Pneumococci - microbiology with the technique of microbiological research. The causative agent of scarlet fever
Pneumococcus. general characteristics
pneumococci - These are extracellular pyogenic gram-positive, immobile, non-spore-forming microorganisms. The temperature optimum is 37°C, they grow better on weakly alkaline media. Since pneumococci produce a large amount of lactic acid, the medium for their cultivation should have a good buffer capacity. More abundant growth is observed on media supplemented with hormones or on blood agar.
Streptococcus pneumoniae, well studied as the main causative agent of pneumonia, in typical cases is represented by lanceolate cocci arranged in pairs (diplococci). In the human body, or in the secretion of the respiratory tract, a pair of microbes is usually surrounded by a capsule. Can be detected and single cells, short chains.
pneumococci grow equally well in the presence and absence of oxygen. The lack of catalase and peroxidase enzymes requires special environments, since under normal cultivation conditions, H 2 O 2 can accumulate in toxic concentrations. Catalase can be obtained by pneumococci from erythrocytes when cultivated on blood agar.
Virulent, encapsulated strains, under aerobic conditions, form shiny dome-shaped colonies 0.5 to 3 mm in diameter on the surface of blood agar, surrounded by a green zone of incomplete hemolysis. With long-term cultivation in an artificial environment pneumococci lose the ability to form a capsule. They are not stable and cannot exist outside the body. In the aerosol that occurs when cocs are excreted from the mouth and nose, they remain in the light for no more than 1.5 hours. In whole sputum - up to 1 month. Not resistant to drying at room temperature and more sensitive than other bacteria to disinfectants. At a temperature of 52 ° C, they are destroyed within 10 minutes.
If autolytic enzymes are activated, then pneumococci show a significant ability to autolysis (self-destruction). This is the basis for the use of the bacterial cell lysis test in the presence of bile, which makes it possible to distinguish pneumococci from other α-streptococci. Bile salts, being surface-active agents, easily initiate this reaction in pneumococci and very rarely in other cocci. In practice, if an identifiable microorganism is not destroyed by bile, it is not pneumococcus.
Pneumococcus. Types (serovars).
pneumococci similar in morphological and cultural properties, but their immunological differences are clearly expressed. This discovery was made in 1910, when animals were immunized with various cultures of pneumococci, and the blood serum of these animals was used to agglutinate pneumococci isolated from many other sources.
With growth pneumococci tend to release water-soluble capsular polysaccharides. These specific soluble substances (SSS) refer to typical characteristics of pneumococci. They can be determined in the precipitation reaction with a pneumococcal culture, as well as in the blood and urine of patients with pneumonia.
At least 88 variants and subvariants have been described. Everyone can cause pneumonia. Nearly 80% of all cases of pneumonia are caused by pneumococcus. In adults, options 1, 2, 3, 4, 6, 7, 14, 18 and 19; in children, primary pneumonia is caused by types 19, 23, 14, 3, b and 1 (in decreasing frequency).
Pneumococcus 3 variant is the most virulent and differs from others in a dense capsule and slimy growth on a nutrient medium. It does not have a lanceolate shape. The presence of the capsule determines the higher virulence of variant 3 and the greater frequency of fatal outcomes from the pneumonia it causes. This option is most dangerous for older patients.
Pneumococcus. Toxic Products
pneumococci have virulence factors, the main of which is a capsule that blocks phagocytosis. Virulent capsular strains form smooth colonies, avirulent non-capsular variants form rough ones.
Antiphagocytic activity is associated with the acidic nature of the capsular substance in combination with special hydrophilic properties, due to which, in a liquid medium, cocci absorbed by phagocytes do not undergo splitting and digestion. On the contrary, capsular cocci located on the surface of the mucosa are easily phagocytosed.
Previous lung diseases, such as primary viral infection, are accompanied by mucosal hypersecretion. The liquefied secret does not allow phagocytes to cope with capsular cocci, and the latter get the opportunity for intensive colonization and cell invasion.
pneumococci can be considered as an example of a pathogenic microorganism, in which high invasiveness is combined with minimal toxigenicity. However, some features of the clinic of pneumococcal infection indicate toxemia, despite the fact that the actual toxin has never been identified. Pneumococci produce hemolysins, leukocidins, certain necrotic substances, as well as neuraminidase, which acts on the cell membranes of the mucous membrane of the nasopharynx and bronchi. Many strains produce hyaluronidase, which promotes distribution in tissues.
Pneumococcus. Pathology of infection
pneumococci - the most common cause of pneumonia, meningitis and inflammation of the middle ear. In pneumococcal infection, the most characteristic sign of tissue damage is the presence of fibrin clots at the site of inflammation. With lobar pneumonia, there is a lot of fibrin in the lungs; with pneumococcal meningitis - a lot of fibrin accumulates in the subarachnoid space.
Pneumonia is an inflammation of the alveoli, bronchioles and small bronchi, in which the affected areas are filled with fibrinous exudate. Compaction (radiologically - “blackout”) is the result of filling the air cavities of the lungs with this exudate.
Pneumococci usually cause 2 types of pneumonia:
1. Lobar (lobar) pneumonia, including from 1 to 5 large anatomical structures (lobes) of the lungs;
2. Bronchopneumonia involving terminal bronchioles and adjacent lobes.
Confluent bronchopneumonia is the result of the fusion of foci of bronchopneumonia.
Lobar pneumonia- a severe toxic disease, the manifestation of which is rapid shallow breathing, tachycardia, cyanosis, nausea and cough. In the blood - leukocytosis (30000-40000 / mm3), 90-95% are polymorphonuclear neutrophils. Characteristic is also inflammation of the pleura - pleurisy.
With the resolution of the inflammatory process and recovery, the exudate in the lungs liquefies and is removed, partly by resorption, partly by expectoration. Air exchange in the affected lobes is restored and the lungs return to their original state.
Occasionally, delayed resorption leads to the formation of an abscess or chronic pneumonia (non-absorbable exudate). With liquefaction and resorption, the affected areas are replaced by fibrous tissue and harden. With the introduction of intensive antimicrobial therapy, such dramatic outcomes are rare.
95% of all cases of lobar pneumonia are pneumonia caused by pneumococcus.
Bronchopneumonia is usually caused by pneumococcus, but other microbes, for example, streptococci, staphylococci, Haemophilus influenzae, isolated or combined (mixed infection) can also.
Bronchopneumonia, more often secondary than primary, is a serious complication of measles, influenza, whooping cough, chronic diseases of the heart, blood vessels, lungs and kidneys. The greatest number of cases occurs in the first and last years of life. Often this disease is a terminal event in persons weakened by other diseases. Bronchopneumonia may result from the use of anesthetics or aspiration of infected material into the lungs during surgery. In newborns, this disease may be associated with aspiration of infected amniotic fluid.
Unlike lobar pneumonia, with bronchopneumonia there are scattered small foci of inflammation, the most frequent at the root of the lung. The exudate consists of leukocytes, fluid and bacteria, but does not contain fibrin and few erythrocytes. Pleurisy and empyema are complications. Quite often there is a chronic course. Congestive pneumonia is a bronchopneumonia complicating heart failure.
pneumococci can also cause inflammation of the middle ear, meningitis. There are known cases of pneumococcal endocarditis, arthritis, peritonitis, keratitis, etc.
