streptococci are a genus of coccal (spherical) gram-positive bacteria belonging to the type Firmicutes and Lactobacillales (lactic acid bacteria). Cell division in these bacteria occurs along one axis. Hence, they grow in chains or pairs, hence the name: from the Greek "streptos", that is, easily bent or twisted, like a chain (twisted chain).

... dysfunctional families are the most vulnerable to breastfeeding caries. Breastfeeding caries is an infectious disease and bacteria are its main causative agent. Bacteria not only produce acid, but also thrive in it. High level...

In this they differ from staphylococci, which divide along several axes and form clusters of cells, similar to grape bunches. Most streptococci are oxidase- and catalase-negative, and many are facultative anaerobes.

In 1984, many organisms that were previously considered streptococci were isolated in the genus Enterococcus and Lactococcus... Currently, over 50 species have been recognized in this genus.

Classification and pathogenesis of streptococci

In addition to streptococcal pharyngitis (sore throat), certain types of streptococci are responsible for many cases of conjunctivitis, meningitis, endocarditis, bacterial pneumonia, erysipelas, and necrotizing fasciitis ("carnivorous" bacterial infections). However, many streptococcal species are not pathogenic, but form part of the symbiotic microbiome of the oral cavity, intestines, skin, and upper respiratory tract in humans. In addition, streptococci are an essential ingredient in the production of Emmental ("Swiss") cheese.

Classification Streptococcus carried out on the basis of their hemolytic characteristics - alpha hemolytic and beta hemolytic.

For medicine, the most important are the group of alpha-hemolytic organisms S. pneumoniae and Streptococcus viridans, and beta-hemolytic streptococci from Lancefield groups A and B.

Alpha hemolytic

Alpha hemolytic species cause the oxidation of iron in the hemoglobin molecules in red blood cells, which gives it a greenish color on blood agar. Beta hemolytic species cause complete rupture of red blood cells. On blood agar, it appears as wide areas without blood cells surrounding the bacterial colonies. Gamma-hemolytic species do not cause hemolysis.

Pneumococci

S. pneumoniae (sometimes called pneumococcus) is the leading cause of bacterial pneumonia and sometimes the etiology of otitis media, meningitis, sinusitis, and peritonitis. The main reason why pneumococci cause disease is considered to be inflammation, so it is usually taken into account in the diagnoses associated with them.

Viridans

Streptococcus viridans is large group symbiotic bacteria, which are either α-hemolytic, giving a green color in blood agar plates (hence their name "virindans", ie "green" from the Latin "vĭrĭdis"), or non-hemolytic. They do not possess Lancefield antigens.

Streptococci that are important for medicine

Beta hemolytic

Beta-hemolytic streptococci are characterized by Lancefield serotyping, which is described as the presence of specific carbohydrates on the walls bacterial cells... The 20 described serotypes are divided into Lancefield groups with letters of the Latin alphabet from A to V (except for I and J) in the name.

Group A

S. pyogenes, also known as group A (GAS), cause a wide range of streptococcal infections. These infections can be non-invasive or invasive. In general, non-invasive infections are more common and less severe. The most common infections include impetigo and streptococcal pharyngitis (sore throat). Scarlet fever is also a non-invasive infection, but it has not been so common in recent years.

Invasive infections, caused by group A β-hemolytic streptococcus, are less common, but more severe. This occurs when a microorganism is capable of infecting areas where it would not normally be found, such as blood and organs. Potential illnesses include streptococcal toxic shock syndrome, pneumonia, necrotizing fasciitis, and bacteremia.

GAS infections can cause additional complications, namely acute rheumatic fever and acute glomerulonephritis. Rheumatism, a disease that affects joints, heart valves, and kidneys, is the result of untreated streptococcal GAS infection that is not caused by the bacteria itself. Rheumatism is caused by antibodies created by the immune system to fight infection, which cross-react with other proteins in the body. This "cross-reaction" essentially forces the body to attack itself and cause damage. Globally, GAS infections are estimated to cause more than 500,000 deaths each year, which is why they are among the world's leading pathogens. Group A streptococcal infections are usually diagnosed with a rapid Streptococcus test or culture.

Group B

S. agalactiae or group B streptococci, GBS, cause pneumonia and meningitis in newborns and the elderly, with rare systemic bacteremia. They can also colonize the intestines and the female reproductive tract, increasing the risk of premature rupture of membranes during pregnancy and transmission of pathogens to the newborn. The American College of Obstetricians and Gynecologists, the American Academy of Pediatrics and the US Centers for Disease Control and Prevention recommend that all pregnant women between 35-37 weeks gestation should be tested for GBS infection. Women who test positive should receive antibiotic treatment during labor, which will usually prevent transmission of the virus to the baby.

The United Kingdom has decided to adopt a risk factor protocol rather than a culture-based protocol as in the United States. Current guidelines suggest that if one or more of the following risk factors are present, women should be treated with antibiotics during childbirth:

• Premature birth (<37 недель)
• Prolonged rupture of membranes (\u003e 18 hours)
• Intrapartum fever (\u003e 38 ° C)
• Previously affected infant from GBS infection
• GBS- bacteriuria during pregnancy

The result of this protocol was the treatment of 15-20% of pregnancies, as well as the prevention of 65-70% of cases of early onset of GBS sepsis.

Group C

This group includes S. equichoking on horses, and S. zooepidemicus. S. equi is a clonal descendant or biovariant of ancestors S. zooepidemicus, which is the cause of infection in several mammalian species, including cattle and horses. Moreover, S. dysgalactiae belongs to group C, it is β-hemolytic streptococcus, which potentially causes pharyngitis and other suppurative infections, like group A streptococci.

