Dysentery - this is a painful infection, accompanied by diarrhea with the release of blood, pus and mucus, abdominal pain and symptoms of general intoxication, occurring with a predominant lesion of the large intestine, caused by different species of the genus Shigella(dysentery bacteria).

causative agents of dysentery belong to the department Gracilicutes, family Enterobacteriaceae, kind Shigella.
Dysentery , called Shigella dysenteriae, is more severe than diseases caused by other Shigella, because in addition to the endotoxin that causes intestinal inflammation, this type of bacteria produces a strong exotoxin that acts as a neurotoxin

Bacterial dysentery , or shigellosis, is an infectious disease caused by bacteria of the genus Shigella,

Dysentery.Morphology and tinctorial properties.
Shigella are gram-negative rods with rounded ends, 2–3 µm long, 0.5–7 µm thick, do not form spores, do not have flagella, and are immobile. In many strains, villi of a general type and genital pili are found. Some Shigella have a microcapsule.

Dysentery. Cultivation.
Dysentery sticks are facultative anaerobes. They are undemanding to nutrient media, grow well at a temperature of 37 ° C and a pH of 7.2-7.4. On dense media they form small transparent colonies, in liquid media - diffuse turbidity. Selenite broth is most often used as an enrichment medium for the cultivation of Shigella.

Dysentery.enzymatic activity.
Shigella have less enzymatic activity than other enterobacteria. They ferment carbohydrates with the formation of acid. An important feature that makes it possible to differentiate Shigella is their relationship to mannitol: S. dysenteriae does not ferment mannitol, representatives of groups B, C, D are mannitol-positive. The most biochemically active are S. sonnei, which slowly (within 2 days) can ferment lactose. Based on the relationship of S. sonnei to rhamnose, xylose and maltose, 7 biochemical variants of it are distinguished.

Dysentery.Antigenic structure.
Shigella have O-antigen, its heterogeneity allows serovars and subserovars to be distinguished within groups; in some members of the genus, the K-antigen is found.

Dysentery.pathogenicity factors.
All dysenteric bacilli form endotoxin, which has an enterotropic, neurotropic, pyrogenic effect. In addition, S. dysenteriae - Shigella Grigoriev-Shiga - secrete an exotoxin that has an enterotoxic, neurotoxic, cytotoxic and nephrotoxic effect on the body, which accordingly disrupts water-salt metabolism and the activity of the central nervous system, leads to the death of epithelial cells of the colon. intestines, damage to the renal tubules.

With the formation of exotoxin, a more severe course of dysentery caused by this pathogen is associated. Exotoxin can also be secreted by other types of Shigella. The RF permeability factor has been discovered, as a result of which blood vessels are affected. Pathogenic factors also include invasive protein, facilitating their penetration into epithelial cells, as well as pili and outer membrane proteins responsible for adhesion, and a microcapsule.

Dysentery.resistance.
Shigella have low resistance to various factors. S. sonnei possess greater resistance, which persist in tap water for up to 2.5 months, and in water of open reservoirs survive up to 1.5 months. S. sonnei can not only survive for a long time, but also multiply in products, especially dairy products.

Dysentery.Epidemiology.
Dysentery is an anthroponotic infection: the source is sick people and carriers. The mechanism of transmission of infections is fecal-oral. The routes of transmission can be different - with Sonne's dysentery, the food route predominates, with Flexner's dysentery - water, for Grigoriev-Shiga's dysentery, the contact-household route is characteristic.

Dysentery found in many countries of the world. In recent years, there has been a sharp rise in the incidence of this infection. People of all ages get sick, but children from 1 to 3 years old are most susceptible to dysentery. The number of patients increases in July-September. Different types of Shigella are unevenly distributed in certain regions.

Dysentery.Pathogenesis.
Shigella enters the gastrointestinal tract through the mouth and reaches the large intestine. Possessing tropism for its epithelium, pathogens attach to cells with the help of pili and proteins of the outer membrane. Thanks to the invasive factor, they penetrate inside the cells, multiply there, as a result of which the cells die.

Ulcerations form in the intestinal wall, in place of which scars are then formed. Endotoxin, released during the destruction of bacteria, causes general intoxication, increased intestinal motility, and diarrhea. Blood from the formed ulcers enters the stool. As a result of the action of exotoxin, a more pronounced violation of water-salt metabolism, the activity of the central nervous system, and kidney damage is observed.

Dysentery.clinical picture.
The incubation period lasts from 1 to 5 days. The disease begins acutely with an increase in body temperature to 38-39 ° C, abdominal pain, diarrhea appear. An admixture of blood, mucus is found in the stool. Grigoriev-Shiga dysentery is the most severe.