Pneumococcus. Sources and ways of transmission of infection
Lobar (lobar) pneumonia is usually endemic in the human population. As an epidemic, it is rare and only as a complication of diseases accompanied by a decrease in resistance. Sources of infection are patients with the active form and carriers.
pneumococci penetrate the body and are excreted in the same way - airborne droplets. The infection is usually transmitted directly by inhalation of bacteria secreted by sick people or carriers from the nose and mouth with droplets of moisture. Indirect transmission is also possible through contact with infected objects.
Almost every person can have multiple short-term carriage of pneumococcus. Upon contact with a sick person, carriage can last from several days to several weeks. In carriers not associated with contact with patients, as a rule, low-virulence strains are isolated; the most dangerous variant 3 is not found.
Pneumococcus. Laboratory diagnosis of infection
pneumococci can be detected in sputum and other body fluids, if they are found in large quantities in sputum, by direct microscopy of Gram-stained smears.
For rapid diagnosis, modern methods for detecting antigens and antibodies (enzymatic immunoassay - ELISA, polymerase chain reaction - PCR, etc.) can be used.
A confirmatory method is the isolation of a pure culture and its infection in white mice, which are highly susceptible to pneumococci. The death of animals within 16-20 hours after infection is caused only by virulent strains. Capsular strains do not cause death of animals.
Typing is necessary, first of all, to establish which of the highly virulent pneumococci is present in the pathological material. To do this, you can use methods based on the action of agglutinating and precipitating type-specific sera obtained by immunizing animals against different variants of pneumococci.
According to the method developed by Neyfild (Neifeld), a smear of sputum or other test material is mixed with type-specific sera. If the type of pneumococcus corresponds to the serum, its capsule swells rapidly, because due to the antigen-antibody reaction, the density of the capsular substance changes sharply. This phenomenon is called the "Nefeld swelling reaction".
If there are few pneumococci in the sputum or repeated typing fails, white mice can be infected intraperitoneally with the test material and peritoneal exudate can be used for typing after a few hours.
Pneumococcus. Difference from other streptococci
In practice, the following characteristics are used:
1. On blood agar, pneumococci give incomplete hemolysis;
2. pneumococci
in tissues and body fluids they have a capsule, streptococci are extremely rare;
3. If 1 part of bile is added to 3 parts of liquid culture, pneumococci dissolve, streptococci do not;
4. pneumococci
ferment inulin, streptococci do not;
5. pneumococci
more pathogenic for white mice than streptococci;
6. For more detailed differentiation, agglutination and precipitation with specific sera are used.
Pneumococcus. immunity to infection
Natural immunity in humans is quite high. Pneumococcal pneumonia in most cases develops in individuals with reduced resistance. The transferred disease leads to the development of immunity to the type of pneumococcus that caused the disease. The duration of immunity is from 6 months to a year.
Pneumococcus. Infection prevention
1. Limiting contact with patients with pneumonia.
2. Discharge from the patient's mouth and nose should be collected and disinfected.
3. After examining the patient, the hands of the staff should be treated with disinfectant.
4. The patient should take measures to limit the spread of drops of moisture when coughing and talking.
Conclusion
- The capsule is the main virulence factor of pneumococci, since it protects the microbe from phagocytosis in the human body, which is the natural host of this microbe.
– pneumococci form little catalase and peroxidase, but they grow well on enriched media, producing a sufficient amount of lactic acid. facultative anaerobes. Unlike other streptococci, they dissolve in bile.
– Water-soluble capsular polysaccharides determine the type-specificity of pneumococci. At least 88 variants and subvariants of Streptococcus pneumoniae can cause disease. Variant 3 is the most virulent, having a thickened capsule and forming slimy colonies on the medium.
– pneumococci are the cause of three main diseases: pneumonia (lobar and bronchopneumonia), meningitis and inflammation of the middle ear. A hallmark of pneumococcal disease is the formation of fibrin in the focus of inflammation.
- Pneumonia can be caused by different microorganisms. It can occur in outbreaks, often as a nosocomial infection.
Taxonomy. Streptococcaceae family, genus Streptococcus, species St. pneumoniae.
Pneumococci were first described by R. Koch (1871)
Morphology. Pneumococci are diplococci in which the sides of the cells facing each other are flattened and the opposite sides are elongated, so they have a lanceolate shape resembling a candle flame. The size of pneumococci is 0.75-0.5 x 0.5-1 μm, they are arranged in pairs, single cocci or short chains are found in sputum and pus (4). In liquid nutrient media, they often form short chains, resembling streptococci. Pneumococci are non-motile, do not have spores, in humans and animals they form a capsule surrounding both cocci. The capsule contains a heat-resistant substance antifagin. When growing on artificial nutrient media, pneumococci lose their ability to form capsules. Pneumococci are gram positive. Gram-negative bacteria are found in old cultures.
Cultivation. Pneumococci are facultative anaerobes. Grow at a temperature of 36-37 about C and pH 7.2-7.4. Growth improves with higher CO 2 levels, and anaerobic conditions also enhance pneumococcal growth. They are demanding on media, since they cannot synthesize many amino acids, therefore they grow only on media with the addition of native protein. On serum agar, they form small, round, delicate, rather transparent colonies, initially dome-shaped, and with aging - with a flat top (center) and raised edges. On agar with blood, moist greenish-gray colonies grow, surrounded by a green zone, which is the result of the conversion of hemoglobin to methemoglobin (α-hemolysis, but it is very strong and sometimes mistaken for β-hemolysis). Pneumococci grow well in broth with the addition of 0.2% glucose and in broth with whey. Growth in liquid media is characterized by diffuse turbidity and dusty sediment at the bottom. Pneumococcus receives most of its energy from the fermentation of glucose, which produces a large amount of lactic acid, which inhibits the growth of pneumococcus. Therefore, when cultivating pneumococcus in sugar broth, it is necessary to periodically (6 hours after sowing) neutralize the broth culture with alkali (1N solution). With aging, pneumococci tend to spontaneous lysis (autolysis - there was a colony and there is none, only the hemolysis zone remains), which is enhanced by surfactants.
Enzymatic properties. Pneumococci have a fairly pronounced saccharolytic activity. They break down: lactose, glucose, sucrose, maltose, inulin with the formation of acid, but do not ferment mannitol. Their proteolytic properties are poorly expressed: they coagulate milk, do not liquefy gelatin, and do not form indole. Pneumococci dissolve in 10% bovine bile within a few minutes or, with the addition of 2% sodium deoxycholate, are easily lysed by surfactants. Breakdown of inulin, dissolution in bile, sensitivity to optochin (ethylhydrocuprein hydrochloride) are important diagnostic features used to differentiate pneumococcus from viridescent streptococcus.
Toxin formation and pathogenicity factors. Pneumococci produce endotoxin, hemolysin, leukocidin. The virulence of pneumococci is also associated with the presence of antiphagin in the capsule. Pneumococci produce hyaluronidase, fibrinolysin, etc.
Antigenic structure and classification. Pneumococci lack a polysaccharide antigen in their cell wall, so they are classified as nongrouping streptococci. In the cytoplasm of pneumococci there is a protein antigen common to the entire group, and in the capsule there is a polysaccharide antigen. According to the polysaccharide antigen, all pneumococci are divided into 84 serovars. Serovars I, II, III are the most common pathogens for humans. In adults, up to 80% falls on types 1-8 and 18, which give more than half of the deaths in pneumococcal bacteremia, and children - 6, 14, 19, 23. Any population of pneumococcus contains a small amount of microorganisms that do not produce capsular polysaccharide and part colonies may be in the R-form (3-5%).