Group D (enterococci)

Many group D streptococci have been reclassified and transferred to the genus Enterococcus (including E. faecium, E. faecalis, E. aviumand E. durans). For example, Streptococcus faecalis is now Enterococcus faecalis.

Other non-enterococcal group D strains include Streptococcus equinus and Streptococcus bovis.

Rarely, nonhemolytic streptococci cause disease. However, beta-hemolytic streptococcus and Listeria monocytogenes (actually a gram-positive bacillus) should not be confused with non-hemolytic streptococci.

Group F

In 1934, Long and Bliss described group F organisms among the "smallest hemolytic streptococci." They are also known as Streptococcus anginosus (according to the Lancefield classification system) or as group members S. milleri (according to the European system).

Group G

Usually (not exclusively) these streptococci are hemolytic. S. canis considered an example of GGS organisms typically found in animals but potentially causing infection in humans.

Group H

These streptococci are infectious agents in medium-sized dogs. In rare cases, they cause illness in humans unless they come into direct contact with the mouth of the animal. One of the most common ways of transmission is human-to-animal contact and mouth-to-mouth contact. However, a dog can lick a person's hand and the infection can spread as well.

Streptococcus video

Molecular taxonomy and phylogenetics

The division of streptococci into six groups is based on their 16S rDNA sequences: S. mitis, S. anginosus, S. mutans, S. bovis, S. pyogenesand S. salivarius... 16S groups were confirmed by complete genome sequencing. Important pathogens S. pneumoniae and S. pyogenes belong to groups S. mitisand S. pyogenes, respectively. And here is the causative agent of caries, Streptococcus mutans, is the main one for the streptococcal group.

Genomics

Hundreds of species' genomes have been sequenced. Most of the genomes of streptococci are 1.8 to 2.3 Mb in size and are responsible for 1700-2300 proteins. The table below lists some of the important genomes. 4 types indicated in the table ( S. pyogenes, S. agalactiae, S. pneumoniae and S. mutans) have an average pairwise protein sequence identity of approximately 70%.

Property	S. agalactiae	S. mutans	S. pyogenes	S. pneumoniae
Base pairs
Open reading frames

The textbook is divided into seven parts. Part one - "General Microbiology" - contains information about the morphology and physiology of bacteria. Part two is devoted to the genetics of bacteria. Part three - "Microflora of the Biosphere" - examines the microflora of the environment, its role in the cycle of substances in nature, as well as human microflora and its significance. Part four - "The doctrine of infection" - is devoted to the pathogenic properties of microorganisms, their role in the infectious process, and also contains information about antibiotics and their mechanisms of action. Part five - "The doctrine of immunity" - contains modern views about immunity. The sixth part - "Viruses and the diseases they cause" - provides information about the main biological properties of viruses and the diseases that they cause. Part seven - "Private medical microbiology" - contains information about the morphology, physiology, pathogenic properties of pathogens of many infectious diseases, as well as modern methods their diagnosis, specific prevention and therapy.

The textbook is intended for students, graduate students and teachers of higher medical educational institutions, universities, microbiologists of all specialties and practical doctors.

5th edition, revised and enlarged

Book:

Streptococci belong to the family Streptococcaceae (genus Streptococcus). They were first discovered by T. Billroth in 1874 with erysipelas; L. Pasteur - in 1878 with postpartum sepsis; isolated in pure culture in 1883 by F. Feleisen.

Streptococci (Greek ... streptos - chain and coccus - grain) - gram-positive, cytochrome-negative, catalase-negative spherical or ovoid cells with a diameter of 0.6 - 1.0 microns, grow in the form of chains of various lengths (see color incl., Fig. 92) or in the form of tetracocci; motionless (except for some representatives of serogroup D); the content of G + C in DNA is 32 - 44 mol% (for the family). Do not form a dispute. Pathogenic streptococci form a capsule. Streptococci are facultative anaerobes, but there are also severe anaerobes. Temperature optimum 37 ° C, optimum pH 7.2 - 7.6. On ordinary nutrient media, pathogenic streptococci either do not grow, or grow very poorly. Sugar broth and blood agar containing 5% defibrinated blood are usually used for their cultivation. The medium should not contain reducing sugars, as they inhibit hemolysis. On the broth, the growth is near-parietal in the form of a crumbly sediment, the broth is transparent. Streptococci forming short chains cause the broth to cloud. On solid media, streptococci of serogroup A form colonies of three types: a) mucoid - large, shiny, resemble a drop of water, but have a viscous consistency. Such colonies form freshly isolated virulent strains having a capsule;

b) rough - larger than mucoid, flat, with an uneven surface and scalloped edges. Such colonies form virulent strains with M antigens;

c) smooth, smaller colonies with smooth edges; form non-virulent cultures.

Streptococci ferment glucose, maltose, sucrose and some other carbohydrates to form acid without gas (except S. kefirwhich forms acid and gas), milk is not curdled (except S. lactis), do not possess proteolytic properties (except for some enterococci).

Classification of streptococci. The genus of streptococci includes about 50 species. Among them, 4 pathogenic ( S. pyogenes, S. pneumoniae, S. agalactiаeand S. equi), 5 opportunistic and more than 20 opportunistic species. For convenience, the entire genus is subdivided into 4 groups using the following features: growth at a temperature of 10 ° C; growth at 45 ° C; growth on a medium containing 6.5% NaCl; growth on a medium with a pH of 9.6;

growth on a medium containing 40% bile; growth in milk with 0.1% methylene blue; growth after heating at 60 ° C for 30 min.

Most of the pathogenic streptococci belong to the first group (all of these signs are usually negative). Enterococci (serogroup D), which also cause various diseases people belong to the third group (all of the listed signs are usually positive).