Dysentery.Immunity.
After a disease, immunity is species-specific and variant-specific. It is short lived and unstable. Often the disease becomes chronic. Repeated diseases were noted even within one season.

Dysentery.laboratory diagnostics.
The patient's feces are taken as the test material. The basis of diagnosis is the bacteriological method, which allows to identify the pathogen, determine its sensitivity to antibiotics, conduct intraspecific identification (determine the biochemical variant, serovar or colicinogenovar). With a protracted course of dysentery, it can be used as an auxiliary serological method, which consists in staging RA, RNHA (by increasing the antibody titer during repeated formulation of the reaction, the diagnosis can be confirmed).

Dysentery.Treatment.
Patients with severe forms of dysentery Grigorieva-Shish and Flexner are treated with broad-spectrum antibiotics with the obligatory consideration of the antibiogram, since among Shigella there are often not only antibiotic-resistant, but also antibiotic-dependent forms. In mild forms of dysentery, antibiotics are not used, since their use leads to dysbacteriosis, which aggravates the pathological process, and disruption of regenerative processes in the mucous membrane of the colon.

Dysentery.Prevention.
The only drug that can be used in the foci of infection for prophylactic purposes is dysenteric bacteriophage. The main role is played by nonspecific prophylaxis.

Non-specific prevention provides for proper sanitary and hygienic arrangement of people's lives, supplying them with high-quality water and food.

In the environment of the patient, measures must be taken to prevent the spread of the pathogen.

Microbiology: lecture notes Tkachenko Ksenia Viktorovna

3. Shigella

3. Shigella

They belong to the genus Shigella.

They are the causative agents of dysentery. The morphology is the same as that of other members of the Enterobacteriaceae family. They are immobile and do not form capsules.

They grow well on simple nutrient media. Colorless colonies form on Endo's medium.

The genus includes four species that differ in biochemical properties (the ability to ferment mannitol and lactose) and antigenic structure:

1) Sh. disenteriae; do not ferment lactose and mannitol; according to antigenic properties within the species are divided into 12 serovars; one of them - shigella Grigorieva-Shiga - the most pathogenic;

2) Sh. flexneri; only ferments mannitol; according to antigenic properties, it is divided into 6 serovars, which are divided into subserovars;

3) Sh. boydii; only ferments mannitol; according to the antigenic structure, it is divided into 18 serovars;

4) Sh. sonnei; ferments only lactose; antigenically, the species is homogeneous; fermentovars, fagovars, and koletsinovars are distinguished within the species.

Shigella, bypassing the stomach and small intestine, enter the large intestine. They attach to colonocyte membrane receptors and penetrate through the outer membrane protein. Cell death leads to the formation of erosions and ulcers surrounded by perifocal inflammation.

Pathogenic factors:

1) proteins of the outer membrane (provide the ability for invasion and intracellular reproduction);

2) contact hemolysin (promotes lysis of cell vacuole membranes);

3) exotoxin (has enterotropic, cyto- and neurotoxic effects);

4) endotoxin (has a general toxic effect on the body and protects the Shigella that have entered the body from the action of the protective forces of the macroorganism).

There are three clinical forms of dysentery, which differ in pathogens, epidemiology and partly in the clinic:

1) Grigoriev-Shiga dysentery. The causative agent is Sh. disenteriae, serovar - shigella Grigorieva-Shiga. Ways of transmission - alimentary, contact-household. Features of the clinic: it is difficult, bloody diarrhea with blood is characteristic, symptoms of CNS damage, there may be bacteremia;

2) Flexner's dysentery. Pathogens - Sh. flexneri and Sh. boydii. Water transmission route. Features of the clinic: proceeds as a typical dysentery of varying severity;

3) Sonnei dysentery. food transmission route. Features of the clinic: there may be symptoms of food poisoning, vomiting.

Diagnostics:

1) bacteriological examination;

2) immunoindication (ELISA);

3) serodiagnosis (has a retrospective value).

Specific prophylaxis: dysenteric bacteriophage (used in foci of infection).

Etiotropic therapy: in the moderate and severe degree of the disease, antibiotics are prescribed (those that are excreted by the intestines), taking into account the sensitivity of the pathogen.

Shigellosis is an acute infectious inflammation of the large intestine, characterized by high contagiousness. Bacterial dysentery is manifested by cramping abdominal pain, vomiting, bloody diarrhea, tenesmus, signs of intoxication. This anthroponosis is more common than other intestinal diseases.

