Streptococcus biological properties. Medical microbiology, immunology and virology. Growth and conditions

Streptococci are gram-positive cocci, mostly aerobes.

The classification of streptococci is based on the type of hemolysis they cause on blood agar and on the antigenic properties of the cell wall polysaccharide. According to the type of hemolysis, α-hemolytic, β-hemolytic and γ-non-hemolytic streptococci are distinguished. According to antigenic differences, 20 groups of streptococci are distinguished, designated by Latin letters from A to V (classification by R. Lancefield).

The most pathogenic streptococcus is α-hemolytic streptococcus group A - Streptococcus pyogenes. It causes sore throat, scarlet fever, erysipelas, impetigo and sepsis. Sensitization can cause erythema nodosum, rheumatism, and acute glomerulonephritis. In addition to the polysaccharide antigen, Streptococcus pyogenes also has other surface antigens (types M, T and R), they are used for epidemiological studies.

The M antigen is an important virulence factor; it is associated with the development of type-specific immunity; some streptococci that have the M antigen cause glomerulonephritis. Streptococcus pyogenes produces the following types of exotoxins.

Streptolysin O: damages cells by binding to cholesterol in membranes; has a cardiotoxic effect in many animals, possibly in humans; powerful antigen.

Streptolysin S: has hemolytic activity, its mechanism of action is unknown; does not have antigenic properties.

Deoxyribonuclease, streptokinase, hyaluronidase: may contribute to the spread of infection in tissues.

Erythrogenic (pyogenic) toxin: only some strains produce it; has antigenic properties.

Streptococcus viridans (α-hemolytic streptococcus) is the main causative agent of subacute infective endocarditis; anaerobic streptococci often cause surgical and postpartum sepsis.

Streptococcus pyogenes infections are common in countries temperate climate. Children are more often infected, the incidence increases in winter. The infection is often asymptomatic, up to 20% of children are bacteria carriers.

The source of infection is a bacteriocarrier or a patient (especially with an upper respiratory tract infection). Children are more likely to become carriers of infection than adults. A recovering person is more contagious than a carrier. In carriers, the infection is more often localized in the pharynx than in the nose, but in the latter case, the number of bacteria and their virulence is higher.

The most common route of transmission of infection is airborne: with saliva or sputum when coughing and sneezing. Another way is contact-household: through handshakes and household items. Consumption of contaminated foods (most often milk) can cause outbreaks of sore throats and scarlet fever.

The outcome of infection depends on the virulence of the bacteria and the resistance of the organism. With high antibacterial immunity, streptococci die or remain on the surface of the skin without causing harm. With a decrease in immunity or high virulence of streptococci, a superficial infection causes angina or impetigo, and a deeper infection causes lymphadenitis and sepsis. If bacteria produce a lot of erythrogenic toxin, and antitoxic immunity is reduced, scarlet fever develops.

Pathogen

1. Streptococci: pus smear (Gram stain). Streptococci are gram-positive bacteria of a round or oval shape with a diameter of 0.5-0.75 microns, interconnected in pairs or in chains of unequal length. They are immobile and do not form spores. May form a capsule in fresh culture; most streptococci are aerobes or facultative anaerobes, and only a few are obligate anaerobes or microaerophiles.

2. Culture on blood agar. Some aerobic streptococci produce soluble hemolysin, which causes a clear zone of hemolysis to form on fresh blood agar. This phenomenon is called hemolysis. The colonies are less than 1 mm in diameter and are surrounded by a clear, colorless zone, within which the erythrocytes are completely lysed. Hemolysis is especially pronounced when cultivating Streptococcus pyogenes under anaerobic conditions; in the presence of oxygen, hemolysis may not be. With α-hemolysis, the hemolysis zone is opaque and has a greenish tint.

Infections of the skin and mucous membranes

3. Streptococcal angina: lips. Lips become glossy and take on a cherry red hue. Weeping cracks are sometimes visible in the corners of the mouth.

4. Cervical lymphadenitis. The spread of infection from the palatine tonsils can cause purulent cervical lymphadenitis. In children younger age swelling of the neck can be quite significant even with moderate changes in the tonsils. In such cases, mumps is sometimes misdiagnosed.

5. Catarrhal angina. Catarrhal angina can be both viral and streptococcal in nature, so it is difficult to judge the etiology without laboratory diagnostics. The picture shows that hyperemia spreads along the roof of the sky to the edematous uvula. In children under three years of age, local manifestations are mild, there are usually no raids. In the absence of treatment, the disease becomes protracted, subfebrile temperature persists for a long time. Diagnosis can be difficult with abdominal pain and vomiting.

6. Catarrhal angina. In older children and adults, the onset is acute and is manifested by sore throat, malaise, fever, and headache. The pharynx is inflamed, the tonsils are edematous, in more than half of the cases they are covered with a white or yellowish coating. The cervical and submandibular lymph nodes are enlarged and painful. In this age group, the disease usually resolves quickly.

7. Follicular tonsillitis. The severity of hyperemia of the mucosa is different, the tissues around the festering follicles are sometimes almost unchanged.

8. Peritonsillar abscess. The penetration of streptococci from the tonsils into the surrounding soft tissues leads to a rapid increase in edema, and often to suppuration. It becomes difficult to open the mouth, there is severe pain when swallowing, the voice becomes nasal. The front wall of the pharynx bulges, shifting the tongue in the opposite direction. In the future, an abscess is formed, as evidenced by the appearance of a yellow spot on the mucous membrane; in this place then there is an opening and emptying of the abscess. When antibiotics are prescribed for early stage disease, as a rule, it is possible to stop the development of infection and prevent the formation of an abscess.

9. Angina Ludwig: front view. Phlegmon of the submandibular region (Ludwig's angina) - very dangerous complication tonsillitis, caries or lymphadenitis. Most often, Ludwig's angina is caused by streptococci, less often by mixed anaerobic flora.