The simplest classification is based on the ratio of streptococci to erythrocytes. Distinguish:

-? -Hemolytic streptococci - when growing on blood agar around the colony, there is a clear hemolysis zone (see color incl., Fig. 93a);

-? -Hemolytic streptococci - greenish staining and partial hemolysis around the colony (greening is due to the conversion of oxyhemoglobin into methemoglobin, see color incl., Fig. 93b);

-? 1-hemolytic streptococci, in comparison with? -Hemolytic streptococci, form a less pronounced and unclear hemolysis zone;

-? - and? 1-streptococci are called S. viridans (green streptococci);

-? -Nehemolytic streptococci do not cause hemolysis on a solid nutrient medium.

Serological classification is of great practical importance. Streptococci have a complex antigenic structure: they have a common antigen for the whole genus and various other antigens. Among them, group-specific polysaccharide antigens localized in the cell wall are of particular importance for classification. According to these antigens, at the suggestion of R. Lansfeld, streptococci are divided into serological groups, designated by the letters A, B, C, D, F, G, etc. Now, 20 serological groups of streptococci (from A to V) are known. Streptococci pathogenic to humans belong to group A, to groups B and D, less often to C, F and G. In this regard, the determination of the group belonging of streptococci is a decisive moment in the diagnosis of the diseases they cause. Group polysaccharide antigens are determined using the corresponding antisera in the precipitation reaction.

In addition to group antigens, type-specific antigens were found in hemolytic streptococci. In group A streptococci, they are proteins M, T and R. Protein M is thermally stable in an acidic environment, but is destroyed by trypsin and pepsin. It is detected after hydrochloric acid hydrolysis of streptococci using a precipitation reaction. Protein T is destroyed when heated in an acidic environment, but is resistant to the action of trypsin and pepsin. It is determined using an agglutination reaction. The R antigen is also found in streptococci of serogroups B, C and D. It is sensitive to pepsin, but not to trypsin, degrades when heated in the presence of acid, but is stable when heated moderately in a weak alkaline solution. According to the M-antigen, hemolytic streptococci of serogroup A are subdivided into a large number of serovariants (about 100), their determination has epidemiological significance. According to the T-protein, streptococci of serogroup A are also subdivided into several dozen serovariants. In group B, there are 8 serovariants.

Streptococci also have cross-reacting antigens common to antigens of the basal layer of the skin epithelium and the epithelial cells of the cortical and medullary zones of the thymus, which may be the cause of the autoimmune disorders caused by these cocci. An antigen (receptor II) was found in the cell wall of streptococci, which is associated with their ability, like staphylococci with protein A, to interact with the Fc-fragment of the IgG molecule.

Diseases caused by streptococci distributed in 11 classes. The main groups of these diseases are as follows: a) various suppurative processes - abscesses, phlegmon, otitis media, peritonitis, pleurisy, osteomyelitis, etc .;

b) erysipelas - wound infection (inflammation of the lymphatic vessels of the skin and subcutaneous tissue);

c) purulent complications of wounds (especially in wartime) - abscesses, phlegmon, sepsis, etc.;

d) sore throats - acute and chronic;

e) sepsis: acute sepsis (acute endocarditis); chronic sepsis (chronic endocarditis); postpartum (puerperal) sepsis;

f) rheumatism;

g) pneumonia, meningitis, creeping corneal ulcer (pneumococcus);

h) scarlet fever;

i) dental caries - its causative agent is most often S. mutans... The genes of cariogenic streptococci responsible for the synthesis of enzymes that ensure colonization of the surface of teeth and gums by these streptococci have been isolated and studied.

Although most of the pathogenic streptococci for humans belong to serogroup A, streptococci of serogroups D and B also play an important role in human pathology. Streptococci of serogroup D (enterococci) are recognized as causative agents of wound infections, various purulent surgical diseases, purulent complications in pregnant women, postpartum women and gynecological patients, infect kidneys, bladder, cause sepsis, endocarditis, pneumonia, foodborne toxicoinfections (proteolytic variants of enterococci). Serogroup B streptococci ( S. agalactiae) often cause diseases of newborns - respiratory tract infections, meningitis, septicemia. Epidemiologically, they are associated with the carriage of this type of streptococcus in the mother and staff of maternity hospitals.

Anaerobic streptococci ( Peptostreptococcus), which are found in healthy people as part of the microflora of the respiratory tract, mouth, nasopharynx, intestines and vagina, can also be the culprits of purulent-septic diseases - appendicitis, postpartum sepsis, etc.

The main factors of the pathogenicity of streptococci.

1. Protein M - the main factor of pathogenicity. M-proteins of streptococcus are fibrillar molecules that form fimbriae on the surface of the cell wall of group A streptococci. M-protein determines adhesive properties, inhibits phagocytosis, determines antigenic type-specificity and has superantigen properties. Antibodies to the M-antigen have protective properties (antibodies to the T- and R-proteins do not have such properties). M-like proteins are found in streptococci of groups C and G and, possibly, are factors of their pathogenicity.

2. Capsule. It consists of hyaluronic acid, similar to that which is part of the tissue, so phagocytes do not recognize streptococci with a capsule as foreign antigens.

3. Erythrogenin - scarlet fever toxin, superantigen, causes TSS. There are three serotypes (A, B, C). In patients with scarlet fever, it causes a bright red rash on the skin and mucous membranes. It has pyrogenic, allergenic, immunosuppressive and mitogenic effects, destroys platelets.

4. Hemolysin (streptolysin) O destroys erythrocytes, has a cytotoxic, including leukotoxic and cardiotoxic, effect, it is formed by most streptococci of serogroups A, C and G.

5. Hemolysin (streptolysin) S has hemolytic and cytotoxic effects. Unlike streptolysin O, streptolysin S is a very weak antigen; it is also produced by streptococci from serogroups A, C and G.

