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    Bacterial dysentery( acute shigellosis) is a potentially dangerous and extremely easily transmitted infectious disease of the colon with the enteral mechanism of infection caused by bacteria of the genus Shigella and occurring with intoxication phenomena. Symptoms appear after an incubation period lasting from one to four days, and usually subside after 10 days. In serious cases, the disease can last up to six weeks, but in most cases the disease has a mild form. Dysentery is most common in children aged one to four years. It is common in overpopulated areas with poor sanitation and often occurs in the form of epidemics;To stop the spread of the disease, sick people are isolated and quarantine is introduced in the epidemic. How to use folk remedies for this disease look here.

    Etiology. The causative agent of shigellosis( dysentery) is a group of microorganisms of the genus Shigella. Shigella - immobile, small sticks of 2-3 μm x 0.5-0.7 μm, do not stain Gram, spores do not form, facultative aerobes. Resistant to the effects of physical and chemical factors, can withstand temperatures of 80-85 ° C for 10-15 minutes and low temperatures - up to -35. ..- 40 ° C and even -150. ..- 160 ° C, UV rays. According to the international classification, the genus Shigella includes 4 species( S. dysenteriae, S. flexnery, S. sonnei) and 4 subgroups( A, B, C, D).

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    The classification is based on biochemical signs and antigenic structure( serovar).

    Subgroup A includes the species S. dysenteriae, which includes the 1st to 10th serovars: the first is Grigoriev-Shiga, the 2nd serovar is Stutzer-Schmitz, the 3rd-7th serovars are Larja-Saks;8-10th serovars are provisional. The Newcastle subspecies is S. flexnery, the 6th serovar, which is closer to S. boydii in a number of characters.

    Subgroup B includes the species S. flexnery, which includes 6 serovars, 4 of which are subdivided into sub-serovars.

    Subgroup C is represented by a kind of boydii, including 15 serovars.

    Shigella of subgroup D are united in a single serovar - S. sonnei species.

    Biological properties of shigella. Shigella are characterized by the following biological properties: high degree of virulence( the most virulent of the enterobacteria family), have multiple drug resistance, most often to tetracycline antibiotics, to aminoglycosides and levomycetin and are resistant to high and low temperatures, able to maintain viability and virulence at 30-40 ° С.

    One of the features of their biological properties is the ability to produce exotoxins: thermolabile and thermostable enterotoxins, cytotoxin. Intensity of production of enterotoxins in S. dysenteriae is 1000 times higher than in other species.

    The endotoxin, which is an O-antigen, is released during autolysis of bacteria, leading to antigenemia. Known pathogenicity factors that have the ability to penetrate Hela cells, and invasiveness. The genetic mechanism of invasiveness control associated with the transfer of the plasmid MM 120 MD is identified, with the elimination of which the invasiveness and virulence property is lost.

    Shigella is classified as highly adhesive, highly toxic, highly virulent enterobacteria.

    • Dysentery bacillus - a bacterium that penetrates into the tissues lining the large intestine, can cause dysentery.

    • Other causative agents of dysentery are the amoeba parasite and the bacteria E. coli, Yersinia and others.

    • A dysentery bacillus usually spreads through contact with feces of an infected person.

    • Neglecting careful washing of hands after emptying the intestines can contribute to infection with dysentery.

    • Flies can carry bacteria from feces( usually in areas with poor sanitation).

    • Use of contaminated food or water can lead to infection with dysentery. Epidemiology of shigellosis. Shigellosis is one of the most common diseases, and, according to WHO, is one of the leading places in the structure of diarrheal diseases.

    Specific weight of shigellosis in Russia among intestinal infections is on the average 30%, and the proportion of children in the total incidence of shigellosis is 60-70%.In recent years in the Russian Federation there has been a trend towards an increase in the incidence of shigellosis. Thus, the incidence of shigellosis Flexner increased by 47%, Shigelosis Sonne - by 24%.

    The source of shigellas is a sick person or bacteriostatic. The greatest epidemiological danger is presented by patients, including erased, atypical forms, which excrete in excrement with excrements 30 times more pathogens than bacteriocarditis or convalescence. As a rule, the bacterial release of shigella in 80% of patients discontinues in 2-3 weeks from the onset of the disease, in 20% of patients continues for several weeks and even months. Long-term bacterial release of shigella is facilitated by the patient's chronic diseases of the gastrointestinal tract, liver, intestinal dysbacteriosis, immunodeficiency states, eating disorders, and inefficient feeding, early transfer to artificial feeding, rickets in children of the first year of life. The inadequate therapy of acute shigellosis contributes to the persistent bacteriovirus of Shigella.