10. Angina Ludwig: side view.

11. Angina Ludwig: bottom of the mouth. Inflammatory edema deforms the floor of the mouth and makes it difficult to swallow. Swelling of the larynx can develop suddenly and lead to asphyxia.

Scarlet fever

12. Pale nasolabial triangle and rash on the trunk. Scarlet fever is caused by strains of Streptococcus pyogenes that produce an erythrogenic toxin. The portal of infection is usually the pharynx, less commonly wounds, burns, and other skin lesions, such as vesicles in chickenpox. If the skin serves as the gate of infection, then they talk about wound scarlet fever. Infection of the birth canal can cause postpartum scarlet fever.

Scarlet fever begins with a high fever, sore throat, and vomiting. With a mild course, vomiting may be absent, sometimes there is no sore throat. The rash appears in the first 24-36 hours and spreads down the body from top to bottom. Bright red cheeks and chin contrast with a pale nasolabial triangle. Reddening of other areas of the skin is expressed to varying degrees, against this background, a small spotted spotted rash stands out. It is most noticeable around the neck and on the upper torso. On the distal parts of the extremities, the spots may merge. The pallor of the nasolabial triangle also occurs with other diseases, especially often with croupous pneumonia.

Complications of scarlet fever are divided into two groups: purulent-septic (rhinitis, sinusitis, otitis media and purulent lymphadenitis) and infectious-allergic (rheumatism and glomerulonephritis).

13. Spotted rash on the trunk. The rash is especially noticeable on the neck and chest, where it resembles reddened goose bumps.

14. Rash on thigh. A patchy rash on the extremities can be difficult to distinguish from rubella rash, but the characteristic appearance of the oral mucosa and pharynx allows a correct diagnosis.

15. Wound scarlet fever. In the absence of antitoxic immunity, absorption of the erythrogenic toxin from an infected wound or skin injury leads to scarlet fever. The typical rash occurs even when the streptococci do not spread beyond the wound.

16. Symptom Pastia. With a profuse rash, dark red pigmentation and petechiae often appear in skin folds, for example, in the folds of the elbows (Pastia's symptom). Pigmentation persists even after the rash fades.

17. Peeling on the brush. Peeling of the skin begins 4-5 days after the onset of the rash. First, small areas of peeling appear on the neck and upper body, and by the end of the second week, peeling extends to the hands and feet. The severity of peeling in different occasions is not the same: the more abundant the rash, the stronger it is. When the rash is gone, flaking can help make the diagnosis, although it's not exclusive to scarlet fever. Peeling begins with the formation of small holes, surrounded by a rim of the epidermis, which then exfoliates and turns into scales.

18. Peeling on the brush. By the end of the second week, peeling begins around the nail folds, the thick epidermis of the palms and soles can peel off in large layers.

19. White strawberry tongue. During the first 1-2 days, the tongue is covered with a white coating, through which enlarged red papillae are visible. The sky is covered with dark red spots, sometimes individual petechiae are found on it. The pharynx is bright red, there is a white coating on the tonsils.

20. Red strawberry tongue. After a few days, the plaque peels off from the top and sides of the tongue. The picture shows a red glossy surface of the tongue with protruding papillae and islands of white plaque.

erysipelas

21. Butterfly. The development of erysipelas is often preceded by an upper respiratory tract infection. Degenerative changes in the skin, common in the elderly, also predispose to deep penetration of the infection. Erysipelas is usually localized on the face or on the legs: streptococci fall on them from the fingers. Penetrating through minor skin lesions, streptococci spread with lymph flow. Sometimes erysipelas occurs due to streptococcal infection of the surgical wound, trophic ulcer or umbilical wound in a newborn.

The incubation period does not exceed a week. The disease begins acutely: with fever and chills. Within a few hours, the patient experiences itching and burning in the affected area, then there is a sharp reddening of the skin, which spreads rapidly. The inflamed area has clear boundaries and rises above healthy skin. In the center of redness, a bubble may form, after opening which remains a bare weeping surface. Facial erysipelas often start on one cheek, then spread across the bridge of the nose to the other, taking on the shape of a butterfly.

22. Erysipelas of the face: acute period. In the acute period, the eyelids sometimes swell so much that the eye does not open, while the eyelashes stick together with pus.

23. Erysipelas of the face: recovery period. After the inflammation subsides, hyperpigmentation and flaking remain. These areas are especially sensitive to sunlight and cold for several months.

24. Phlegmonous erysipelas: acute period. The infection can penetrate into the subcutaneous tissues and cause phlegmon (phlegmonous erysipelas). Often a bubble is formed with serous-purulent contents, which is then opened. Necrosis of the affected tissues (gangrenous erysipelas) may develop.

25. Erysipelas of the legs: the period of recovery. The lower leg is edematous, the skin is hyperpigmented and flaky. Lymphangitis leads to chronic lymphostasis: this predisposes to relapses of erysipelas.

Streptococcal impetigo.

26. Impetigo on the face. Impetigo is a form of pyoderma, a highly contagious disease caused by both streptococci and staphylococci. Eczema, pediculosis, scabies and fungal infection predispose to the development of impetigo. Purulent blisters first appear on the face - around the mouth and nose - and very quickly spread to other parts of the body. The blisters dry up and form crusts. Streptococcal impetigo differs from staphylococcal impetigo in the golden color of the crusts.

27. Impetigo on the lower leg. Local application of antibiotics is ineffective, since the access of drugs is difficult due to thick crusts. Skin lesions with nephritogenic strains of streptococcus can cause acute glomerulonephritis.