6. Streptokinase - an enzyme that converts a preactivator into an activator, and it converts plasminogen into plasmin, the latter also hydrolyzes fibrin. Thus, streptokinase, activating blood fibrinolysin, increases the invasive properties of streptococcus.

7. A factor that inhibits chemotaxis (aminopeptidase) inhibits the mobility of neutrophilic phagocytes.

8. Hyaluronidase is an invasion factor.

9. Clouding factor - hydrolysis of serum lipoproteins.

10. Proteases - destruction of various proteins; it is possible that tissue toxicity is associated with them.

11. DNase (A, B, C, D) - DNA hydrolysis.

12. The ability to interact with the Fc-fragment of IgG using the receptor II - suppression of the complement system and the activity of phagocytes.

13. Pronounced allergenic properties of streptococci, which cause sensitization of the body.

Streptococcus resistance. Streptococci tolerate low temperatures well, are quite resistant to drying, especially in a protein environment (blood, pus, mucus), remain viable for several months on objects and dust. When heated to a temperature of 56 ° C, they die after 30 minutes, except for group D streptococci, which withstand heating to 70 ° C for 1 hour, a 3 - 5% solution of carbolic acid and lysol kills them within 15 minutes.

Features of epidemiology. The source of exogenous streptococcal infection are patients with acute streptococcal diseases (tonsillitis, scarlet fever, pneumonia), as well as convalescents after them. The main method of infection is airborne, in other cases - direct contact and very rarely alimentary (milk and other food products).

Features of pathogenesis and clinic. Streptococci are inhabitants of the mucous membranes of the upper respiratory tract, digestive and urinary tracts, therefore, the diseases they cause can be endogenous or exogenous, that is, they are caused either by their own cocci, or as a result of infection from the outside. Having penetrated through damaged skin, streptococci spread from the local focus through the lymphatic and circulatory system... Infection by airborne droplets or airborne dust leads to damage to the lymphoid tissue (tonsillitis), the process involves regional lymph nodes, from where the pathogen spreads through the lymphatic vessels and hematogenously.

The ability of streptococci to cause various diseases depends on:

a) the places of the entrance gates (wound infections, puerperal sepsis, erysipelas, etc.; respiratory tract infections - scarlet fever, tonsillitis);

b) the presence of various pathogenic factors in streptococci;

c) states immune system: in the absence of antitoxic immunity, infection with serogroup A toxigenic streptococci leads to the development of scarlet fever, and in the presence of antitoxic immunity, angina occurs;

d) sensitizing properties of streptococci; they largely determine the peculiarity of the pathogenesis of streptococcal diseases and are the main cause of complications such as nephrosonephritis, arthritis, damage to the cardiovascular system, etc.;

e) pyogenic and septic functions of streptococci;

f) the presence of a large number of serovariants of serogroup A streptococci by the M antigen.

Antimicrobial immunity, which is caused by antibodies to the M protein, has a type-specific character, and since there are a lot of serovariants for the M-antigen, repeated diseases of angina, erysipelas and other streptococcal diseases are possible. The pathogenesis of chronic infections caused by streptococci is more complex: chronic tonsillitis, rheumatism, nephritis. The etiological role of serogroup A streptococci in them is confirmed by the following circumstances:

1) these diseases, as a rule, occur after the transfer of acute streptococcal infections (tonsillitis, scarlet fever);

2) in such patients, streptococci or their L-forms and antigens are often found in the blood, especially during exacerbations, and, as a rule, hemolytic or green streptococci on the pharyngeal mucosa;

3) constant detection of antibodies to various antigens of streptococci. The detection of anti-O-streptolysins and anti-hyaluronidase antibodies in high titers in patients with rheumatism during an exacerbation in the blood is of especially valuable diagnostic value;

4) the development of sensitization to various streptococcal antigens, including the thermostable component of erythrogenin. It is possible that in the development of rheumatism and nephritis, autoantibodies to connective and renal tissue, respectively, play a role;

5) the obvious therapeutic effect of the use of antibiotics against streptococci (penicillin) during rheumatic attacks.

Post-infectious immunity. The main role in its formation is played by antitoxins and type-specific M-antibodies. Antitoxic immunity after scarlet fever is strong and long-lasting. Antimicrobial immunity is also strong and long-term, but its effectiveness is limited by the type-specificity of M-antibodies.

Laboratory diagnostics. The main method for diagnosing streptococcal diseases is bacteriological. The material for the study is blood, pus, mucus from the pharynx, plaque from the tonsils, and discharge from wounds. The decisive stage in the study of the isolated pure culture is the determination of its serogroup. Two methods are used for this purpose.

A. Serological - determination of group polysaccharide using a precipitation reaction. For this purpose, use the appropriate group-specific sera. If the strain is beta hemolytic, its polysaccharide antigen is extracted with HCl and tested with serogroups A, B, C, D, F and G. If the strain does not induce beta hemolysis, its antigen is extracted and tested with antisera from groups B and D only. Group A, C, F, and G antisera often cross-react with alpha-hemolytic and non-hemolytic streptococci. Streptococci that do not cause beta hemolysis and do not belong to groups B and D are identified by other physiological tests (Table 20). Group D streptococci have been identified as an independent genus Enterococcus.

B. Grouping method - based on the ability of aminopeptidase (an enzyme produced by streptococci from serogroups A and D) to hydrolyze pyrrolidine-naphthylamide. For this purpose, commercial kits of necessary reagents are produced for the determination of group A streptococci in blood and broth cultures. However, the specificity of this method is less than 80%. Serotyping of serogroup A streptococci is performed using either precipitation (determine the M-serotype) or agglutination (determine the T-serotype) only for epidemiological purposes.