Environmental resistance. Pneumococci belong to the group of unstable microorganisms. The temperature of 60 ° C destroys in 3-5 minutes. They are quite resistant to low temperatures and drying. In dried sputum, they remain viable for up to 2 months. On a nutrient medium, they remain no more than 5-6 days. Therefore, when cultivating, it is necessary to do reseeding every 2-3 days. Ordinary disinfectant solutions destroy them in a few minutes. Resistant to gentamicin and monomycin.
Animal susceptibility. Humans are the natural host of pneumococci. However, pneumococci can cause illness in calves, lambs, piglets, dogs, and monkeys. Of the experimental animals, white mice are highly sensitive to pneumococcus.
Sources of infection. A sick person and a bacteriocarrier (20-40%, up to 70% of people are carriers of virulent pneumococci).
Transmission routes. Airborne, may be airborne.
entrance gate. The mucous membrane of the upper respiratory tract, eyes and ear. The human mucosa normally has a natural resistance to pneumococcus. Pathological changes in the respiratory tract, other infections (viral), pathological accumulation of mucus (with allergic diseases), blockage of the bronchi (with atelectasis), damage to the respiratory tract by irritants, alcohol or drug intoxication, vascular disorders (pulmonary edema, heart failure) contribute to its decrease. , malnutrition, hypochromic anemia.
Diseases in humans. Pneumococci can cause purulent-inflammatory diseases of different localization. Specific for pneumococci are:
1. Croupous pneumonia
2. Creeping corneal ulcer
The most common disease is croupous pneumonia, which affects one, less often two or three lobes of the lung. The disease is acute, accompanied by high fever, cough. It usually ends critically. Pneumococci are leaders in the etiology of acute pneumonia, pulmonary empyema, can cause sinusitis, meningitis and other diseases, rarely endocarditis.
Immunity. After the illness, unstable immunity remains, since pneumonia is characterized by relapses.
Prevention. It comes down to sanitary and preventive measures. Specific prophylaxis has not been developed.
Treatment. Antibiotics are used - penicillin, tetracycline, etc.
Questions for self-control:
1. How are streptococci and pneumococci stained by Gram?
2. What genus do they belong to?
3. How are streptococci located in smears?
4. What do pneumococci resemble in shape?
5. How are pneumococci located in smears?
6. Are streptococci and pneumococci motile?
7. Under what conditions does pneumococcus form a capsule?
8. What is the role of the capsule in pneumococcus?
9. Due to the content of what substance in the capsule of pneumococcus is it protected from phagocytosis?
10. Are streptococci and pneumococci demanding on nutrient media?
11. Do streptococci grow on simple nutrient media?
12. What media are used for the cultivation of streptococcus and pneumococcus?
13. What 3 groups of streptococci are distinguished depending on their hemolytic activity?
14. What is the growth pattern of streptococcus on sugar or whey broth?
15. What toxins do streptococci secrete?
16. Name the pathogenicity enzymes secreted by streptococci.
17. How many serogroups of streptococci according to Lensfield do you know?
18. How are they designated?
19. What serogroup includes the majority of streptococci pathogenic for humans?
20. What diseases caused by St. pyogenes, are classified as suppurative?
21. Name non-suppurative diseases caused by group A streptococci.
22. Why are group B streptococci considered the scourge of maternity wards?
23. On what grounds are streptococci united in the group of non-groupable streptococci?
24. Who can be the source of infection in streptococcal infections?
25. What are the ways of transmission of the infectious principle in these diseases?
26. What serological group includes pneumococci?
27. Do pneumococci grow on simple nutrient media?
28. What colonies do pneumococci produce on blood agar?
29. What substances cause and enhance autolysis of pneumococcus colonies?
30. What biochemical tests are used to differentiate viridescent streptococcus from pneumococcus?
31. What diseases are caused by pneumococci?
32. What disease is most often caused by pneumococci?
33. Who can be the source of pneumococcal infection?
34. What are the ways of transmission of the infectious beginning in pneumococcal infections?
35. What antibiotics are used to treat streptococcal infections?
36. What measures are taken to prevent streptococcal infections?
Table of contents of the subject "Streptococci. Hemolytic Streptococci. Pneumococcus. Non-Hemolytic Streptococci.":First Pneumococcus identified by Pasteur (1881) while working on the rabies vaccine and initially considered him to be the causative agent of rabies. etiological role pneumococcus in the development of pneumonia in humans proved K. Frenkel and A. Weihselbaum (1884).
pneumococcus bacteria do not contain group antigen and are serologically heterogeneous - 84 serovars are isolated according to antigen of capsular polysaccharides. Known strains that colonize human and animal organisms.
Epidemiology of pneumococcus
Pneumococcus- one of the main causative agents of community-acquired bacterial pneumonia (2-4 cases per 1000 people). At least 500,000 cases are registered annually in the world pneumococcal pneumonia children and the elderly are most susceptible to infection.
Reservoir of pneumococcal infection- patients and carriers (20-50% of preschool children and 20-25% of adults), the main route of transmission of pneumococcus- contact, and during outbreaks also airborne. The peak incidence occurs in the cold season.
In the vast majority of cases clinical forms of pneumococcal infection develop with violations of the body's resistance (including due to cold stress), as well as against the background of concomitant pathology (sickle cell anemia, Hodgkin's disease, HIV infection, myeloma, diabetes mellitus, conditions after splenectomy) or alcoholism.
Morphology of pneumococcus. Cultural properties of pneumococcus
pneumococci represented by oval or lanceolate cocci with a diameter of about 1 µm. In smears from clinical material pneumococci arranged in pairs, each pair is surrounded by a thick capsule (Fig. 12-10).
Encapsulation by pneumococci stimulates the introduction of blood, serum or ascitic fluid into the medium. on agar pneumococci form delicate translucent, well-defined colonies with a diameter of about 1 mm; sometimes they can be flat with a depression in the center. Like other streptococci, colonies never merge with each other. On the CA, the colony is surrounded by a zone of a-hemolysis in the form of a greenish discolored zone.
Pneumococcal infections (A40.3) - a group of diseases of bacterial etiology, clinically manifested by purulent-inflammatory changes in various organs and systems, but especially often in the lungs like lobar pneumonia and in the central nervous system like purulent meningitis.
The proportion of pneumococcal infections in the structure of childhood infectious pathology has not been precisely established. The disease is more common in children aged 6 months to 7 years with a deficiency of humoral immunity.
Infection with pneumococci can occur both exogenously and endogenously. With exogenous infection, croupous pneumonia most often develops. Endogenous infection occurs due to a sharp weakening of the immune defense due to the activation of saprophytic pneumococci on the mucous membranes of the respiratory tract. Under these conditions, pneumococci can cause meningitis, septicemia, endocarditis, otitis media, pericarditis, peritonitis, sinusitis and other purulent-septic diseases.
Etiology. Pneumococcus was originally called Diplococcus pneumoniae. This name has now been changed to Streptococcus pneumoniae. According to modern classification, pneumococci are assigned to the family streptococcaceae, kind Streptococcus.
Pneumococci are Gram-positive cocci of oval or spherical shape, 0.5-1.25 μm in size, arranged in pairs, sometimes in the form of short chains. Since the distal end of each pair is pointed, the cocci are lanceolate, for which they were formerly called lanceolate diplococci. Pneumococci have a well organized capsule. According to its polysaccharide composition, more than 85 serotypes (serovars) of pneumococci are distinguished. Only smooth capsular strains of mainly the first 8 types are pathogenic for humans, the remaining serovars are weakly virulent for humans.