Shigellosis is found everywhere. People of any age and nationality are sensitive to it. The incidence rate is highest in overpopulated countries with a lack of hygienic culture among people. The significance of individual shigellosis in human pathology is constantly changing. At the beginning of the 20th century, during the famine and complete unsanitary conditions, Grigoriev-Shiga shigellosis was widespread. In the 50s, most of the dysentery was caused by Shigella Flexner. At the end of the last century, Shigella Sonne caused pathology in humans.

Persons with II (-) blood group are especially susceptible to shigellosis. They have the most severe symptoms of infection. Urban residents get sick several times more often than rural residents, which is associated with crowding in large cities. Pathogenic shigella affects people with low social status, who consume low-quality foods and insufficiently purified drinking water. The peak incidence occurs in summer and autumn.

Diagnosis of pathology is based on the clinical picture and is confirmed by culture. Treatment consists of rehydration, detoxification and antimicrobial therapy.

Etiological factors

The causative agents of shigellosis belong to the genus Shigella. First A. V. Grigoriev and K. Shig independently discovered the causative agent of dysentery. Other shigella were described some time later by S. Flexner, K. Sonne, J. Boyd, A. Sachs. These scientists at different times studied the microbiology of shigellosis - its pathogen, pathogenesis, morphological processes, clinical symptoms, diagnosis and treatment.

Shigella are non-motile, non-sporing, facultative anaerobic bacterial rods that stain negatively according to Gram and grow well on ordinary nutrient media. In the broth they form uniform turbidity with sediment, and on plate media - round, convex and colorless colonies.

Shigella are viable only in the human body. In the environment, microbes die within one to two weeks. On the paws of flies, bacteria can live up to three days, so flies are considered carriers of shigellosis. The access of these insects to sewage and food may play a role in the spread of dysentery. Sitting on food, insects infect them.

Microbes are sensitive to boiling, direct sunlight and disinfectants - chloramine, active chlorine. Shigella are resistant to physical, chemical and biological environmental factors. They remain viable in dried feces, soil, water, and food. Bacteria are resistant to some antibacterial agents, so not all drugs are suitable for eliminating the disease.

Pathogenicity factors that allow microbes to invade epitheliocytes, multiply and damage them:

• Adhesion and colonization factors - pili, general fimbriae, outer membrane proteins, cell wall lipopolysaccharides,
• Sex pili involved in conjugation,
• Enzymes that destroy mucus and ensure the rapid penetration of bacteria into body tissues,
• Invasion factors - plasmids and chromosomal genes,
• Endotoxin, which has an enterotropic and neurotropic effect, causing intestinal dysfunction,
• Cytotoxin, which destroys intestinal cells,
• Enterotoxin, which stimulates the release of water into the intestinal lumen and thins the stool,
• Neurotoxin, which causes symptoms of intoxication,
• O antigen and K antigen.

Shigella not only have a toxic effect on intestinal cells, but also disrupt the growth of normal microflora. All patients develop dysbacteriosis and disorder of the process of normal digestion.

Epidemiology

A sick person, a convalescent person or a bacteriocarrier are sources of infection. No animal in nature suffers from dysentery. Patients with mild and erased forms of shigellosis, with mild symptoms, are dangerous in epidemiological terms. Infected workers in the food industry and catering also pose a serious danger to others.

Shigellosis is spread by water, alimentary or contact routes.

1. Alimentary way. Microbes get on food products from dirty hands, flies' paws, when fertilizers containing feces with bacteria are used in the garden. Fruits, berries, milk, compotes, side dishes, salads and first courses are a good nutrient substrate for Shigella.
2. Waterway. With the faeces of a sick person, bacteria can enter drinking water through drains. In epidemic terms, wells, small reservoirs, public pools are dangerous. The cause of contamination of tap water can be the washing of infected linen or an accident at a treatment plant. The water way of spreading the infection is relevant in the warm season.
3. shigellosis- disease of dirty hands. In the spread of infection, the contact-household mechanism is of great importance. Feces from the hands fall on household items, and then on the mucous membrane of the mouth. This is especially true for people who do not follow the rules of personal hygiene, as well as for homosexuals.

Susceptibility to shigellosis is high. Almost 100% of people exposed to bacteria develop dysentery. Children are more susceptible to infection than adults. Dysentery Sonne comes to light more often in children's groups - schools and kindergartens.

Pathogenesis

Shigella dysentery penetrates with food or water through the mouth into the human gastrointestinal tract, overcoming the barrier factors of the oral cavity and the acidic contents of the stomach. In this case, some of the Shigella dies, and endotoxin is released. The infectious dose of pathogens is of great importance: the higher it is, the more pronounced the clinical signs of the disease.