Of the serological reactions, coagglutination and latex agglutination reactions are used to detect streptococci of serogroups A, B, C, D, F and G. Determination of the titer of antihyaluronidase and anti-O-streptolysin antibodies is used as an auxiliary method for diagnosing rheumatism and for assessing the activity of the rheumatic process.

For the detection of streptococcal polysaccharide antigens, IFM can also be used.

PNEUMOCOCCI

A special position in the genus Streptococcus takes the form S. pneumoniaewhich plays a very important role in human pathology. It was discovered by L. Pasteur in 1881. Its role in the etiology of croupous pneumonia was established in 1886 by A. Frenkel and A. Weikselbaum, as a result of which S. pneumoniae called pneumococcus. Its morphology is peculiar: cocci have a shape resembling a candle flame: one

Table 20

Differentiation of some categories of streptococci

Note: + - positive, - negative, (-) - very rare signs, (±) - unstable sign; b aerococci - Aerococcus viridans, found in approximately 1% of patients suffering from streptococcal diseases (osteomyelitis, subacute endocarditis, urinary tract infections). Allocated as an independent species in 1976, insufficiently studied.

the end of the cell is pointed, the other is flattened; are usually arranged in pairs (flat ends are facing each other), sometimes in the form of short chains (see color incl., Fig. 94b). They have no flagella, do not form a dispute. In humans and animals, as well as on media containing blood or serum, they form a capsule (see color incl., Fig. 94a). Gram positive, but often gram negative in young and old cultures. Optional anaerobes. The optimum temperature for growth is 37 ° C, at temperatures below 28 ° C and above 42 ° C they do not grow. The optimum pH for growth is 7.2 - 7.6. Pneumococci produce hydrogen peroxide, but they do not have catalase, so for growth they require the addition of substrates containing this enzyme (blood, serum). On blood agar, small round colonies are surrounded by a green zone formed by the action of the exotoxin hemolysin (pneumolysin). Growth on sugar broth is accompanied by turbidity and precipitation. In addition to the O-somatic antigen, pneumococci have a capsular polysaccharide antigen, which is characterized by a wide variety: according to the polysaccharide antigen, pneumococci are divided into 83 serovariants, 56 of them are divided into 19 groups, 27 are presented independently. Pneumococci differ from all other streptococci in morphology, antigenic specificity, and also in that they ferment inulin and exhibit high sensitivity to optochin and bile. Under the influence of bile acids, intracellular amidase is activated in pneumococci. It breaks the bond between alanine and peptidoglycan muramic acid, the cell wall is destroyed, and pneumococcus lysis occurs.

The main factor in the pathogenicity of pneumococci is a polysaccharide capsule. Capsular pneumococci lose their virulence.

Pneumococci are the main causative agents of acute and chronic inflammatory diseases lungs, which occupy one of the leading places in morbidity, disability and mortality of the population of the whole world.

Pneumococci, along with meningococci, are the main culprits of meningitis. Moreover, they cause creeping ulcer cornea, otitis media, endocarditis, peritonitis, septicemia and a number of other diseases.

Post-infectious immunity type-specific, due to the appearance of antibodies against a typical capsular polysaccharide.

Laboratory diagnostics based on selection and identification S. pneumoniae... Sputum and pus are used as research material. White mice are very sensitive to pneumococci, therefore, a biological sample is often used to isolate pneumococci. In dead mice, pneumococci are found in a smear preparation from the spleen, liver, lymph nodes, and when inoculated, a pure culture is isolated from these organs and from the blood. To determine the serotype of pneumococci, an agglutination reaction on glass with typical sera or the phenomenon of "swelling of capsules" is used (in the presence of homologous serum, the capsule of pneumococci swells sharply).

Specific prevention pneumococcal diseases are carried out using vaccines prepared from highly purified capsular polysaccharides of those 12-14 serovariants that most often cause diseases (1, 2, 3, 4, 6A, 7, 8, 9, 12, 14, 18C, 19, 25) ... Vaccines are highly immunogenic.

SCARLATIN MICROBIOLOGY

Scarlet fever (late lat ... scarlatium - bright red color) is an acute infectious disease, which is clinically manifested by angina, lymphadenitis, a small-point bright red rash on the skin and mucous membrane with subsequent peeling, as well as general intoxication of the body and a tendency to purulent-septic and allergic complications.

The causative agents of scarlet fever are group A beta-hemolytic streptococci, which have an M antigen and produce erythrogenin. The etiological role in scarlet fever was attributed to various microorganisms - protozoa, anaerobic and other cocci, streptococci, filterable forms of streptococcus, viruses. The decisive contribution to the elucidation of the true cause of scarlet fever was made by the Russian scientists G. N. Gabrichevsky, I. G. Savchenko and the American scientists, the spouses Dick (G. F. Dick and G. H. Dick). I.G.Savchenko back in 1905 - 1906. showed that streptococcus scarlet fever produces a toxin, and the antitoxic serum obtained by it has a good therapeutic action... Based on the works of I.G.Savchenko, the wife of Dick in 1923 - 1924. showed that:

1) the introduction of a small dose of toxin intradermally to persons who have not had scarlet fever, causes them a positive local toxic reaction in the form of redness and swelling (Dick's reaction);

2) in persons who have had scarlet fever, this reaction is negative (the toxin is neutralized by the antitoxin they have);

3) the introduction of large doses of the toxin subcutaneously to persons who did not suffer from scarlet fever, causes them symptoms characteristic of scarlet fever.