In addition to capsular antigens, pneumococci have 3 somatic antigens: a protein type-specific antigen M and two species-specific antigens C and R. Somatic antigens do not determine the specificity and virulence of the pathogen. In the course of the pathological process, antibodies are produced to all pneumococcal antigens, but antibodies to capsular antigens are most important for protecting the body.
When pneumococci are destroyed, endotoxin and β-hemolysin are released. In addition, pneumococci produce a certain amount of agemolysin and neuraminidase, which have weak hemotoxic, fibrinolytic properties and the ability to destroy leukocytes.
Pneumococci do not grow well on conventional nutrient media, but grow well on serum or ascitic agar, forming small round colonies with a green coloration of the medium. Haze and sediment form on sugar broth.
Pneumococci are relatively stable in the external environment. In dried sputum, they persist for 1-2 months, on infected diapers - 1-2 weeks, when boiled they die instantly, and at a temperature of 50-60 ° C - within 10 minutes. Pneumococci are highly sensitive to conventional disinfectant solutions.
Epidemiology. Pneumococci are practically permanent inhabitants of the human upper respiratory tract and in this sense they can be classified as conditionally pathogenic microorganisms.
In cultures of mucus from the oropharynx, they can be found in most healthy children. The greatest number of pneumococcal carriers is detected among young children, as well as the elderly. The carriage of serovars that do not have pronounced virulent properties predominates. In the course of carriage, most likely, immunity is developed. However, it cannot be called tense and, moreover, it is type-specific. The development of the disease in these cases is possible only with a sharp decrease in the body's immune reactivity (severe forms of influenza and SARS, prolonged use of corticosteroid hormones, cytostatics, X-ray therapy, etc.).
In epidemiological terms, clones of pneumococci with greater virulence and invasiveness are of paramount importance. They are formed in weakened children under adverse environmental conditions (cold season, overcrowding, increased incidence of influenza, SARS, etc.).
The source of infection is always a person - a patient or a carrier of pneumococci. The causative agent is transmitted by airborne droplets and household contact.
Susceptibility to pneumococci has not been clearly established. The disease usually develops in children with a deficiency of type-specific antibodies and is especially severe in children with sickle cell anemia, other forms of hemoglobinopathies, and C 3 deficiency. It is believed that in these cases the disease develops against the background of inadequate opsonization of pneumococci, which makes it impossible to eliminate them by phagocytosis.
Pathogenesis. Pneumococci can affect any organs and systems, but the lungs and respiratory tract should be considered a tropic organ. The reasons that determine the tropism of pneumococci to the bronchopulmonary system have not been established for certain. It is likely that pneumococcal capsular antigens have an affinity for lung tissues and airway epithelium. The introduction of the pathogen into the lung tissue is facilitated by acute respiratory infections, which eliminate the protective function of the epithelium of the respiratory tract and reduce the overall immunoreactivity. Various congenital and acquired defects in the system of elimination of bacterial antigens are also important: defects in the surfactant system of the lung, insufficient phagocytic activity of neutrophils and alveolar macrophages, impaired bronchial patency, decreased cough reflex, etc. A special place in the pathogenesis of lung damage during pneumococcal infection is assigned to impaired function of the ciliated epithelium bronchi, as well as changes in the chemical composition and rheological properties of bronchial secretions.
As a result of the interaction of micro- and macroorganism in the bronchopulmonary system, an inflammation focus is formed with a characteristic morphological substrate characteristic of certain clinical forms of the disease (bronchitis, pneumonia, pleurisy, etc.).
From the primary lesion, pneumococci begin to spread with the flow of lymph and blood, forming a prolonged bacteremia. Clinically, this may manifest as an infectious toxic syndrome, but asymptomatic bacteremia is also possible.
In debilitated children, pneumococci sometimes cross the blood-brain barrier and cause purulent meningitis or meningoencephalitis.
The spread of infection by contact bronchogenic way can lead to the occurrence of purulent pleurisy, sinusitis, otitis media, mastoiditis, pericarditis, epidural abscess, empyema. Pneumococcal bacteremia sometimes ends with the development of osteomyelitis, purulent arthritis, brain abscess.
Severe forms of pneumococcal infection are formed almost exclusively in young children, while the severity of clinical forms is determined not only by the reactivity of the macroorganism, but also by the virulence of the pathogen. The infection is especially severe with massive bacteremia and a high concentration of capsular antigen in the blood.
In severe cases, pneumococcal infection is accompanied by the development of rheological and hemodynamic disorders up to the occurrence of disseminated intravascular coagulation, acute adrenal insufficiency, edema and swelling of the brain substance.
clinical picture. Depending on the lesion, lobar pneumonia, pneumococcal meningitis, otitis media, osteomyelitis, endocarditis, peritonitis are distinguished.
Croupous pneumonia (English croup - croak) is an acute inflammation of the lungs, characterized by rapid involvement in the process of the lobe of the lung and the adjacent area of the pleura.
The disease occurs mainly in older children. In infants and young children, croupous pneumonia is extremely rare, which is explained by insufficient reactivity and features of the anatomical and physiological structure of the lungs (relatively wide intersegmental connective tissue layers that prevent contact spread of the inflammatory process). Croupous pneumonia is more often caused by pneumococcal serotypes I, III, and especially IV; other serotypes rarely cause it.
With croupous pneumonia, staging of morphological changes is noted. Usually, the pathological process begins in the posterior and posterolateral sections of the right lung in the form of a small focus of inflammatory edema, which rapidly increases, forming a phase of hyperemia and serous exudation (tide stage) with pneumococcal exudate multiplying; in the future, the pathological process enters the phase of leukocyte migration and fibrin prolapse (hepatization stage), followed by gradual resorption of exudate elements - leukocytes and fibrin (resolution stage). In children, the pathological process rarely extends to the entire lobe, more often only a few segments are affected.
The disease begins acutely, often with chills and pain in the side, aggravated by deep breathing. From the first hours there is a dry cough, headache, weakness, weakness, high fever (up to 39-40 ° C). Children are excited, sometimes delirious. Symptoms of croupous pneumonia quickly appear: a short, painful cough with a small amount of viscous glassy sputum, flushing of the cheeks, swelling of the wings of the nose, rapid shallow breathing, herpetic eruptions on the lips and wings of the nose, sometimes cyanosis of the lips and fingertips; on the side of the lesion, one can see lagging of the chest during breathing and limitation of mobility of the lower edge of the lung. When the process is localized in the lower lobe of the right lung, due to damage to the pleura, pain is felt not only in the chest, but also in the abdomen, simulating a disease of the abdominal organs (appendicitis, peritonitis, pancreatitis, etc.). At the same time, repeated vomiting, frequent loose stools, and bloating are possible in children, which makes it difficult to differentiate with acute intestinal infection. When the process is localized in the upper lobe of the right lung, meningeal symptoms may appear in children (neck muscle stiffness, convulsions, frequent vomiting, severe headache, delirium),
Changes in the lungs undergo a very characteristic evolution. On the 1st day of illness, in typical cases, a tympanic shade of percussion sound can be noted on the side of the lesion, then within a few hours this sound is gradually replaced by dullness. By the end of the 1st day, at the height of inhalation, crepitus and small bubbling wet and dry rales begin to be heard.