28. Phlegmon. The penetration of streptococci through the skin and mucous membranes can lead to the development of phlegmon. The defeat of the lymphatic vessels leads to lymphangitis and lymphadenitis, and the penetration of streptococci into the bloodstream causes sepsis. With phlegmon, the inflamed area has less clear boundaries than with erysipelas, and is accompanied by suppuration.

29. Sepsis. The penetration of Streptococcus pyogenes into the bloodstream leads to metastatic lesions, for example, as in this case, to phlegmon. In the clinical picture of sepsis, the leading place is occupied by a violation of the general condition, so the defeat of individual organs fades into the background.

30. Abscess of the brain. The entry into the bloodstream of a small amount of low-virulence streptococci can cause only a slight violation of the general condition. However, they can settle in internal organs (such as the brain), leading to abscesses. Usually such streptococci are microaerophiles or anaerobes. Abscesses can be asymptomatic for a long time.

31. Subacute infective endocarditis. Streptococcus viridans (α-hemolytic streptococcus, viridans streptococcus) is part of the normal microflora of the mouth. In diseases of the teeth and gums, Streptococcus viridans can enter the bloodstream and cause infective endocarditis (especially on diseased valves). The only manifestation of infective endocarditis may be prolonged fever. The main diagnostic methods are blood cultures and echocardiography.

In subacute infective endocarditis, the vegetations on the valves are more massive, soft and loose than in rheumatism. The valves themselves are damaged to a lesser extent than in acute infective endocarditis (the most common causative agent of which is Staphylococcus aureus). Small emboli, detached from the outer layer of the vegetation, mostly settle in the kidneys and brain. They rarely contain bacteria, and therefore the heart attacks caused by them proceed without complications. (Arrows show vegetations.)

32. Subacute infective endocarditis: histological specimen of a heart valve. Vegetations consist of three layers: the outer one has an eosinophilic color and a granular structure. It is made up of fibrin and platelets. Streptococci are located in the middle layer, and the inner one is formed by an inflamed valve leaflet. Outer layer - frequent source small emboli (A - myocardium, B - valve leaflet, C - outer layer of vegetation).

33. Subacute infective endocarditis: subungual hemorrhages. The deposition of immune complexes in the walls of blood vessels can lead to hemorrhages in the conjunctiva, oral mucosa and under the nails. Small painful nodules form on the pads of the fingers and toes - Osler's nodules. Glomerulonephritis often develops.

Sensitization to streptococci

34. Erythema nodosum: localization of the rash. The rash in erythema nodosum consists of painful nodules 1-5 cm in diameter. The rash is usually localized on the shins; the hands and face may also be affected. Erythema nodosum is more common in young people. It is caused by sensitization, including to β-hemolytic streptococci. The general condition is disturbed to varying degrees; there is often fever and swollen lymph nodes.

35. Erythema nodosum. Initially, the nodes are red and painful, in the process of reverse development, they change color, like a bruise. The nodes do not ulcerate and do not leave scars.

36. Ring-shaped erythema. Erythema annulare is also caused by sensitization to streptococci. The rash looks like annular red spots, localized on the trunk. Erythema annulare is more common in children, sometimes against the background of a rheumatic attack.

streptococci(Streptococcus) - causative agents of a large number of human and animal infections, they cause erysipelas, sepsis and purulent infections, scarlet fever, tonsillitis. There are non-pathogenic varieties that live in the human mouth and intestines. Anaerobic strains of streptococci have a low degree of activity, and they are usually found in the human oral cavity and digestive tract. In some cases, they cause chronic inflammatory processes and are the causative agents of wound infections. Significantly greater value in the pathogenesis of human streptococcal infections have facultative anaerobes, which are divided according to the nature of hemolysis on agar with blood into the following types:

beta-hemolytic streptococci;
alpha-hemolytic streptococci;
gamma-hemolytic streptococci that do not cause visible hemolysis on solid nutrient media with blood.

The greatest pathogenicity possess beta-hemolytic streptococci, which are the causative agents of most streptococcal infections in a person. The pathogenicity of alpha-hemolytic streptococci is less pronounced. They are found in the pharyngeal mucus of healthy people, but in some cases in chroniosepsis, subacute septic endocarditis, oral infections. Gamma-hemolytic streptococci are saprophytes of the upper respiratory tract and the human intestinal tract. In some cases, they cause subacute septic endocarditis, urinary tract infections, wound infections.

Morphology of streptococci

these are immobile spherical or oval cocci with a diameter of 0.8-1 microns, forming chains of various lengths and positively staining according to Gram. Some strains form a capsule. The length of the chains is related to the growing conditions. In a liquid nutrient medium, they are longer; on dense media, they are often arranged in the form

short chains and bundles. Cocci may be ovoid before division. The division occurs perpendicular to the chain. Each coccus is divisible by 2.

Biology of streptococci

cultural properties: on agar with blood, streptococcus forms small (1-2 mm in diameter) translucent rods, grayish or colorless, which are well removed by a loop. The size of the hemolysis zone varies in different strains: group A forms a hemolysis zone slightly larger than the diameter of the colony, group B gives a large hemolysis zone. Type A streptococci form a greenish or greenish-brown hemolysis zone, cloudy or transparent, varying in size and color intensity. In some cases, the colony itself acquires a greenish coloration. In liquid nutrient media, streptococci are characterized by benthic, often rising along the walls, growth. When shaken, a granular or flaky suspension. Common growing media: meat-peptone agar with the addition of rabbit or sheep blood, semi-liquid agar with serum.

Good growth and toxin formation can be achieved on "combination broth" or on media containing casein hydrolysate and yeast extract. Hemolytic streptococci metabolize glucose with the formation of lactic and other acids, which is a factor limiting the growth of microbes in a nutrient medium. Resistance to physical and chemical factors.

Group A hemolytic streptococci can persist for a long time on objects, in dust in a dried state. However, these cultures, while maintaining viability, lose their virulence.