Finally, by infecting volunteers with a culture of streptococcus, they were able to reproduce scarlet fever. Currently, the streptococcal etiology of scarlet fever is generally accepted. The peculiarity here lies in the fact that scarlet fever is caused not by any one serotype of streptococci, but by any of the beta-hemolytic streptococci, which have an M antigen and produce erythrogenin. However, in the epidemiology of scarlet fever in different countries, in their different regions and in different time the main role is played by streptococci with different serotypes of the M-antigen (1, 2, 4 or other) and producing erythrogenins of different serotypes (A, B, C). A change in these serotypes is possible.

The main factors in the pathogenicity of streptococci in scarlet fever are exotoxin (erythrogenin), pyogenic-septic and allergenic properties of streptococcus and its erythrogenin. Erythrogenin consists of two components - a heat-labile protein (the toxin itself) and a heat-stable substance with allergenic properties.

Infection with scarlet fever occurs mainly by airborne droplets, but any wound surface can be the entrance gate. The incubation period is 3 - 7, sometimes 11 days. The pathogenesis of scarlet fever reflects 3 main points associated with the properties of the pathogen:

1) the action of scarlet toxin, which causes the development of toxicosis - the first period of the disease. It is characterized by damage to peripheral blood vessels, the appearance of a small-point rash of bright red color, as well as an increase in temperature and general intoxication. The development of immunity is associated with the appearance and accumulation of antitoxin in the blood;

2) the action of the streptococcus itself. It is nonspecific and manifests itself in the development of various purulent-septic processes (otitis media, lymphadenitis, nephritis appear on the 2nd - 3rd week of the disease);

3) sensitization of the body. It is reflected in the form of various complications such as nephrosonephritis, polyarthritis, cardiovascular diseases, etc. on the 2nd - 3rd week. disease.

In the clinic of scarlet fever, I (toxicosis) and stage II are also distinguished, when purulent-inflammatory and allergic complications are observed. In connection with the use of antibiotics (penicillin) for the treatment of scarlet fever, the frequency and severity of complications decreased significantly.

Post-infectious immunity durable, long-term (repeated diseases are observed in 2-16% of cases), due to antitoxins and immune memory cells. Those who have recovered also remain allergic to the scarlet fever allergen. It is detected by intradermal administration of killed streptococci. In those who had recovered from the injection site, redness, swelling, soreness (Aristovsky-Fanconi test). To check for the presence of antitoxic immunity in children, the Dick reaction is used. With its help, it was found that passive immunity in children of the 1st year of life persists during the first 3 - 4 months.

The content of the article

Entitled " streptococcal infection»Combine diseases caused by hemolytic streptococcus. They are very diverse, starting with scarlet fever, erysipelas, with mild localized inflammatory processes in the pharynx, nose, nasopharynx, ears, on the skin, and ending with the most severe expediting pneumonia, sepsis, septicopyemia. All of them are closely related by a common etiology, have epidemiological connections, common pathogenetic, morphological, clinical manifestations and are directly related to infectious pathology. Description of scarlet fever, erysipelas is given in special chapters, this chapter provides a brief description of the main general patterns inherent in the entire group of streptococcal infections.

Etiology of streptococcal infection in children

The causative agent is hemolytic streptococcus (streptococcus haemolyticus). This is a spherical or oval microbe, forms chains of various lengths in smears, is stained according to Gram; from the entire group of streptococci it is distinguished by the nature of hemolysis on solid media with the addition of blood. Streptococci on this basis are divided into α-greening - their colonies are surrounded by a greenish hemolysis zone, β-hemolytic, forming a hemolysis zone around the colony, and non-hemolytic.

Among β-hemolytic streptococci, 17 groups are distinguished according to the precipitation reaction, designated by letters of the alphabet from A to S f Lancefield, 1933: Griffits, 1935). Diseases in humans are caused by streptococci mainly of group A. However, in recent years, there have been indications of the importance of group B streptococci in pathology, especially in newborns and weakened ones, as well as in premature babies. Among streptococci of group A, about 60 different serological types were identified, which are determined by the agglutination reaction with the corresponding sera of immunized animals.

Attempts to link the different manifestations of streptococcal infection with certain types of streptococci have not been successful. It is considered established that different serological types of streptococcus can cause the same clinical forms of streptococcal infection. On the other hand, the same type causes both carriage and various streptococcal diseases, including scarlet fever and erysipelas.
The regularity is that with a variety of streptococcal diseases, a large number of types are determined, which increases with milder forms and especially with streptococcal disease, while with scarlet fever, the number of serotypes is more limited.

Bacterial components determine the invasiveness, aggressive properties of hemolytic streptococcus, they are type-specific. In accordance with this response are type-specific antibodies:
precipitins, agglutinins, bacteriotropins, complement-binding and protective... Thus, antibacterial immunity is predominantly type-specific, that is, directed against one specific type of streptococcus. In addition, it is fragile, which, with a wide variety of types of hemolytic streptococcus, determines the frequency, recurrence of streptococcal infection in the same child in the form of tonsillitis, rhinitis, otitis media and other forms.

Exotoxins cause general intoxication, they are heterogeneous and consist of several components. The main one is Dick's erythrogenic toxin, it is also called a general action toxin, or rash toxin. In addition to it, streptococci secrete toxins of "private application" (V.I. Ioffe) - streptolysin (O and S), leukocidin, enterotoxin and enzymes - hyaluronidase, streptokinase, amylase, proteinase, etc. Dick's erythrogenic toxin causes general intoxication and the development of the syndrome scarlet fever, and other toxins and enzymes facilitate its penetration into tissues. Different serological types of streptococci emit a qualitatively homogeneous toxin, to which a homogeneous antitoxin is produced in the patient's body. Therefore, antitoxic immunity does not possess type-specificity, and with subsequent infection with other types of streptococcus, even with high toxigenicity, local inflammatory processes occur, but not scarlet fever.
A feature of antitoxic immunity is its stability, it persists for life.