At the height of clinical manifestations (2-3 days of illness), dullness in the affected area becomes pronounced and bronchial breathing begins to be heard above the lesion, sometimes pleural friction rub, as well as voice trembling and bronchophony. At the same time, the cough intensifies, becomes less painful and more moist, sometimes the sputum becomes reddish-brown, shortness of breath increases, cyanosis of the lips and face intensifies.
In the peripheral blood at the height of the disease, neutrophilic leukocytosis is noted, the content of stab cells increases to 10-30%, sometimes there is a shift in the formula to young and myelocytes, toxic granularity of neutrophils is often detected, aneosinophilia, moderate monocytosis are typical; ESR increased.
The resolution stage usually begins on the 5-7th day of illness. Symptoms of intoxication weaken, the body temperature drops critically or lytically. In the lungs, bronchial breathing weakens, voice trembling and bronchophony disappear, and abundant crepitus reappears. In the process of resorption of the exudate, bronchial breathing becomes hard, and then vesicular, the shortened percussion sound disappears.
On the radiograph, you can see the main stages of the development of croupous pneumonia. In the stage of the tide, there is a slight decrease in transparency in the area of the affected area, an increase in the pulmonary pattern due to the plethora of blood vessels. In the stage of hepatization, a pronounced decrease in the transparency of the area of the affected lung is revealed, resembling a picture of atelectasis.
The resolution stage is manifested by the slow restoration of the transparency of the affected area of the lung. In some cases, fluid is determined in the pleural cavity (pleuropneumonia). The total duration of the disease is about 3-4 weeks, the duration of the febrile period is an average of 7-10 days, complete restoration of the structure and function of the lungs occurs after 1-1.5 months.
Pneumococcal meningitis is the most severe form of purulent meningitis in children. The disease usually occurs in children of the second half of life. In children of the first 5 months of life, pneumococcal meningitis is rare. At an older age, pneumococcal meningitis is often preceded by trauma to the skull or it occurs in children with chronic diseases of the paranasal sinuses, as well as in children with congenital or acquired immunity disorders. Especially often children suffering from sickle cell anemia, oncological diseases, who have undergone splenectomy get sick.
Meningeal involvement usually occurs secondary to other manifestations of pneumococcal infection. In rare cases, the primary focus cannot be established. The causative agent penetrates the meninges as a result of bacteremia. It is believed that the serovar of the pathogen with which the child is infected is important in the development of pneumococcal bacteremia and meningitis. Most patients with pneumococcal meningitis have serotypes 1-7, as well as 14, 18, 23, less often others.
The disease usually begins acutely, with an increase in body temperature to high values, but in weakened children, the temperature may remain subfebrile and even normal. Children become restless, scream, often spit up. Often the first symptoms are convulsions, tremors, hyperesthesia, bulging of the large fontanelle and loss of consciousness. The meningeal syndrome is often incomplete and mild. In severe cases, it may be absent altogether. In most patients, the disease immediately begins as meningoencephalitis. In these cases, from the 1st day, consciousness is disturbed, tremors of the limbs, convulsions, sharp psychomotor agitation, turning into stupor and coma, appear. Focal symptoms of damage to the cranial nerves appear early, often abducens, oculomotor and facial, mono- and hemiparesis are possible. In older children, there is often a clinical picture of edema and swelling of the brain with its wedging into the foramen magnum.
The cerebrospinal fluid is turbid, purulent, greenish-gray in color. When settling, a precipitate quickly falls out, neutrophilic pleocytosis is noted (500-1200 cells in 1 μl). The protein content is usually high, the amount of sugar and chlorides is reduced.
In the peripheral blood, leukocytosis with a sharp shift to the left, aneosinophilia, monocytosis are detected, moderate anemia and thrombocytopenia are possible; ESR increased.
Pneumococci are relatively often the causative agents of otitis media, purulent arthritis, osteomyelitis, pericarditis, endocarditis, primary peritonitis, etc. All these conditions can be in patients with pneumonia, bronchitis, tracheitis, or occur independently, as a result of bacteremia. Usually they are observed in young children, especially in premature infants and in the 1st month of life. Clinically, they cannot be distinguished from diseases caused by other pyogenic bacteria.
Diagnostics. It is possible to accurately diagnose pneumococcal infection only after the pathogen has been isolated from the lesion or blood. For research, sputum is taken for lobar pneumonia, blood for suspected sepsis, purulent discharge or inflammatory exudate for other diseases. Pathological material is subjected to microscopy. The detection of gram-positive lanceolate diplococci surrounded by a capsule provides a basis for preliminary diagnosis of pneumococcal infection. To establish whether the isolated diplococci belong to pneumococci, combined type-specific sera containing high titers of antibodies to all pneumococcal serotypes are used. In the early days of pneumococcal meningitis, the pathogen can be found in the cerebrospinal fluid, where it is located both extra- and intracellularly. In order to isolate a pure culture, the test material is inoculated on blood, serum or ascitic agar. On nutrient media, pneumococcus gives rise to small transparent colonies. A biological sample can be used to isolate a pure culture. For this purpose, white mice are intraperitoneally infected with the test material. In the presence of pathogenic pneumococci in the material, mice die within 24-48 hours. To detect pneumococcal antigens, the method of solid-phase immunoelectrophoresis can be used.
Treatment. Therapy for pneumococcal infection should be comprehensive. In severe cases, antibiotics must be prescribed.
In mild and moderate forms (nasopharyngitis, bronchitis, otitis media, etc.), phenoxymethylpenicillin (vepicombin) can be prescribed at 50,000-100,000 IU / (kg. Day) in 4 oral doses or penicillin at the same dose 3 times a day intramuscularly in for 5-7 days, or azithromycin (Sumamed) at the rate of 10 mg/kg per day for 3 days. Patients with lobar pneumonia or meningitis are prescribed a 3rd and 4th generation cephalosporin antibiotic. In the course of antibiotic treatment, it is advisable to check the sensitivity of isolated pneumococci to the prescribed drug and, if necessary, replace it. In the last 2 years, strains of pneumococci resistant to many antibiotics have become increasingly isolated.
In severe forms of pneumococcal infection, in addition to antibiotics, infusion, pathogenetic, restorative and symptomatic therapy is prescribed, the principles of which are the same as for other infectious diseases.
Forecast. With pneumococcal meningitis, the mortality rate is about 10-20% (in the pre-antibiotic era - 100%). In other forms of the disease, deaths are rare. They occur, as a rule, in children with congenital or acquired immunodeficiency, long-term treatment with immunosuppressive drugs, in children with congenital malformations.
Prevention. For the prevention of pneumococcal infection, it is proposed to administer the polyvalent polysaccharide vaccine "PNEUMO 23" manufactured by Sanofi Pasteur (France), which is a mixture of purified capsular polysaccharides of the 23 most common pneumococcal serotypes. 1 dose of such a vaccine contains 25 micrograms of each type of polysaccharide, as well as isotonic sodium chloride solution and 1.25 mg of phenol as a preservative. The vaccine does not contain other impurities. It is recommended to administer it to children over 2 years of age at risk for pneumococcal infection, which include children with immunodeficiencies, asplenia, sickle cell anemia, chronic pathology of the kidneys, heart, as well as people over 60 years old. The vaccine is administered once at a dose of 0.5 ml subcutaneously or intramuscularly. This vaccine is highly immunogenic and rarely causes adverse reactions. The duration of post-vaccination immunity has not been precisely established, but antibodies in the blood after vaccination persist for up to 5 years. A contraindication to the introduction of pneumococcal vaccine is hypersensitivity to the constituent components of the vaccine.