Group A streptococcus is highly sensitive to penicillin, which has a bactericidal effect on it. Sulfanilamide acts on streptococcus A bacteriostatically.

Modern classification of streptococci

based on their serological differences. There are 17 known serological groups: A, IN,

C, D, E, F, etc. The division into groups is based on the presence of a specific polysaccharide (substance C) in representatives of different groups. Streptococci of group A are pathogenic for humans. Streptococci of different groups differ not only in their ability to cause diseases in humans and animals and in their natural habitat, but also in biochemical and cultural characteristics.

In addition to serological differences, when differentiating strains, the following indications are taken into account:

source of selection;
nature of hemolysis;
the ability to form soluble hemolysis;
resistance to various temperatures;
feature to grow in milk with methylene blue;
fermentation of sugars;
liquefaction of gelatin.

Serological serotypes: By agglutination on glass, strains of beta-hemolytic streptococcus isolated from scarlet fever and other streptococcal infections and from healthy carriers were divided into 50 serological types. Cultures of 46 types are assigned to group A, types 7, 20, 21 - to group C, and type 16 - to group D.

The division of streptococci into types is also carried out using the precipitation reaction. The results of type determination by the agglutination reaction and in the precipitation reaction usually give the same results. Scarlet fever usually predominates

1 or 2-3 types. Common antigenic substances were found in strains belonging to groups A, C, Q.

Streptococcal (with scarlet fever) toxin contains

2 factions:

thermolabile or true scarlatinal toxin;
thermostatic, which has the properties of an allergen.

The true erythrogenic toxin is a protein. It is a streptococcal exotoxin that causes the Dick reaction in people susceptible to scarlet fever. Purified erythorogenic toxin is used for skin tests to determine the level of antitoxic immunity (Dick reaction).

For bacteriological examination, the material collected with a swab from the mucous membrane of the pharynx and nose is inoculated on a Petri dish with blood agar, placed in a thermostat for 3-4 hours at 37 °C. In the presence of streptococci, characteristic rods grow on the agar in a day. For microscopic examination, an isolated colony is subcultured into a liquid nutrient medium (meat-peptone broth with whey) and after 24 hours of cultivation in a thermostat, it is subjected to research. Smears are stained according to Gram or methylene blue according to Loeffler. Then, the biochemical properties of the cultures are studied and the type of streptococcus is determined using an agglutination test on glass and a precipitation test with typical sera. Of the serological reactions, the complement fixation reaction (CFR) is used with the serum of an immunized rabbit.

DOMAIN → Bacteria; TYPE → Firmicutes; CLASS → Vasilli; ORDER → Lactobacillales;

FAMILY → Streptococcaceae; GENUS → Streptococcus; SPECIES → Streptococcus species (up to 50 species)

The main features of the genusStreptococcus:

1. Cells of spherical or oval (lanceolate) shape 0.5-2.0 microns. Arranged in a chain or in pairs.

2. Motionless, no dispute. Some species have a capsule.

3. Gram-positive. Chemoorganotrophs, demanding on nutrient media, facultative anaerobes

4. Ferment sugars to form acid, but this is not a reliable differentiator within the genus

5. Unlike staphylococci, there is no catalase activity and cytochromes.

6. Usually, erythrocytes are lysed. According to hemolytic properties: beta (complete), alpha (partial), gamma (none). Capable of forming L-shapes.

Antigenic structure of the genusStreptococcus:

Cell wall polysaccharide on the basis of which they are divided into 20 groups, denoted by Latin letters. Pathogenic species belong primarily to the A. group and less often to other groups. There are species without a group antigen.

Type-specific protein antigens (M, T, R). M-protein is possessed by pathogenic species. In total, there are over 100 serotypes, most of which belong to group A streptococci. The M-protein is located superficially in the form of filamentous formations braiding the cell - fimbriae.

Capsular streptococci have capsular antigens of various chemical nature and specificity.

There are cross-reactive antigens

Group A streptococci are part of the nasopharyngeal microflora and are not normally found on the skin. The most pathogenic for humans are hemolytic streptococci of group A, belonging to the species S. pyogenes

Group A streptococci cause infections at any age and are most common in children between 5 and 15 years of age.

Group A pathogenicity factors

1) Capsule (hyaluronic acid) → Antiphagocytic activity

2) M-protein (fimbriae) → Antiphagocytic activity, destroys complement (C3b), superantigen

3) M-like proteins → Bind IgG, IgM, alpha2-macroglobulin

4) F-protein → Microbe attachment to epithelial cells

5) Pyrogenic exotoxins (erythrogenins A, B, C) → Pyrogenic effect, increased HRT, immunosuppressive effect on B-lymphocytes, rash, superantigen

6) Streptolysins: S (oxygen stable) and

O (oxygen sensitive) → Destroy white blood cells, platelets, red blood cells. Stimulate the release of lysosomal enzymes.

7) Hyaluronidase → facilitates invasion by disintegrating connective tissue

8) Streptokinase (fibrinolysin) → Destroys blood clots (thrombi), promotes the spread of microbes in tissues

9) DNase → Demolymerizes extracellular DNA in pus

10) C5a-peptidase → Destroys the C5a component of complement, chemoattractant

The pathogenesis of infections caused byS. pyogenes:

It most commonly causes a localized infection of the upper respiratory tract or skin, but can infect any organ.

Most frequent suppurative processes: abscesses, phlegmon, tonsillitis, meningitis, pharyngitis, sinusitis, frontal sinusitis. lymphadenitis, cystitis, pyelitis, etc.

Local inflammation leads to leukocytolysis in the peripheral blood, followed by tissue infiltration with leukocytes and local pus formation.

Non-suppurative processes causedS. pyogenes:

erysipelas,

streptoderma,

impetigo,

scarlet fever,

rheumatoid infection (rheumatic fever),

glomerulonephritis,

toxic shock,

sepsis, etc.