    Shigella spreads through a fecal-oral transmission mechanism that involves the transmission of an infectious agent to the aquatic, food and domestic routes, and also through flies. And for each type of shigell there are major and additional ways of transmission. The main transmission path, ensuring the preservation of a particular pathogen as a species, is for shigella Grigoriev-Shiga household,

    Flexner - water, Sonne - food. Transmission factors can be respectively infected water, milk, sour cream, cottage cheese. If the sanitary and hygienic standards are not respected, they can become infected and serve as transmission factors and other products.

    In young children, the shigell transmission route is predominantly contact-household, in older children it is more often food and water.

    Shigellosis is an infection characterized by high susceptibility of all age groups. However, the highest incidence is recorded in childhood( up to 60-70% of all patients).The incidence rate in different age groups of children is not the same. Most often, children from 2 to 7 years old( specific weight - up to 70%), who visit children's groups. The incidence of shigellosis among "organized" children is 3.5 times higher than the incidence rate among children who do not attend children's institutions. Children of the first year of life suffer from shigellosis much less often.

    Factors of nonspecific defense of the body against shigella. Of the nonspecific defense factors encountered in the shigella path, hydrochloric acid, bile and enzymes secreted by the mucosa of the gastrointestinal tract should be indicated first.

    The function of a mechanical barrier is performed by peristalsis, which facilitates the mechanical removal of shigella from the intestinal lumen, and intact intestinal epithelium.

    A certain barrier role is played by a normal intestinal microflora that competes with pathogenic pathogens for attachment to the mucous membrane, producing a number of substances that inhibit the growth of pathogenic bacteria and determine the activity of the intestinal epithelium.

    Local immunity factors( secretory immunoglobulins of class A, macrophages, properdin, lysozyme) are of great importance.

    Nonspecific resistance of the body depends on a number of factors: nutrition of patients, their age, the presence of concomitant acute and chronic diseases, the state of the environment.

    • First, watery diarrhea. She can go to diarrhea with mucus and blood.

    • Stress in the bowels, accompanied by pain in the rectum.

    • Abdominal pain;pain in the whole body.

    • Nausea and vomiting.

    • Fever.

    • Rapid dehydration and weight loss( small children and elderly people are particularly prone to dehydration).

    Conditions for the development of acute shigellosis. The development of acute shigellosis is determined both by the state of the organism and by the characteristic of the pathogen.

    Factors predisposing to the development of acute shigellosis are chronic diseases of the liver, gastrointestinal tract, intestinal dysbiosis, dysfermentosis, disorders in the local immunity system, hereditary enzymopathies.

    The development of the infectious process is also determined by the properties and number of pathogens, the density of their distribution on the surface of the intestine. A large number of shigellas contained in infected food, getting into the child's body, can cause the development of severe forms of the disease with a short incubation period and the development of neurotoxicosis, infectious-toxic shock. At the same time, in children of the first years of life with an immunodeficient state, the disease can arise as a result of infection even in small doses of shigella.

    The main pathogenetic mechanisms of acute shigellosis. The disease develops only when the pathogen enters the gastrointestinal tract through the mouth. Throughout the gastrointestinal tract, under the influence of nonspecific factors of the macroorganism's defense, shigella is killed with the release of endotoxin, which is absorbed into the blood. The phase of toxemia in shigellosis is characterized by the involvement of all organs and systems, primarily the nervous system, in the pathological process, and is of a nonspecific character. Primary infectious toxicosis develops.

    Colonization and adhesion of shigella occurs mainly in the large intestine, in the distal part of it. Inflammation is formed, peristalsis and intestinal motility are disrupted. All of the above leads to the development of the syndrome of invasive diarrhea.

    Primary toxic lesions of glands of both thick and small intestines are observed in infants and in case of massive invasion( food path of infection), leading to disruption of digestion and absorption of food ingredients, accumulation of osmotically active substances in the small intestine and development of entero-colic variantflow of shigellosis.