Children with an immunodeficiency state in case of contact with a patient with pneumococcal infection can be given gamma globulin at 0.2 ml / kg intramuscularly.
scarlet fever cause various serotypes of beta-hemolytic streptococci with M-antigen and producing erythrogenin (toxigenic streptococci of serogroup A) - (Streptococcus pyogenes). In the absence of antitoxic immunity, scarlet fever occurs, in the presence of angina.
Clinical picture
Intoxication - fever, general malaise, headaches.
Scarlatina rash - finely punctate, with moderate pressure with a glass spatula, the spots are more clearly visible. When pressed harder, the rash gives way to a golden-yellowish skin tone. It appears on the 1-3rd day of illness and is localized mainly on the cheeks, in the groin, on the sides of the body. The skin of the nasolabial triangle remains pale and rash-free. The rash usually lasts 3-7 days, then fades away, leaving no pigmentation. Characterized by a thickening of the rash on the folds of the limbs - axillary, elbow, popliteal areas.
Scarlet tongue - on the 2-4th day of illness, the patient's tongue becomes pronounced grainy, bright red, the so-called "crimson" tongue.
Angina is a constant symptom of scarlet fever. It can be more severe than the usual sore throat.
Peeling of the skin - occurs after the disappearance of the rash (14 days after the onset of the disease): in the area of the palms and feet it is large-lamellar, starting from the fingertips; on the trunk, neck, auricles scaly peeling.
Pneumococci, taxonomy. Properties. Serological groups. Distinctive features from other streptococci. Caused diseases. Principles and methods of laboratory diagnostics.
Morphology and biological properties. Pneumococci (Streptococcus pneumoniae) are paired cocci of an oval, slightly elongated lanceolate shape, resembling a candle flame. They can also be located in short chains, resembling streptococci. They are non-motile, do not form spores, and are Gram-positive.
They are grown on media with the addition of protein: blood, serum, with ascitic fluid. On blood agar, pneumococcal colonies are small, resembling dewdrops, transparent in transmitted light, with a depressed center, surrounded by a zone of incomplete hemolysis, a greenish tint, similar to the colonies of viridescent streptococcus. On liquid media, they give a gentle turbidity, sometimes forming a precipitate. They are quite active biochemically: they decompose glucose, lactose, maltose, inulin and other carbohydrates with the formation of acid, do not liquefy gelatin, do not form indole. The splitting of inulin is a differential diagnostic feature that helps to distinguish pneumococci from streptococci, which do not decompose inulin. An important distinguishing feature is the ability of pneumococci to dissolve in bile, while streptococci are well preserved in it.
Pathogenesis and clinic. Pneumococci are the causative agents of lobar pneumonia in humans. They can also cause creeping corneal ulcers, upper respiratory catarrhs, meningitis, endocarditis, joint damage, and other diseases.
After the disease, immunity is low-tensioned, short-term, type-specific.
Microbiological diagnostics. The material for the study is sputum, blood, throat swab, cerebrospinal fluid. Due to the fact that pneumococcus dies quickly, pathological material must be delivered to the laboratory as soon as possible for research.
Meningococcus. Taxonomy, properties. Antigenic structure of meningococci, classification. Pathogenesis of meningococcal infection, clinical manifestations. Principles and methods of microbiological diagnostics. Differentiation of the causative agent of meningococcal infection and other meningococci. specific prophylaxis.
N. meningitidis (meningococci).
Meningococcus is the causative agent of meningococcal infection - a severe anthroponosis with airborne droplet transmission of the pathogen. The main source is carriers. The natural reservoir is the human nasopharynx. Morphological, cultural and biochemical properties are similar to gonococcus. Differences - they ferment not only glucose, but also maltose, produce hemolysin. They have a capsule that is larger and has a different structure than that of the gonococcus.
antigenic composition. They have four main antigenic systems.
1. Capsular group-specific polysaccharide antigens. Serogroup A strains most commonly cause epidemic outbreaks.
2. Protein antigens of the outer membrane. According to these antigens, meningococci of serogroups B and C are divided into classes and serotypes.
3. Genus- and species-specific antigens.
4. Lipopolysaccharide antigens (8 types). They have a high toxicity, cause a pyrogenic effect.
pathogenicity factors. Adhesion factors and colonization - pili and outer membrane proteins. Invasiveness factors - hyaluronidase and other produced enzymes (neuraminidase, proteases, fibrinolysin). Of great importance are capsular polysaccharide antigens that protect microorganisms from phagocytosis.
Immunity resistant, antimicrobial.
Laboratory diagnostics based on bacterioscopy, isolation of the culture and its biochemical identification, serological diagnostic methods. The inoculation of the material is carried out on solid and semi-liquid nutrient media containing blood, ascitic fluid, and blood serum.
Oxidase positive cultures are considered to belong to the genus Neisseria. Meningococcus is characterized by the fermentation of glucose and maltose. Belonging to the serogroup is determined in the agglutination test (RA).
Gonococcus. Taxonomy, properties. Pathogenesis of gonococcal infection, features of immunity. Principles and methods of laboratory diagnostics of acute and chronic gonorrhea, blennorrhea. RSK Borde-Zhangu, purpose, mechanism, response accounting. Prevention of blennorrhea in newborns. Prevention and treatment of gonorrhea. specific therapy.
N.gonorrheae (gonococcus).
Gonococcus is the causative agent of gonorrhea, a sexually transmitted disease with inflammatory manifestations in the urinary tract. The substrate for colonization is the epithelium of the urethra, rectum, conjunctiva of the eye, pharynx, cervix, fallopian tubes and ovary.
Diplococci stain well with methylene blue and other aniline dyes, pleomorphic (polymorphism). Very whimsical to the conditions of cultivation and nutrient media. Of the carbohydrates, only glucose is fermented.
Antigenic structure very variable - characterized by phase variations (disappearance of antigenic determinants) and antigenic variations (changes in antigenic determinants).
pathogenicity factors. The main factors are drank, with the help of which gonococci carry out adhesion and colonization of epithelial cells of the mucous membrane of the urinary tract, and lipopolysaccharide(endotoxin, released during the destruction of gonococci). Gonococci synthesize IgAI, a protease that cleaves IgA.
Laboratory diagnostics. Bacterioscopic diagnosis includes Gram stain and methylene blue. Typical signs of gonococcus are gram-negative staining, bean-shaped diplococci, intracellular localization.
Sowing is carried out on special media (KDS-MPA from rabbit meat or bovine heart with serum, ascites-agar, blood agar).
Causative agents of gaseous anaerobic infection. Taxonomy. Properties. characteristics of toxins. Pathogenesis, clinical forms. Principles and methods of laboratory diagnostics, drugs for specific prevention and treatment.
Gas gangrene is an anaerobic polyclostridial (i.e. caused by various types of clostridia) wound (traumatic) infection. Of primary importance is C.perfringens, less often C.novyi, as well as other types of clostridia in persistent associations with each other, aerobic pyogenic cocci and putrefactive anaerobic bacteria.