Treatment of streptococcal infections:It is carried out primarily with antibiotics: cephalosporins, macrolides, lincosamides

Prevention of streptococcal infections:

General sanitary and hygienic measures, prevention and treatment of acute local streptococcal infections are important. To prevent relapse (rheumatic fever) - antibiotic prophylaxis.

An obstacle to the creation of vaccines is a large number of serotypes, which, taking into account the type-specificity of immunity, makes their production hardly realistic. In the future, the synthesis of M-protein polypeptides and the hybridoma route for its production.

Associated drugs are produced abroad for the immunotherapy of infections caused by opportunistic microbes - from 4 to 19 types. These vaccines include S.pyogenes and S.pneumoniae.

Immunoprophylaxis of pneumococcal infections - a vaccine from polysaccharides of 12-14 serovariants, which often cause diseases.

A vaccine against caries is being developed.

The textbook consists of seven parts. Part one - "General Microbiology" - contains information about the morphology and physiology of bacteria. Part two is devoted to the genetics of bacteria. The third part - "Microflora of the biosphere" - considers the microflora of the environment, its role in the cycle of substances in nature, as well as the 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 ideas about immunity. The sixth part - "Viruses and the diseases they cause" - provides information about the main biological properties of viruses and the diseases they cause. Part seven - "Private Medical Microbiology" - contains information about the morphology, physiology, pathogenic properties of pathogens of many infectious diseases, as well as about 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 practitioners.

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.

Streptococcus (gr. . streptos- chain and coccus- grain) - gram-positive, cytochrome-negative, catalase-negative cells of spherical or ovoid shape with a diameter of 0.6 - 1.0 microns, grow in the form of chains of various lengths (see color inc., Fig. 92) or in the form of tetracocci; immobile (except for some representatives of serogroup D); the content of G + C in DNA is 32 - 44 mol % (for the family). Dispute does not form. Pathogenic streptococci form a capsule. Streptococci are facultative anaerobes, but there are also strict anaerobes. The temperature optimum is 37 ° C, the optimum pH is 7.2 - 7.6. On conventional nutrient media, pathogenic streptococci either do not grow or grow very poorly. For their cultivation, sugar broth and blood agar containing 5% defibrinated blood are usually used. The medium should not contain reducing sugars, as they inhibit hemolysis. On the broth, the growth is near-wall in the form of a crumbly sediment, the broth is transparent. Streptococci, forming short chains, cause turbidity of the broth. On dense media, serogroup A streptococci 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 having M antigens;

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

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

Streptococcus classification. The genus Streptococcus includes about 50 species. Among them, 4 pathogens are distinguished ( S. pyogenes, S. pneumoniae, S. agalactiae And S. equi), 5 opportunistic and more than 20 opportunistic species. For convenience, the entire genus is divided into 4 groups using the following features: growth at 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 pathogenic streptococci belong to the first group (all of these signs are usually negative). Enterococci (serogroup D), which also cause various diseases of a person 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:

– β-hemolytic streptococci – when growing on blood agar around the colony, there is a clear zone of hemolysis (see color inc., Fig. 93a);

– α-hemolytic streptococci – around the colony greenish coloration and partial hemolysis (greening is due to the conversion of oxyhemoglobin to methemoglobin, see color inc., Fig. 93b);

– α1-hemolytic streptococci, compared with β-hemolytic streptococci, form a less pronounced and cloudy zone of hemolysis;

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

– β-non-hemolytic streptococci do not cause hemolysis on solid nutrient medium.

Serological classification has gained 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, denoted by the letters A, B, C, D, F, G, etc. Now 20 serological groups of streptococci are known (from A to V). Streptococci pathogenic for 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 affiliation of streptococci is a decisive moment in the diagnosis of the diseases they cause. Group polysaccharide antigens are determined using the appropriate 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. The M protein is thermostable 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 the 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, and is destroyed by heating in the presence of acid, but stable by moderate heating in a weak alkaline solution. According to the M antigen, hemolytic streptococci of serogroup A are divided into a large number of serovariants (about 100), their determination is of epidemiological significance. According to the T-protein, serogroup A streptococci are also divided into several dozen serovariants. In group B, 8 serovariants are distinguished.

Streptococci also have cross-reactive antigens common to the antigens of the cells of the basal layer of the epithelium of the skin 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. In the cell wall of streptococci, an antigen (receptor II) was found, with which their ability, like staphylococci with protein A, is associated, to interact with the Fc fragment of the IgG molecule.

Diseases caused by streptococci divided into 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 war time) - abscesses, phlegmon, sepsis, etc.;

d) angina - acute and chronic;

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

e) rheumatism;

g) pneumonia, meningitis, creeping ulcer of the cornea (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 the colonization of the surface of teeth and gums by these streptococci have been isolated and studied.

Although most streptococci pathogenic to humans belong to serogroup A, important role streptococci of serogroups D and B also play in human pathology. Streptococci of serogroup D (enterococci) are recognized as the causative agents of wound infections, various purulent surgical diseases, purulent complications in pregnant women, puerperas and gynecological patients, infect the kidneys, bladder, cause sepsis, endocarditis, pneumonia, food poisoning (proteolytic variants of enterococci). Streptococcus serogroup B ( S. agalactiae) often cause diseases of the newborn - 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 pathogenicity factors of streptococci.

1. Protein M is 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 T- and R-proteins do not have such properties). M-like proteins have been found in group C and G streptococci and may be factors in their pathogenicity.

2. Capsule. It consists of hyaluronic acid, similar to that which is part of the tissue, so phagocytes do not recognize encapsulated streptococci 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 a pyrogenic, allergenic, immunosuppressive and mitogenic effect, 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 a hemolytic and cytotoxic effect. Unlike streptolysin O, streptolysin S is a very weak antigen, it is also produced by streptococci of serogroups A, C and G.