In the small intestine, microbes settle on enterocytes, invade them, multiply and secrete enterotoxin and cytotoxin. They disrupt metabolism, cause polyhypovitaminosis. Cytotoxins contribute to the destruction of cells, and enterotoxins cause diarrhea.

When there are a lot of bacteria, they populate the entire large intestine. With the help of special proteins, bacteria are fixed on epitheliocytes and colonocytes, act on receptors and penetrate into cells. Then the microbes secrete mucin and other pathogenicity factors that cause adhesion and invasion of pathogens into the cells of the submucosal layer.

Inflammation quickly spreads to healthy areas of the intestine. Its walls become loose and edematous, destruction of the mucous membrane occurs. The process of absorption of nutrients and fluid is disturbed, it enters the intestinal lumen, diarrhea develops. Gradually, ulcerative colitis develops with bleeding erosions and ulcers that coalesce and enlarge the exposed surface of the intestinal wall. Against the background of ulcerative or fibrinous-necrotic inflammation of the intestine, an active release of toxins occurs.

Symptoms

Incubation for shigellosis lasts an average of a week, and more often 2-3 days. The disease begins acutely. In patients, the temperature rises sharply to febrile values, fever and chills occur. Intoxication is the body's response to the appearance of shigellosis toxins in the blood. Then there is lethargy, weakness, pain in the muscles and joints, aches all over the body, cephalgia, apathy.

Diarrhea is the main symptom of the disease, appearing on the second day of illness. At first, the stool simply liquefies, and then becomes lean to a “rectal spit”, mucus and blood appear in it. The frequency of stool per day is 10-30 times. In this case, painful painful sensations arise due to irritation and tension of the intestinal wall and peritoneum. Abdominal pain has a different localization and severity: from diffuse, moderate to sharp and cramping. Before a bowel movement, it increases, and immediately after a bowel movement, relief occurs.

Among other dyspeptic symptoms, the most common are nausea, vomiting, tenesmus. In patients, the heartbeat becomes more frequent, shortness of breath, blood pressure decreases, heart sounds are muffled, noises appear at its top. In infants with dysentery, the limbs become cold, they constantly burp, sleep becomes restless and bad. Specialists during the examination find in patients a dry and furred tongue, palpation - soreness and spasm of the colon.

Damage to the nervous system is manifested by insomnia and general anxiety, soreness along the nerve fibers, hand tremors and skin hypersensitivity. When the central nervous system is affected, delusions and hallucinosis occur.

Clinical forms of shigellosis infection:

• Light- stool up to 5 times a day, without impurities with intermittent and mild pain in the abdomen.
• Moderate- fever, abdominal pain like contractions, loose bloody stools with lumps of mucus.
• heavy- shaking chills, excruciating pain in the abdomen, watery stools up to 50 times a day, dyspepsia, tachycardia, hypotension.
• Atypical form- dyspepsia, intoxication, watery stools.
• Hypertoxic form- neurotoxicosis, damage to the heart, blood vessels, nervous structures, shock, renal failure, cyanosis of the skin, sticky sweat, convulsive syndrome, confusion.
• Erased form- double stool, short-term pain in the abdomen.

Clinical signs of the disease subside by day 14, and complete recovery and restoration of the intestinal mucosa occurs within 4 weeks.

1. Shigella Sonne causes light and erased forms of dysentery without destruction of the intestinal mucosa.
2. Shigella Flexnera causes typical inflammation, occurring in moderate or severe form.
3. Dysentery Grigoriev-Shigi always characterized by a severe course with dehydration, intoxication, sepsis, a drop in blood pressure and a deterioration in the blood supply to vital organs.

There is a chronic form of dysentery, the duration of which reaches three or more months. Its pathogenetic and pathomorphological processes are not well understood. It is believed that the pathology is based on autoimmune reactions, the development of which is facilitated by existing diseases of the gastrointestinal tract, immune status disorders, intestinal dysbiosis and other loci of the body, malnutrition, alcohol abuse, prolonged and uncontrolled use of antibacterial agents.

Complications

The severe course of dysentery in the absence of timely treatment leads to the development of severe complications, which include:

• state of shock
• severe dysbiosis,
• perforation of the intestinal wall,
• Purulent inflammation of the peritoneum,
• Paresis and invagination of the intestine,
• anal fissure,
• prolapsed hemorrhoids,
• Postdiarrheal inflammation of the intestine,
• Inflammation of the pancreas
• myocarditis,
• Toxic inflammation of the liver
• gangrenous enterocolitis,
• Bronchopneumonia,
• hypovitaminosis,
• malabsorption syndrome,
• kidney failure,
• Cardiovascular insufficiency,
• convulsions,
• Violation of consciousness.