C.perfringens is a normal inhabitant of the intestines of humans and animals, it enters the soil with feces. It is the causative agent of wound infection - it causes disease when the pathogen enters the wound under anaerobic conditions. It is highly invasive and toxigenic. Invasiveness is associated with the production of hyaluronidase and other enzymes that have a destructive effect on muscle and connective tissues. Main pathogenicity factor - exotoxin, which has hemo-, necro-, neuro-, leukotoxic and lethal effects. In accordance with the antigenic specificity of exotoxins, they are isolated serotypes pathogen. Along with gas gangrene, C. perfringens causes food poisoning (they are based on the action of enterotoxins and necrotoxins).
Features of pathogenesis. In contrast to purulent diseases caused by aerobes, anaerobic infection is not dominated by inflammation, but necrosis, edema, gas formation in tissues, poisoning with toxins and tissue decay products.
Immunity- predominantly antitoxic.
Laboratory diagnostics includes bacterioscopy of wound discharge, isolation and identification of the pathogen, detection and identification of toxin in bioassays using a neutralization reaction with specific antitoxic antibodies.
Prevention and treatment. The prevention of gas gangrene is based on timely and correct surgical treatment of wounds. In case of severe wounds, antitoxic serums are administered against the main types of clostridium, 10 thousand IU each, for medicinal purposes - 50 thousand IU each.
Clostridia tetanus. Taxonomy. Properties, characteristics of toxins. The pathogenesis of the disease. Descending tetanus. Clinic. Principles and methods of laboratory diagnostics. The purpose of bacteriological research, preparations for specific prevention and treatment.
Tetanus is an acute wound infection characterized by lesions neurotoxin motor cells of the spinal cord and brain, which manifests itself in the form of spasms of the striated muscles. People and farm animals get sick. Soil, especially contaminated with human and animal feces, is a constant source of tetanus infection.
Pathogen - C.tetani - a large spore-forming gram-positive bacillus. Spores are located terminally (a type of drumstick), mobile due to flagella - peritrichous. Mandatory anaerobic. The spores are very resistant.
antigenic properties. The causative agent has O- and H- antigens.
pathogenicity factors. The main factor is the strongest exotoxin. Its two main fractions are distinguished - tetanospasmin (neurotoxin) and tetanolysin (hemolysin). Neurotoxin in the central nervous system penetrates into the area of myoneural synapses, is transmitted from neuron to neuron in the area of synapses, accumulates in the motor areas of the spinal and brain, blocks synaptic transmission. Death occurs from paralysis of the respiratory center, asphyxia (damage to the muscles of the larynx, diaphragm, intercostal muscles) or paralysis of the heart.
Laboratory diagnostics. Microbiological diagnostics includes bacterioscopy of raw materials, culture for isolation of the pathogen and its identification, detection of tetanus toxin.
Isolation of the pathogen is carried out according to the standard scheme for anaerobes, using various dense and liquid (Kitt-Tarozzi medium) media, identification is based on morphological, cultural, biochemical and toxigenic properties.
The simplest and most effective method of microbiological diagnostics is a bioassay on white mice. One group is infected with the test material, the second (control) - after mixing the samples with antitoxic tetanus serum. In the presence of tetanus toxin, the experimental group of mice dies, while the control group remains alive.
Treatment and emergency prevention. Donor tetanus immunoglobulin (antitoxin), antitoxic serum (350 IU/kg), antibiotics (penicillins, cephalosporins) are used. To create vaccine immunity, tetanus toxoid is used, more often as part of the DTP vaccine (tetanus toxoids, diphtheria and killed whooping cough).
Clostridia botulinum. Taxonomy. Properties. Characteristics of toxins, difference from exotoxins of pathogens of other foodborne infections. Principles and methods of laboratory diagnostics. Drugs for specific prevention and treatment.
Botulism is a severe food poisoning associated with the use of products contaminated with C.botulinum, and is characterized by a specific lesion of the central nervous system. It got its name from lat. botulus - sausage.
Exciter properties. Large polymorphic gram-positive rods, motile, have peritrichous flagella. Spores are oval, located subterminally (tennis racket). Eight types of toxins are formed, differing in antigenic specificity, and, accordingly, 8 types of pathogen are isolated. Among the most important characteristics is the presence or absence of proteolytic properties (casein hydrolysis, production of hydrogen sulfide).
The toxin has a neurotoxic effect. The toxin enters the body with food, although it can probably accumulate when the pathogen multiplies in the tissues of the body. The toxin is thermolabile, although boiling for up to 20 minutes is necessary for complete inactivation. The toxin is rapidly absorbed in the gastrointestinal tract, penetrates into the blood, selectively acts on the nuclei of the medulla oblongata and ganglion cells of the spinal cord. Neuroparalytic phenomena develop - swallowing disorders, aphonia, dysphagia, ophthalmo-plegic syndrome (strabismus, double vision, eyelid drooping), paralysis and paresis of the pharyngeal and laryngeal muscles, respiratory and cardiac arrest.
Laboratory diagnostics. The principles are common to clostridia.
Treatment and prevention. The basis is the early use of antitoxic sera (polyvalent or, when the type is established, homologous). Prevention is based on the sanitary and hygienic regime in the processing of food products. Home-made canned mushrooms and other products stored under anaerobic conditions are especially dangerous.
11. Pseudomonas aeruginosa. Taxonomy. Properties. Caused diseases.
Role in nosocomial infections. Principles and methods of laboratory diagnostics.
The genus pseudomonas, P. aeruginosa (Pseudomonas aeruginosa) is one of the main causative agents of local and systemic purulent-inflammatory processes in medical hospitals.
The pathogen is ubiquitous (water, soil, plants, animals), occurs normally in humans (most often in the intestines, on the skin and mucous membranes). Morphology- Gram-negative straight or slightly curved rod, movable, located in smears singly, in pairs or in short chains. Synthesizes mucus (capsular substance), especially more virulent mucoid strains.
cultural properties. It is an aerobe and has a set of enzymes corresponding to the type of respiration (cytochromes, cytochrome oxidase, dehydrases). On liquid media it forms a grayish-silver film. On dense media, the phenomenon of iridescent lysis is often observed. By the end of the day due to pigment synthesis pyocyanin a blue-green color of the culture appears.
biochemical properties. Pseudomonas aeruginosa is characterized by low saccharolytic activity (oxidizes only glucose), high proteolytic activity, and the formation of a beta-hemolysis zone on blood agar. Synthesizes trimethylamine, which gives crops a pleasant smell of jasmine. Produces the production of bacteriocins - pyocins.
Antigenic and pathogenic properties. The main antigens of Pseudomonas aeruginosa are a group-specific somatic O-antigen and a type-specific flagellar H-antigen. O-antigenic complex - an aggregate of LPS with proteins and lipids of the cell wall, has the properties of endotoxin, is one of the main factors of pathogenicity. Pseudomonas aeruginosa has a large set of pathogenicity factors - endotoxin (LPS, similar to other gram-negative bacteria), a number of exotoxins - cytotoxin, exoenzyme S, hemolysins, exotoxin A (the most important, resembles diphtheria exotoxin), enzymes (collagenase, neuraminidase, proteases).
Laboratory diagnostics. P.aeruginisa received its name for the bluish - green staining of the detachable wounds and dressings. The main diagnostic method is bacteriological. Important is the detection of the pigment pyocyanin. Treatment and specific prevention. There is no specific prevention. With food poisoning and intestinal dysbacteriosis caused by Pseudomonas aeruginosa, a complex intesti - bacteriophage, which includes pseudomonas phage, is effective. Of the antibacterial drugs, aminoglycosides, cephalosporins and quinolones are more often used.