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

7. The 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; possibly associated with tissue toxicity.

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

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

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

Streptococcus resistance. Streptococci are well tolerated low temperatures, 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 can 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 genitourinary tracts, so the diseases they cause can be endogenous or exogenous in nature, 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 systems. Infection by airborne or airborne dust leads to damage to the lymphoid tissue (tonsillitis), regional lymph nodes are involved in the process, from where the pathogen spreads through the lymphatic vessels and hematogenously.

The ability of streptococci to cause various diseases depends on:

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

b) the presence of various pathogenicity factors in streptococci;

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

d) sensitizing properties of streptococci; they largely determine the peculiarity of the pathogenesis of streptococcal diseases and are the main cause of such complications as nephronephritis, arthritis, lesions of cardio-vascular system and etc.;

e) pyogenic and septic functions of streptococci;

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

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

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

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

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

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

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

Postinfectious immunity. The main role in its formation is played by antitoxins and type-specific M-antibodies. Antitoxic immunity after scarlet fever has a strong long-term character. Antimicrobial immunity is also strong and long lasting, 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 throat, plaque from the tonsils, wound discharge. The decisive step in the study of isolated pure culture is the determination of its serogroup. For this purpose, two methods are used.

A. Serological - determination of a group polysaccharide using a precipitation reaction. For this purpose, appropriate group-specific sera are used. If the strain is beta-hemolytic, its polysaccharide antigen is extracted with HCl and tested with antisera from serogroups A, B, C, D, F, and G. If the strain does not cause beta-hemolysis, its antigen is extracted and tested with antisera from groups B and D only. Groups 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 a separate genus. Enterococcus.

B. Grouping method - based on the ability of aminopeptidase (an enzyme produced by streptococci of serogroups A and D) to hydrolyze pyrrolidine-naphthylamide. For this purpose, commercial kits of the 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 M-serotype) or agglutination (determine T-serotype) reaction for epidemiological purposes only.

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 anti-hyaluronidase and anti-O-streptolysin antibodies is used as an auxiliary method for diagnosing rheumatism and for assessing the activity of the rheumatic process.

IFM can also be used to detect streptococcal polysaccharide antigens.

PNEUMOCOCCIS

Special position in the genus Streptococcus takes the form S. pneumoniae which plays a very important role in human pathology. It was discovered by L. Pasteur in 1881. Its role in the etiology of lobar 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, (±) – changeable sign; b aerococci - Aerococcus viridans, is found in approximately 1% of patients suffering from streptococcal diseases (osteomyelitis, subacute endocarditis, urinary tract infections). Separated into an independent species in 1976, not studied enough.

the end of the cell is pointed, the other is flattened; usually arranged in pairs (flat ends facing each other), sometimes in the form of short chains (see color incl., fig. 94b). They do not have flagella, they do not form spores. In humans and animals, as well as on media containing blood or serum, they form a capsule (see color inc., Fig. 94a). Gram-positive, but often Gram-negative in young and old cultures. facultative anaerobes. The temperature optimum for growth is 37 °C, at temperatures below 28 °C and above 42 °C they do not grow. The optimal pH for growth is 7.2 - 7.6. Pneumococci form 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 as a result of the action of the exotoxin hemolysin (pneumolysin). Growth in sugar broth is accompanied by turbidity and a slight precipitation. In addition to the O-somatic antigen, pneumococci have a capsular polysaccharide antigen, which is very diverse: 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 are highly sensitive to optochin and bile. Under the influence of bile acids in pneumococci, intracellular amidase is activated. It breaks the bond between alanine and peptidoglycan muramic acid, the cell wall is destroyed, and pneumococcal lysis occurs.

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

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

Pneumococci along with meningococci are the main culprits of meningitis. In addition, they cause creeping corneal ulcers, otitis, 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 isolation and identification S. pneumoniae. The material for the study is sputum and pus. White mice are very sensitive to pneumococci, so 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 sowing from these organs and from the blood, a pure culture is isolated. To determine the serotype of pneumococci, an agglutination reaction on glass with typical sera or the phenomenon of “capsule swelling” is used (in the presence of homologous serum, the pneumococcal capsule swells sharply).

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

MICROBIOLOGY OF SCARLET FINA

Scarlet fever(Late Late . scarlatium- bright red color) - spicy infection, which is clinically manifested by tonsillitis, lymphadenitis, small-pointed bright red rash on the skin and mucous membrane, followed by 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 the 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 Russian scientists G. N. Gabrichevsky, I. G. Savchenko and the American scientists G. F. Dick and G. H. Dick. I. G. Savchenko back in 1905 - 1906. showed that scarlatinal streptococcus produces a toxin, and the antitoxic serum obtained by it has a good therapeutic effect. Based on the works of I. G. Savchenko, the Dick spouses in 1923 - 1924. showed that:

1) intradermal administration of a small dose of toxin to persons who have not suffered from scarlet fever causes 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 have not suffered 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 recognized. 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 that has the M-antigen and produces erythrogenin. However, in the epidemiology of scarlet fever in different countries, in different regions and at different times, the main role is played by streptococci that have different M-antigen serotypes (1, 2, 4 or another) and produce erythrogenins of different serotypes (A, B, C). It is possible to change these serotypes.

The main factors of 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 thermolabile protein (actually a toxin) and a thermostable substance with allergenic properties.

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

1) the action of scarlatinal 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-pointed rash of bright red color, as well as fever 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, 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 nephronephritis, polyarthritis, cardiovascular diseases, etc. on the 2nd - 3rd week. illness.

In the clinic of scarlet fever, stage 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 have decreased significantly.