Diagnostic measures

Diagnosis of shigellosis begins with a conversation with a doctor. He collects an anamnesis and listens to the complaints of the patient. Palpation of the abdomen reveals soreness, tension in the abdomen, and intestinal spasm.

Laboratory diagnostics:

1. The main diagnostic method is microbiological. Examine native feces, rectal swab, vomit or washings of the stomach or intestines. The biomaterial is seeded on selective media - Endo and Ploskirev, as well as on accumulation media - selenite broth or magnesium medium. Crops are incubated at 37 degrees during the day. On the second day, the formed colonies are studied: flat or convex, round, small, transparent, with a smooth or jagged edge. Lactose-negative colonies are removed on Kligler's polycarbohydrate medium. The next day, the results are recorded. Then a pure culture is isolated for further study of biochemical and antigenic properties. For this, a Hiss color series and an agglutination reaction with shigellosis sera are put.
2. After isolation of the infectious agent, its sensitivity to antimicrobial agents and dysenteric bacteriophage is determined.
3. Serodiagnosis allows you to quickly confirm or refute the alleged diagnosis. For this, they put RPGA, ELISA, RIF, RNGA, RSK.
4. An auxiliary diagnostic method is an allergic test with dysentery.
5. To determine the Shigella DNA in the biomaterial, PCR is performed.
6. Microbiological examination of feces for dysbacteriosis reveals significant changes in the normal intestinal microflora: a decrease in lacto- and bifidobacteria, the presence of pathogenic shigella, an increase in the number of opportunistic microbes.

Instrumental diagnostics consists in conducting sigmoidoscopy, which allows you to make a diagnosis in doubtful situations. With shigellosis, the intestinal mucosa is red, edematous, loose, with small shallow ulcers, mucus lumps and foci of atrophy. This is a non-specific diagnostic method, since similar signs can appear with other intestinal infections.

General therapeutic measures

Treatment of pathology is carried out on an outpatient basis, if the patient's condition remains satisfactory. Hospitalization is indicated for patients with moderate and severe disease, the presence of concomitant pathologies, persons from decreed groups and young children.

Patients need the most benign diet that does not irritate the mucous membrane of the digestive tract. Eat a decoction of rice, grated soups, jelly, vegetable and low-fat chicken broths, stale bread or crackers. Eat food should be fractional: in small portions, 5-6 times a day. Three days after the normalization of the stool, you can return to normal nutrition.

Medical treatment for shigellosis:

The chronic form of dysentery during the period of exacerbation is treated in the same way as the acute one. After elimination of exacerbation symptoms, microclysters with infusions of eucalyptus, chamomile, rosehip and sea buckthorn oils, physiotherapy, eubiotics and vitamins have a good therapeutic effect. In severe cases, plasmapheresis is indicated - a method of cleansing blood plasma from toxins.

Patients remain disabled with a mild form of infection for 7-10 days, with moderate - up to 20 days, and with severe - more than a month. Patients from the decreed groups are allowed to work after receiving two negative results of stool cultures.

Prevention

Shigellosis is a highly contagious infectious disease, for the prevention of which the following rules must be observed:

1. Destroy flies and other insects in the food area,
2. Drink good quality water or boil it,
3. Do not eat spoiled fruits and expired products,
4. Wash your hands every time before eating
5. Clean up the territories of populated areas and protect water bodies from pollution by sewage,
6. To undergo hygiene training for all persons employed in food enterprises, catering facilities and food trade,
7. Alert the public about outbreaks of infection,
8. To accept children in the team after a survey on the intestinal flora,
9. Isolate and monitor patients and carriers of bacillary dysentery.

Currently, specific prophylaxis of shigellosis in children and adults is carried out by introducing an antidysenteric vaccine.

Shigellosis is a fairly common disease, which can be prevented by observing simple sanitary-hygienic and anti-epidemic rules. In the early stages, dysentery responds well to treatment. With timely seeking medical help, the prognosis for complete recovery is favorable. Timely complex treatment of acute forms of shigellosis infection prevents chronicity of the process.

Video: dysentery in the program “Live healthy!”

Bacteria of the genus Shigella are the causative agents of bacillary dysentery, or shigellosis. Dysentery is a polyetiological disease. It is caused by various types of bacteria named Shigella in honor of A. Shiga. They are currently assigned to the genus Schigella, which is subdivided into four species. Three of them - S. dysenteriae, S. flexneri and S. boydii - are divided into serovars, and S. flexneri is further divided into subserovars.