Streptococcus resistance to physical and chemical influences is quite high. When heated in a humid environment up to 70 ° C, some strains remain viable for up to 1 hour, and at 65 ° C for up to 2 hours. But as a rule, they die after 30 minutes at a temperature of 60 ° C. and after 15 minutes under the influence of chemical disinfectants. Streptococci tolerate freezing well; in dried up pus or blood persists for weeks and months; quickly die under the action of disinfectants. They are very sensitive to the action of penicillin, erythromycin, oleandomycin and other antibiotics, more moderately sensitive to streptomycin.

Epidemiology of streptococcal infection in children

The source of streptococcal infection is a patient and a streptococcal carrier; the importance of healthy carriers is small. Patients can be sources of infection in any form of the disease, but the most dangerous are patients with damage to the upper respiratory tract and throat. Streptococci are sprayed with droplets of saliva during conversation, coughing, sneezing. When dry, they can mix with dust and circulate in the air. With purulent lesions on the hands, streptococcus can be introduced into food (milk, jelly, cream, etc.), where it can multiply. As a result of eating contaminated food, foodborne infections can occur. Infection with streptococcal infection through objects and through a "third party" is possible, but in the spread of infection, this path is of little importance.
Susceptibility to streptococcus, apparently, universal, it is highest in childhood and young age and decreases after 40-50 years.
Morbidity different forms of streptococcal infection is very large. Due to the lack of registration and registration of all diseases caused by hemolytic streptococcus, there are no data fully characterizing its distribution. Among adults working in enterprises, the incidence of streptococcal sore throats alone reaches 10-20%, the incidence of children is much higher. Streptococcal diseases are more common in autumn and winter. Carriage can reach significant proportions, however, among children, when streptococcus is isolated, mild or erased forms of infection are usually determined.

Pathogenesis of streptococcal infection in children

The place of introduction of streptococcus most often is the tonsils and lymphoid tissue of the upper respiratory tract, less often damaged skin (diaper rash, burns, wounds), where a primary inflammatory focus occurs with the reproduction of streptococci, the accumulation of toxins and decay products of tissues and microbial bodies. From a local inflammatory focus, streptococci spread, toxins, protein breakdown products are absorbed, and a pathological process develops in the body, in which three syndromes or three lines of pathogenesis are distinguished: infectious (or septic), toxic and allergic.

Infectious Syndrome includes changes directly related to the reproduction and vital activity of streptococci. At the site of the introduction of the microbe, catarrhal inflammation occurs, it can turn into a purulent, necrotic (primary focus).
Hemolytic streptococcus has aggressiveness, which is expressed and its rapid spread from the primary focus to the surrounding tissues, to regional lymph nodes, the formation of a primary complex (V.D. Tsinserling), periadenitis, phlegmon can develop. With the most frequent lesion of the pharynx, streptococcus can spread intracanalicularly through the Eustachian tube, into the middle ear and cause otitis media, mastoiditis, etc.; spread into the nasopharynx can contribute to the development of sinusitis, ethmoiditis. Of all foci of inflammation, hematogenous dissemination and the development of metastatic purulent foci in any organ (septicopyemia) are possible. With a good adaptive ability of the body, the rapid development of immune reactions, especially with etihasty treatment, the process can stop at any stage.

Toxic syndrome develops due to the absorption of the toxin of hemolytic streptococcus and its spread in the body. The main manifestations of intoxication are fever, tachycardia, and impaired well-being. sometimes vomiting. The degree of their severity is different, it depends on the state of the patient's antitoxic immunity and on the properties of the pathogen. The presence of a toxic effect even in milder forms of streptococcal infection is confirmed by the development of antitoxic immunity. detected by increasing titers of immunological reactions.

Allergic syndrome due to the allergenic effect of streptococcal protein, which, absorbed during the course of the disease, causes an allergic mood and creates the prerequisites for the development of nephritis, rheumatism, collagenosis.
The clinical diversity of streptococcal infection forms depends on the localization of the process, the various relationships between the goxygenicity and virulence of the pathogen and the state of the macroorganism, the degree of its antibacterial and antitoxic immunity, allergic mood, and nonspecific resistance.

Clinic of streptococcal infection in children

The clinical manifestations of streptococcal infection are very diverse - from the mildest forms to severe septic diseases.
Despite the huge variety of clinical manifestations, the entire group of streptococcal infection has common clinical features due to the specific properties of hemolytic streptococcus. In severe diseases, these features are very clearly expressed and can be diagnosed; as the severity decreases, they are erased and more difficult to identify.

The incubation period is short - from a few hours to 4-5 days. Characterized by an acute onset of the disease, the rapid development of a local inflammatory focus and general intoxication. The clinical feature is the severity of signs of inflammation (soreness, hyperemia and tissue infiltration in the local inflammatory focus). The same inflammatory reaction, accompanied by soreness and a tendency to suppuration, occurs in the regional lymph nodes. Characterized by the appearance of leukocytosis, neutrophilia, often with a shift to the left, increased ESR.
In the classification of streptococcal infection, mainly local infectious processes and generalized forms are distinguished, differing in the severity and nature of the course of the disease. Scarlet fever, which differs from other forms by the pronounced action of the erythrogenic toxin of streptococcus, and erysipelas are described in the relevant sections. Mostly local streptococcal diseases are distinguished by localization. Skin and subcutaneous streptococcal processes include streptoderma, phlegmon, abscesses, lymphadenitis, lymphangitis, inflammation of wounds and burns. Bone and articular lesions are manifested in the form of arthritis, osteomyelitis.
Lesions of the pharynx, nasopharynx and accessory cavities - this rhinitis, pharyngitis, tonsillitis, tonsillitis, adenoiditis, otitis media, mastoiditis, sinusitis.
Respiratory system disorders develop in the form laryngitis, bronchitis, tracheitis, pneumonia, abscess, empyema.
When damage to the cardiovascular system arise endocarditis, pericarditis.
IN digestive organs streptococcus may cause abscess, peritonitis, cholecystitis, foodborne toxicoinfection.
Streptococcal infection genitourinary system may manifest nephritis, cystitis, pyelitis, postpartum infections.
When damage to the nervous system arise purulent meningitis, brain abscesses.
Essentially, a person does not have a single organ that could not be affected by streptococcus.