Post-infectious immunity strong, long-term (repeated diseases are observed in 2-16% of cases), due to antitoxins and immune memory cells. In those who have been ill, the allergic state to the scarlatinal allergen also persists. It is detected by intradermal injection of killed streptococci. In patients who have been ill at the injection site - redness, swelling, soreness (Aristovsky-Fanconi test). To test for the presence of antitoxic immunity in children, the Dick reaction is used. With its help, it was established that passive immunity in children of the 1st year of life is preserved during the first 3-4 months.

QUESTIONS AND ANSWERS

MICROBIOLOGY

"PRIVATE MICROBIOLOGY"

Questions and answers

Microbiology

Manual for self-preparation for the final lesson in the section

"Private microbiology"

Version 1.00

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Used Books:

Lecture notes;
Computer version of the lectures of Kaskevich L.I.;
Borisov.
and other available literature

1. Staphylococci, general characteristics. role in human pathology. Pathogenicity factors and mechanisms of pathogenesis of staphylococcal infections. Microbiological diagnostics. Prevention and treatment. 5

2. Streptococci, classification. General characteristics. pathogenicity factors. Antigenic structure. Pathogenesis, immunity, microbiological diagnosis of streptococcal infections. 6

3. Classification of Neisseria. Meningococci, general characteristics. Meningococcal infections, mechanisms of pathogenesis, immunity, diagnostic methods, prevention. IDS. 8

4. Gonococci, general characteristics. Mechanisms of pathogenesis and immunity. Microbiological diagnosis of acute and chronic gonorrhea. 9

5. General characteristics of the Enterobacteriaceae family. 11

6. General principles bacteriological diagnosis of acute intestinal infections (AII). Nutrient media for enterobacteria. Classification, principles of operation, application. eleven

7. Materials for research in AEI: methods of taking and nature of the material depending on the clinical form of the disease and the stage of pathogenesis. 12

8. General principles of serological diagnosis of acute intestinal infections. 13

9. Escherichia coli, general characteristics. The biological role of Escherichia coli. Diseases caused by Escherichia. 13

10. Salmonella. General characteristics. Genus representatives. Serological classification according to Kaufman-White. Molecular biological typing. 14

11. Causative agents of typhoid fever, paratyphoid A and B, general characteristics. Phage typing. Vi-antigen and its significance. 15

12. Mechanisms of pathogenesis and methods of microbiological diagnosis of typhoid fever and paratyphoid fever. 15

13. Immunity in typhoid fever. Serological diagnosis of typhoid fever and paratyphoid fever. specific prophylaxis. 16

14. Etiology of food intoxications and toxic infections of a bacterial nature. Materials and diagnostic methods. 16

15. Salmonellosis. Characteristics of pathogens and diagnostic methods. Nosocomial salmonellosis. 17

16. Causative agents of dysentery. Classification. Characteristic. Pathogenesis, immunity to dysentery. Methods of microbiological diagnostics of acute and chronic dysentery. 18

17. Klebsiella. Classification, general characteristics. Pathogenesis, immunity, methods of microbiological diagnostics of Klebsiellosis. 19

18. Pseudomonas aeruginosa, general characteristics, pathogenicity factors. role in human pathology. 19

19. Causative agents of intestinal yersiniosis, general characteristics. Pathogenesis. Methods for the diagnosis of yersiniosis. 20

20. Causative agent of diphtheria, general characteristics. Differences from non-pathogenic corynebacteria. Mechanisms of pathogenesis. Methods of microbiological and molecular biological diagnostics of diphtheria. 21

21. Diphtheria toxin and its properties. Anatoxin. Immunity in diphtheria and its nature. Determination of the intensity of antitoxic immunity. specific immunotherapy and specific prophylaxis. 22

22. Pertussis causative agent, general characteristics. Differentiation with the causative agent of parapertussis. Pathogenesis, immunity. Microbiological diagnostics. Specific prophylaxis of whooping cough. 23

23. General characteristics of causative agents of tuberculosis. Pathogenesis, immunity, diagnostic methods and specific prevention of tuberculosis. Mycobacteriosis. 24

24. The causative agent of leprosy. Characteristics, pathogenesis, immunity of the disease. 26

25. Especially dangerous infections (SDI). Classification Basic rules for the mode of operation, collection, transfer of infectious material during OOI. General principles for diagnosing ASI .. 27

26. Causative agents of cholera. Systematics. General characteristics. Differentiation of biovars. Pathogenesis, immunity, specific prevention. Methods of microbiological diagnostics. 28

27. Plague causative agent, general characteristics. plague pathogenesis. Immunity, prevention. 29

28. The causative agent of anthrax, characteristics. Pathogenesis, immunity, specific prevention of anthrax. 29

29. The causative agent of tularemia, general characteristics. Pathogenesis. Immunity. specific prophylaxis. 30

30. Causative agents of brucellosis, general characteristics. Differentiation of Brucella species. Pathogenesis. Immunity. specific prophylaxis. 31

31. Spirilla family. Campylobacter, characteristics, role in human pathology. Helicobacter. 31

32. Classification and general characteristics of anaerobes. Clostridia. Bacteroides, peptococci and other non-spore-forming anaerobes. pathogenicity factors. role in human pathology. 33

33. The causative agent of tetanus, general characteristics. pathogenesis and immunity. Specific therapy and prevention. 34

34. Causative agents of gas gangrene, general characteristics. Pathogenesis. Specific prevention of gas gangrene. 34

35. The causative agent of botulism, general characteristics. Pathogenesis. Specific therapy and prevention of botulism. Clostridial gastroenteritis. 35

36. Methods for diagnosing anaerobic infections. 36

37. Classification and general characteristics of spirochetes. 36

38. Classification of treponema and treponematoses. Characteristics of the causative agent of syphilis. Pathogenesis, immunity, diagnostic methods of syphilis. 37