Morphology and physiology. In their morphological properties, Shigella differ little from Escherichia and Salmonella. However, they lack flagella and are therefore non-motile bacteria. Many strains of Shigella have pili. Different species of Shigella are identical in their morphological properties. The causative agents of dysentery are chemoorganotrophs, undemanding to nutrient media. On dense media, when isolated from the patient's body, as a rule, S-forms of colonies are formed. Shigella species Schigella sonnei form two types of colonies - S-(I phase) and R-forms (II phase). Phase I bacteria form both types of colonies during subculturing. Shigella are less enzymatically active than other enterobacteria: when fermenting glucose and other carbohydrates, they form acidic products without gas formation. Shigella do not break down lactose and sucrose, with the exception of S. sonnei, which slowly (on the second day) break down these sugars. It is impossible to distinguish the first three species by biochemical characteristics.

Antigens. Shigella, like Escherichia and Salmonella, have a complex antigenic structure. Their cell walls contain O-, and in some species (Shigella Flexner) and K-antigens. In chemical structure, they are similar to Escherichia antigens. The differences are mainly in the structure of the terminal links of LPS, which determine the immunochemical specificity, which makes it possible to differentiate them from other enterobacteria and among themselves. In addition, Shigella have antigenic cross-links with many serogroups of enteropathogenic Escherichia, which cause mainly dysentery-like diseases, and with other enterobacteria.

Pathogenicity and pathogenesis. The virulence of Shigella is determined by their adhesive properties. They adhere to colonic enterocytes due to their microcapsule. Then they penetrate enterocytes with the help of mucinase, an enzyme that destroys mucin. After colonization of enterocytes, Shigella enter the submucosal layer, where they are phagocytosed by macrophages. In this case, the death of macrophages occurs and a large number of cytokines are released, which, together with leukocytes, cause an inflammatory process in the submucosal layer. As a result, intercellular contacts are disturbed and a large number of Shigella penetrate into the enterocytes activated by them, where they multiply and spread to neighboring cells without entering the external environment. This leads to the destruction of the epithelium of the mucous membrane and the development of ulcerative colitis. Shigella produce enterotoxin, the mechanism of action of which is similar to the heat-labile enterotoxin of Escherichia. Shigella Shiga produce a cytotoxin that affects enterocytes, neurons, and myocardial cells. This indicates the presence of three types of activity in it - enterotoxic, neurotoxic and cytotoxic. At the same time, the destruction of shigella releases endotoxin - LPS of the cell wall, which enters the bloodstream and has an effect on the nervous and vascular systems. All information about the pathogenicity factors of Shigella is encoded in a giant plasmid, and the synthesis of Shiga toxin is encoded in a chromosomal gene. Thus, the pathogenesis of dysentery is determined by the adhesive properties of pathogens, their penetration into the enterocytes of the colon, intracellular reproduction and production of toxins.

Immunity. With dysentery, local and general immunity develops. With local immunity, secretory IgA (SIgA) are essential, which are formed in the 1st week of the disease in the lymphoid cells of the intestinal mucosa. By coating the intestinal mucosa, these antibodies prevent Shigella from attaching and penetrating into epithelial cells. In addition, during the infection, the titer of serum antibodies IgM, IgA, IgG increases, which reaches a maximum at the 2nd week of the disease. The greatest amount of IgM is found in the 1st week of illness. The presence of specific serum antibodies is not an indicator of the intensity of local immunity.

Ecology and epidemiology. The habitat of Shigella is the human large intestine, in the enterocytes of which they multiply. The source of infection are patients, people and bacteria carriers. Infection occurs by ingestion of contaminated food or water. Thus, the main route of infection transmission is alimentary. However, cases of contact-household transmission are described. The resistance of different types of Shigella to environmental factors is not the same - the most sensitive are S. dysenteriae, the least sensitive are S. sonnei, especially in the R-form. They remain in feces for no more than 6-10 hours.

Laboratory diagnostics. A pure culture of the pathogen is isolated by sowing the patient's feces on a differential diagnostic nutrient medium (Ploskirev's, Levin's, etc.) medium, followed by its identification on variegated media and by antigenic properties in the agglutination reaction to determine the species and serovar. The percentage of positive results is quite low, especially in chronic dysentery.

Specific prevention and treatment. Obtaining various vaccines (heated, formalized, chemical) did not solve the problem of specific prevention of dysentery, since all of them had low efficiency. For treatment, fluoroquinolones are used and, less commonly, antibiotics.

The first causative agent of dysentery was discovered by A. V. Grigoriev (1891), and in 1898 the Japanese scientist Shiga studied and described it. In subsequent years, other representatives of this genus were isolated and described: Flexner (1900), Sonne (1915), Stutzer-Schmitz (1917), Large-Sachs (1934).