The main generalized form of streptococcal infection is septicopyemia with metastases in any tissues and organs. Currently, it does not occur with antibiotic treatment.
The severity of streptococcal processes is determined by intoxication, the degree of which is usually in direct proportion to the nature of the local inflammatory focus. Subclinical, mild forms are widespread, occurring at normal or subfebrile temperatures, mainly with catarrhal changes in the local focus (catarrhal tonsillitis, rhinitis, etc.). There may be inapparent forms, which are detected only on the basis of immunological changes. Moderate forms occur with moderate intoxication at a temperature of 38-39 ° C with severe symptoms of impaired well-being (headache, poor appetite, weakness, vomiting may occur) and are accompanied by tachycardia. These are localized, predominantly purulent processes, for example, follicular, lacunar tonsillitis, with pronounced inflammatory changes, with a reaction in the regional lymph nodes.

Severe forms are characterized by high temperature, changes in the cardiovascular system (tachycardia, deafness of heart sounds, a drop in blood pressure), impaired consciousness, vomiting, etc., such intoxication occurs mainly with purulent lesions of the lungs, empyema, septicopyemia, etc. Mild streptococcal processes in in the form of catarrhal tonsillitis, rhinitis can take a protracted, chronic course; the duration of the disease especially contributes to the allergization of the body. The diagnosis in the most pronounced forms can be based on clinical changes, but, as a rule, it must be confirmed bacteriologically - by excretion of hemolytic streptococcus from pus or from mucus of the throat, nose. In diagnostics, immunological reactions can be important, but for general practice they are complex and almost inaccessible.

Features of streptococcal infection in modern conditions

Streptococcal infection until the 50s, before the appearance of etiotropic drugs, caused a large number of violently proceeding severe diseases with high mortality: abscessing pneumonia, empyema, septicopyemia, meningitis, etc. This infection was spread as a nosocomial cross-infection in maternity hospitals, surgical departments, infectious children's hospitals, as a secondary infection with measles, whooping cough, diphtheria, was common reason severe complications and deaths. After the introduction of penicillin into practice, which has a quick effect on streptococcus, severe forms with damage to internal organs and bones began to disappear; nosocomial streptococcal infection has practically disappeared among the causes of death, but its importance in the pathology of children is still very high. Moderate, mild, subclinical forms are widespread. Currently, mainly local processes are observed with localization in the pharynx, on the skin. The most common are pyoderma, rhinitis, tonsillitis, nasopharyngitis, otitis media, lymphadenitis, which is one of the reasons for the spread of scarlet fever, allergization of children, the occurrence of renal diseases, rheumatism, heart damage, chronic tonsillitis, etc.

Treatment of streptococcal infection in children

Treatment for streptococcal infection should be etiotropic. In the first place among etiotropic agents is penicillin, to which streptococci, as a rule, remain sensitive, despite its more than 30 years of use. The introduction of penicillin, as a rule, interrupts the streptococcal process at any stage of development. To obtain a bactericidal effect, the dose and course of treatment with penicillin should be sufficient. In severe forms, penicillin is administered at the rate of 50,000-100,000 U / (kg day), with streptococcal infection moderate and in other forms, this dose can be reduced to 30,000-40,000 U / (kg day). In the best way the introduction of penicillin is intramuscular with an interval between injections of 3-4 hours, in milder forms, a 2-time injection or 4-5 doses of phenoxymethylpenicillin is sufficient. The duration of the course is 5-7 days.
With streptococcal infection in children over 3 years old, durant penicillin preparations - bicillin-3 can also be used.
Bicillin-3 is absorbed quickly and appears in the blood within an hour, in bacteriostatic concentration it lasts for 7-8 days, therefore it is especially convenient for the treatment of acute forms of streptococcal infection. The drug is administered once at a dose of 20,000 U / (kg-day), but not more than 800 OOO U. Previously, to determine the sensitivity to penicillin, do skin test... A 0.1% solution of penicillin is injected intradermally at a dilution of 1:10 000 (on the inner surface of the forearm). The reaction is checked after 20 hours. If penicillin is intolerant, its semisynthetic preparations (oxacillin) are used. Sulfanilamide drugs are ineffective.

Symptomatic therapy in the past with tonsillitis, nasopharyngitis almost always included rinsing, irrigation of the throat. Currently, they are used less often, but they certainly have a hygienic value (usually furacilin is used at a dilution of 1: 5000).
Vitamins are widely used for all forms of streptococcal infection, especially vitamin C and B vitamins.
With otitis media, lymphadenitis, phlegmon, physiotherapeutic procedures are used, mainly UHF; with acute suppurative processes, early surgical intervention is necessary.
With streptococcal infection of moderate and severe, bed rest is prescribed. The diet can be general with the exception of salty, smoked foods and spices, with an increased content of vitamins.

Prevention of streptococcal infection in children

All forms of streptococcal infection are contagious and highly contagious; there are close epidemiological links between different forms. Prevention is very difficult due to the wide distribution of light, worn out, subclinical forms. The main preventive measure Is the isolation and sanitation of patients (penicillin therapy).
Sanitation is carried out by carrying out general measures aimed at strengthening the body.