39. Leptospira. General characteristics. Leptospirosis pathogenesis, immunity, specific prevention. Microbiological diagnosis of leptospirosis. 38

40. Borrelia, general characteristics. Pathogenesis, immunity in relapsing fever. Microbiological diagnostics. The causative agent of Lyme borreliosis. 38

41. Systematic position and characteristics of rickettsiae. causative agents of rickettsiosis. Pathogenesis, immunity, methods of diagnosing typhus. 39

42. Characteristics of chlamydia. Causative agents of trachoma, ornithosis, respiratory and urogenital chlamydia. Mechanisms of pathogenesis and methods of diagnosis of chlamydia. 41

43. General characteristics of mycoplasmas. role in human pathology. Methods for the diagnosis of mycoplasmosis. 42

Staphylococci, general characteristics. role in human pathology. Pathogenicity factors and mechanisms of pathogenesis of staphylococcal infections. Microbiological diagnostics. Prevention and treatment.

DOMAIN → Bacteria; TYPE → Firmicutes; CLASS → Vasilli; ORDER → Vasillalles; FAMILY → Staphylococcaceae; genus → Staphylococcus; SPECIES → Staphylococcus species;

The genus Staphylococcus has 28 species, of which 14 live on the skin and mucous membranes. Some species cause disease in humans, most often these are:

S. aureus(golden),

S. epidermidis(epidermal),

S.saprophiticus(saprophytic).

Morphology.

Spherical shape, cluster-like arrangement (Greek - staphylos - bunch). There is no dispute. Motionless. Gram-positive.

facultative anaerobes. Chemoorganotrophs. Grow on normal media, can grow in the presence of 6-10% NaCl. The colonies are pigmented.

Biochemically active. Catalase positive. Oxidase negative. Contains cytochromes.

They live on the skin and mucous membranes of humans and animals. There are various ecological options. Hospital ecovars of pathogens have special properties.

Sustainability

The most resistant bacteria that do not form spores. They tolerate drying well (up to 50 days at room temperature). UV kills in 10-12 hours, boils in seconds

Resistant to NaCl, fatty acids, acidic pH. (provides nourishment to the skin)

Nosocomial strains (especially S. aureus) are characterized by increased resistance to antibiotics, antiseptics and disinfectants.

Pathogenic factors:

1) Capsule → Inhibition of phagocytosis

2) Protein A → Interaction with the Fc fragment of antibodies, sensitization

3) Peptidoglycan → Stimulation of the production of endogenous pyrogens, leukocyte chemoattractant (formation of abscesses)

4) Teicic acids → Bind fibronectin

5) Membranotoxins, or hemolysins (alpha, beta, gamma, delta toxins), leukocidin → Toxic to many cells, including erythrocytes, leukocytes, macrophages, fibroblasts. Alpha toxin is an example of a pore-forming toxin.

6) Exfoliative toxin (A, B) → Causes the "scalded skin" syndrome, destroying cell contacts - desmosomes in the granular layer of the epidermis. Superantigen

7) Toxin of toxic shock syndrome → Neurotropic, vasotropic effects. Superantigen

8) Enterotoxins (A-E) → Action on enterocytes (food intoxication). Neurotropic effects Superantigen.

9) Plasmocoagulase → Transfer of fibrinogen to fibrin, preventing contact with phagocytes

10) Hyaluronidase → Destruction of connective tissue

11) Lipase, lecithinase → Hydrolysis of lipids, lecithin

12) Fibrinolysin → Destruction of fibrin clots

13) Deoxyribonuclease → DNA cleavage, pus liquefaction

14) Keratinoid enzymes → Inactivation of bactericidal oxygen species

15) Resistance to NaCl, fatty acids → Reproduction in sweat and sebaceous glands.

Transmission mechanisms: Contact (main), Aerosol, fecal-oral

Infection can take place both exogenously and endogenously.

Features of pathogenesis. Staphylococci are opportunistic pathogens. The development of the disease and its clinical form depend on a number of conditions: impaired immunity; damage to the covers; properties of the pathogen (a set of pathogenicity factors), its quantity, entrance gate.

The development of the pathological process is possible in any biotope.

Staphylococcal infections often develop:

1) against the background of other diseases (secondary infections), for example, after influenza or other viral infections

2) in medical institutions (nosocomial infections)

Diseases: more than 100 nosological forms. The main pathogen is S. aureus

Local suppurative processes

Diseases of the bones and joints

· Defeats internal organs: pneumonia (in children and the elderly), kidney damage (pyelonephritis), cystitis (often S. epidermidis and S. saprophiticus)

· Peritonitis. After operations on the abdominal organs.

CNS lesions

· Sepsis. Septicopyemia.

· Toxic shock syndrome.

Syndrome of "scalded babies". In newborns (infection through the umbilical vein), there is a detachment of the skin with blisters, intoxication. Older children have a syndrome of "scalded skin" (erythema, blisters, intoxication).

· Food poisoning.

Prevention principles

Specific

A) Staphylococcal toxoid.

b) Associated Staphylo-Protein-Pseudomonas aeruginosa vaccine ( Contains concentrated toxoids of staphylococcus aureus and Pseudomonas aeruginosa, cytoplasmic antigens of staphylococcus and chemical proteus vaccine.

Non-specific prophylaxis

1) Compliance with the sanitary and anti-epidemic regime

2) Monitoring of pathogens and their drug resistance.

3) Restrictive measures.

a) invasive procedures - carried out according to strict indications.

b) immunosuppressive drugs and methods (immunosuppressants, antibiotics, chemotherapy, radiotherapy) - also according to strict indications.

Streptococci, classification. General characteristics. pathogenicity factors. Antigenic structure. Pathogenesis, immunity, microbiological diagnosis of streptococcal infections.