According to the International Classification, all bacteria that cause dysentery are combined in honor of Shiga into one genus - Shigella.

Morphology. Shigella are small (2-3 × 0.4-0.6 µm) rods with rounded ends. They differ from other members of the Enterobacteriaceae family in the absence of flagella. They do not have spores or capsules. Gram-negative.

cultivation. Shigella are facultative anaerobes. Unpretentious to nutrient media. They multiply on MPA and MPB at a temperature of 37 ° C and pH 7.2-7.4. Elective and differential diagnostic environments for them are Ploskirev, Endo, EMS environments. Grow in the form of small, translucent, grayish, round colonies, 15-2 mm in size in an S-shape. An exception is Sonne's Shigella, which often dissociate, forming large, flat, cloudy, R-shaped colonies with jagged edges (Fig. 44). In liquid nutrient media, Shigella give a uniform turbidity, R-forms form a precipitate.

Enzymatic properties. The enzymatic properties of Shigella are less pronounced than those of other representatives of Enterobacteriaceae: they break down carbohydrates without gas formation, do not break down lactose and sucrose. The exception is Sonne shigella, which break down these carbohydrates on the 2nd-3rd day.

The proteolytic properties of Shigella are not very pronounced - the formation of indole and hydrogen sulfide is inconsistent, they coagulate milk, and do not thin gelatin.

In relation to mannitol, all shigella are divided into splitting and non-cleaving mannitol (Table 37).

Note. to - splitting with the formation of acid.

Sonne shigella are currently divided into four enzymatic types. They differ in their ability to break down rhamnose and xylose (Table 38).

Note. + splitting; (+) splitting after 3-5 days; - does not change.

toxin formation. Shigella have endotoxin. An exception is Shigella Shigi, which, in addition to endotoxin, secrete exotoxin, which has a neurotoxic effect.

Antigenic structure and classification. Shigella contain somatic antigens, which include group and type antigens. According to the International Classification, Shigella is divided into four groups, denoted by Latin capital letters A, B, C, D.

Group A S. dysenteriae: 1 - Grigorieva - Shigi; 2 - Stutzer - Schmitz; 3-7 - Large - Saks and 8-10 - provisional. Representatives of this group have only typical antigens, denoted by Arabic numerals.

Group B S. flexneri. Microbes of this group have a more complex antigenic structure - they contain typical antigens, denoted by Roman numerals, and group antigens, denoted by Arabic numerals. Shigella Flexner has 6 serotypes. Shigella Flexner 6 was formerly designated as a subspecies of S. newcastle.

Group C S. boydii. Has only typical antigens. There are 15 serological types in this group.

Group D S. sonnei has its own species antigen (Table 39).

In a microbiological study, the answers indicate the serovariant and subserovariant of the isolated culture. For example, a culture of Shigella Flexner 1a was isolated.

Environmental resistance. A temperature of 100°C kills Shigella instantly. A temperature of 60 ° C kills them in 20-30 minutes. Shigella are resistant to low temperatures - they remain in river water for up to 3 months, on vegetables and fruits - up to 10-15 months. Sunlight kills them in 2-3 hours, and Shigella Shigi - in 20 minutes. Commonly used concentrations of disinfectant solutions destroy them in 20-30 minutes. Group A shigella are the least resistant to external factors, and Sonne shigella are the most resistant.

Animal susceptibility. Animals are not sensitive to pathogens of dysentery, with the exception of monkeys. Experimental infection of rabbits and white mice causes intoxication and death in them.

Sources of infection. A person suffering from acute and chronic forms of dysentery, and a bacteriocarrier.

Transmission routes. Food. Of great importance is the waterway, vegetables, fruits, various items contaminated with shigella, and flies.

Pathogenesis. Once in the intestine with food, Shigella penetrate into the epithelial cells of the mucous membrane of the large intestine, where they multiply. Some of them die. The endotoxin formed during the destruction of bacteria sensitizes the mucous membrane, the permeability of blood vessels increases, and the endotoxin is absorbed into the blood, causing intoxication. The defeat of the mucous membrane is accompanied by swelling, necrosis, hemorrhage. In addition, the toxin affects the central nervous system, which leads to trophic disorders. Especially severe is the disease caused by Shigella Shigi, which penetrate deep into the mucous membrane of the colon, causing severe hyperemia, swelling and bloody diarrhea. The exotoxin formed by them causes severe intoxication.

The magnitude of the infectious dose is important for the occurrence of the disease.