Conditionally pathogenic gram-negative bacteria - causative agents of purulent-inflammatory processes (Proteus, Klebsiella, miraculous rod, etc.), taxonomy. General characteristics of enterobacteria. Principles and methods of laboratory diagnostics.
Genus Klebsiella.
The genus Klebsiella belongs to the Enterobacteriaceae family. A feature of the representatives of the genus is the ability to form a capsule. The main species is K. Pneumoniae. Cause opportunistic lesions - nosocomial pneumonia, urinary tract infections, diarrhea in newborns. Klebsiella cause mastitis, septicemia and pneumonia in animals, are constantly found on the skin and mucous membranes of humans and animals. Klebsiella - straight, motionless sticks of various sizes. facultative anaerobes. Oxidase - negative, catalase - positive.
pathogenicity factors. These include a polysaccharide capsule (K-antigen), endotoxin, fimbriae, siderophore system (binds ferrous ions and reduces their content in tissues), thermolabile and thermostable exotoxins.
Clinical manifestations. K.pneumoniae (subsp. pneumoniae) is characterized by hospital bronchitis and bronchopneumonia, lobar pneumonia, urinary tract infections, lesions of the meninges, joints, spine, eyes, as well as bacteremia and septicopyemia. The subspecies ozaenae causes a special form of chronic atrophic rhinitis - lake.
Laboratory diagnostics. The main method is bacteriological. Treatment. One of the features of Klebsiella is their multidrug resistance and the development of lesions against the background of a decrease in the body's resistance. Antibiotics are used for generalized and sluggish chronic forms of Klebsiellesis, usually in combination with drugs that stimulate the immune system.
Genus Proteus.
The genus Proteus belongs to the Enterobacteriaceae family. The genus was named in honor of the son of Poseidon Proteus, capable of changing his appearance. Representatives of the genus are able to change the external manifestations of growth on dense nutrient media, and are also distinguished by the greatest pleomorphism (morphology variability) compared to other Enterobacteria.
Proteins break down tyrosine, restore nitrates, oxidase is negative, catalase is positive. They live in the intestines of many species of vertebrates and invertebrates, soil, sewage, and decaying organic residues. Can cause urinary tract infections in humans, as well as septic lesions in patients with burns and after surgery. Quite often they also cause food poisoning. P.vulgaris and P.mirabilis have the most common role in pathology.
cultural properties. Proteas grow on simple media over a wide range of temperatures. The optimum pH is 7.2-7.4, the temperature is from +35 to 37 degrees Celsius. Proteus colonies in the O-form are rounded, semi-transparent and convex, H-forms give continuous growth. The growth of proteas is accompanied by a putrid odor. The phenomenon of swarming is characteristic, H-forms give on MPA a characteristic creeping growth in the form of a bluish-smoky delicate veil. When sowing according to the Shushkevich method in the condensation moisture of freshly cut MPA, the culture gradually rises in the form of a veil up the surface of the agar. Diffuse turbidity of the medium with a thick white sediment at the bottom is noted on the BCH.
pathogenicity factors. These include LPS of the cell wall, the ability to “swarm”, fimbria, proteases and urease, hemolysins and hemagglutinins.
Laboratory diagnostics. The main method is bacteriological. Differential diagnostic media (Ploskirev), enrichment media and MPA are used according to the Shushkevich method. Treatment. In case of intestinal dysbacteriosis associated with proteas (colitis), it is possible to use proteus phage and preparations containing it (intestifag, coliproteus bacteriophage).
"Wonderful stick" (Serratia marcescens), type of bacteria from among the pigment microorganisms. Gram-negative motile (peritrichous) non-spore-bearing rods. By type of exchange - facultative anaerobe. On the surface of the agar forms smooth or granular dark and bright red colonies with a metallic sheen. Lives in soil, water, food. Developing on bread (at high humidity), in milk, it colors them red; such products are not allowed to be sold. Conditionally pathogenic for animals and humans; may cause suppuration.
13. Escherichia. Taxonomy. Diseases caused by Escherichia coli. Pathogenic variants of diarrheagenic Escherichia. Antigenic structure, classification. Features of microbiological diagnostics. Differentiation of diarrheagenic Escherichia from conditionally pathogenic.
Escherichia are the most common aerobic intestinal bacteria that, under certain conditions, can cause a wide group of human diseases, both intestinal (diarrhea) and extraintestinal (bacteremia, urinary tract infections, etc.) localization. The main species - E. coli (E. coli) - the most common causative agent of infectious diseases caused by enterobacteria. This pathogen is an indicator of faecal contamination, especially water.
cultural properties. On liquid media, E. coli gives diffuse turbidity, on dense media it forms S- and R-forms of colonies. On the Endo medium for Escherichia, lactose-fermenting Escherichia coli form intensely red colonies with a metallic sheen, non-fermenting - pale pink or colorless colonies with a darker center, on Ploskirev's medium - red with a yellowish tint, on Levin's medium - dark blue with a metallic sheen .
biochemical properties. Escherichia coli in most cases ferments carbohydrates (glucose, lactose, mannitol, arabinose, galactose, etc.) with the formation of acid and gas, forms indole, but does not form hydrogen sulfide, and does not liquefy gelatin.
The main pathogenicity factors of diarrheal E.coli.
1. Factors of adhesion, colonization and invasion associated with pili, fimbrial structures, outer membrane proteins. They are encoded by plasmid genes and promote colonization of the lower small intestine.
2. Exotoxins: cytotonins (stimulate hypersecretion of fluid by intestinal cells, disrupt water-salt metabolism and contribute to the development of diarrhea) and enterocytotoxins (act on cells of the intestinal wall and capillary endothelium).
3. Endotoxin (lipopolysaccharide).
Depending on the presence of various pathogenicity factors, diarrheagenic Escherichia coli are divided into five main types: enterotoxigenic, enteroinvasive, enteropathogenic, enterohemorrhagic, enteroadhesive.
4. Pathogenic E. coli is characterized by the production of bacteriocins (colicins).
Enterotoxigenic E. coli have a high molecular weight thermolabile toxin, similar in action to cholera, cause cholera-like diarrhea (gastroenteritis in young children, traveler's diarrhea, etc.).
Enteroinvasive Escherichia coli able to penetrate and multiply in the cells of the intestinal epithelium. They cause profuse diarrhea with an admixture of blood and a large number of leukocytes (an indicator of an invasive process) in the stools. Clinically resembles dysentery. The strains have some similarities with Shigella (non-motile, do not ferment lactose, have high enteroinvasive properties).
Enteropathogenic E.coli- the main causative agents of diarrhea in children. At the heart of the lesions is the adhesion of bacteria to the intestinal epithelium with damage to the microvilli. Characterized by watery diarrhea and severe dehydration.
Enterohemorrhagic Escherichia coli cause diarrhea mixed with blood (hemorrhagic colitis), hemolytic-uremic syndrome (hemolytic anemia in combination with renal failure). The most common serotype of enterohemorrhagic Escherichia coli is O157:H7.
Enteroadhesive E.coli do not form cytotoxins, are poorly studied.
Laboratory diagnostics. The main approach is the isolation of a pure culture on differential diagnostic media and its identification by antigenic properties. They put RA with a set of polyvalent OK (to O- and K-antigens) sera.