Immunity. A person has a natural resistance to dysentery infection. After the disease, immunity is unstable, and after Sonne's dysentery is practically absent. With a disease caused by Shigella dysentery 1 (Grigorieva - Shigi), a more stable antitoxic immunity is developed.

Prevention. General sanitary and anti-epidemic measures: isolation, early diagnosis, disinfection.

Specific prophylaxis has not found wide application. Persons who have been in contact with patients are given a polyvalent dysenteric bacteriophage.

Treatment. Complex, sulfonamides with antibiotics. There is no specific treatment.

test questions

1. Name the representatives of the genus Shigella - the causative agents of dysentery.

2. Relation to what carbohydrate is the basis for dividing Shigella into two groups? What types of Shigella are included in each of these groups?

3. What are the routes of entry of Shigella and what part of the intestine do they affect?

4. What type of Shigella often grows in an R-shape?

5. Which Shigella have type and group antigens?

Microbiological research

The purpose of the study: detection and identification of Shigella for diagnosis; detection of bacteria carriers; detection of shigella in foods.

Research material

1. Bowel movements.

2. Sectional material.

3. Food products.

Basic research methods

1. Microbiological.

2. Serological.

Research progress

Second day of research

The seeded cups are removed from the thermostat, viewed with the naked eye or through a magnifying glass. Suspicious colonies (colorless) in the amount of 4-6 are screened on Russell's medium and mannitol. Sowing is done by strokes on a sloping surface and an injection into an agar column. The inoculated Russell medium is placed in a thermostat for 18-24 hours (in parallel, reseeding from the selenite medium to differential media is done).

Third day of research

Take out the cultures made on Russell's medium from the thermostat. Cultures that have not broken down lactose are subjected to further study: smears are made, stained according to Gram and microscopically. In the presence of gram-negative rods, inoculation is carried out on Hiss media, broth with indicator papers (to detect indole and hydrogen sulfide) and litmus milk. The inoculated media are placed in a thermostat for 18-24 hours.

Fourth day of research

Take out the crops from the thermostat and take into account the result. Cultures suspicious for their enzymatic and cultural properties against Shigella (see Table. 37) are subjected to serological identification. In the absence of such cultures give a negative answer.

Serological identification

The species, serovar, subserovar of the isolated culture is determined using adsorbed sera. Analysis of the antigenic structure begins with an agglutination test on glass with mixture No. 1. This mixture includes sera with antibodies to Sonne, Newcastle shigella and polyvalent serum to Flexner's shigella. With a positive agglutination reaction with the mixture, the isolated culture is agglutinated separately with each serum included in the mixture.

A positive agglutination test with adsorbed serum against Shigella Sonne and Newcastle gives the right to answer. To establish the serovar and subserovar of Shigella Flexner, it is necessary to additionally perform agglutination reactions with typical (I, II, III, IV, V) and group (1-3, 4-6-7, 8) sera. For example, the isolated culture gave a positive reaction with type II serum and group serum 3, 4. As can be seen from the table, the Flexner Shigella culture, serovar 2, podserovar 1a, was isolated. Answer: Shigella Flexner 2a are isolated.

In the absence of agglutination with mixture No. 1, an agglutination reaction is performed with other polyvalent sera.

When setting up an agglutination reaction, one should take into account the ratio of the culture under study to mannitol and, depending on this, use one or another serum. So cultures that do not break down mannitol are tested with polyvalent sera to Shigella dysentery Grigoriev-Shiga and Stutzer-Schmitz (1, 2), Large-Sachs (3-7), provisional types (8-10).

Mannitol degrading cultures are tested with Mix No. 1 and Boyd's Shigella polyvalent sera.

In the presence of agglutination of the isolated culture of one of these sera, a culture test is carried out with each of the sera included in the polyvalent one. A positive result with one of the sera determines the serovariant of the isolated culture.

When using serum for Boyd's shigella, agglutination is started with the serum of the serovar that is most common in the area. In our country, Boyd's shigella of serovariants 4, 5, 7, 9 and 12 are more often isolated (see Fig. 44).

As accelerated methods of microbiological research in dysentery, fluorescent microscopy and a biological test on guinea pigs are used. With the introduction of virulent strains of Shigella into the conjunctival sac (under the lower eyelid), by the end of the 1st day, the animals develop conjunctivitis.

test questions

1. What material is used for bacteriological examination in the diagnosis of dysentery and how is it collected?

2. The breakdown of what carbohydrate gives the right to give a negative answer?

3. What sera can be used to determine the type, subspecies, serovar and subserovar of Shigella Flexner?

4. What serums are included in Blend #1?

Study the dysentery study chart by day.

Nutrient media

Environments Ploskirev, Endo, EMS(see chapter 19).