    Features of immunity after acute acute shigellosis. Immunity after the transferred shigellosis species-specific and antimicrobial. In the blood of a patient with shigellosis, agglutinins, precipitin, hemagglutinins and complement-binding antibodies accumulate. The titer of specific antibodies is low, rapidly decreases, and after 5-15 months.antibodies completely disappear. Specific humoral immunity has a monospecific character. Of great importance is local, mucosal immunity, which is cell-tissue. Immunity of intestinal epitheliocytes to the causative agent arises due to the increased production of secretory immunoglobulins of class A, activation of tissue macrophages, mast cells, histiocytes, lysozyme.

    Pathomorphological changes in shigellosis. Morphological changes in shigellosis in children are detected in all parts of the gastrointestinal tract, but mainly in the distal parts of the large intestine. The severity of morphological changes can be very different: from acute catarrhal inflammation to fibrinous-necrotic, fibrinous-ulcerative. Diphtheric colitis is less common.

    In children of the first year of life, catarrhal and follicular-ulcerative lesions of the large intestine predominate.

    The most significant changes in the large intestine, as a rule, develop in the shigella of Grigoriev-Shiga, less severe - with Flexner's shigellosis, the easiest - with shigellosis Sonne.

    Almost always along with colitis there is catarrhal, less often - catarrhal-hemorrhagic enteritis and catarrhal, less often - erosive gastritis.

    Histological examination of the sigmoid and rectum reveals damage to the musculoskeletal( Auerbach) and submucosal( Meisnerian) plexuses.

    Mucosal repair of the gastrointestinal tract occurs much later than clinical recovery( from 5 weeks to 2-3 months).

    Dystrophic changes are observed in many organs. In the lungs there are edema, perivascular hemorrhages with secondary leukocyte reaction, in the myocardium - swelling and lumpy decay of cardiomyocytes, in the liver - degenerative changes in hepatocytes, in the brain - perivascular edema, hemorrhages.

    Causes of death: infectious-toxic shock - in 60-70%, cerebral edema - in 15-20%, acute heart failure - in 10-15%, pneumonia - in 5-7% of deaths.

    I. By form:

    1. Typical.

    2. Atypical: erased, asymptomatic, hypertoxic, dyspeptic.

    3. Bacteriovenism.

    II.By the severity of the process:

    1. Light.

    2. Medium-heavy.

    3. Heavy:

    a) with a predominance of common changes;B) with prevalence of local changes;C) mixed form.

    III.In the course of the disease:

    a) acute( up to 1 month);B) subacute;

    c) protracted( up to 3 months);

    d) chronic( more than 3-4 months) - continuous, relapsing.

    IV.By the nature of complications: otitis media, intestinal dysbiosis, anemia, etc.

    V. Mixt infection.

    Clinic. The incubation period varies from 6-8 hours to 7 days, on average 2-3 days.

    When the child is infected by the food, the incubation period is short-lived, and the disease is characterized by a violent onset, expressed by a general infectious syndrome, possible development of neurotoxicosis, infectious-toxic shock.

    The contact-household way of infection leads to the manifestation of the infection in 4-7 days, which manifests itself in the form of a typical intestinal syndrome and mild symptoms of intoxication.

    The reference diagnostic criteria for acute shigellosis, occurring typically:

    • Acute onset of the disease.

    • Temperature rise to subfebrile and febrile digits lasting from 1 to 3 days.

    • Development of intoxication of different severity, possible formation of infectious toxicosis, neurotoxicosis.

    • Clinical signs of distal colitis.

    • Invasive diarrhea.

    Clinical manifestations of toxicosis in acute shigellosis. Specific shigellosis toxemia develops more often in older children, manifests as a primary neurotoxicosis with a characteristic clinical picture. The defeat of the toxins of the cardiovascular system can be accompanied by a drop in blood pressure and the development of a collapoid state. In addition, increased permeability and fragility of the vascular wall lead to the development of local hemorrhagic syndrome, and in patients with severe forms - DIC syndrome.

    Clinical features of distal colitis in patients with acute shigellosis. The manifestations of distal colitis in a patient with acute shigellosis are:

    • lean liquid stool with mucus, herbs, blood veins, fecal( "rectal spitting");

    • painful defecation - tenesmus;

    • spasmodic and soreness of the sigmoid colon during palpation of the abdomen;

    • compliance or gaping of the anus;

    • "false urges" for defecation.

    Distal colitis is recorded in patients with typical Shigellosis forms.

    Symptomatics of a mild form of acute shigellosis .The mild form of shigellosis occurs in 50-60% of patients and is characterized by the absence or mild symptoms of intoxication( subfebrile temperature, slight lethargy, decreased appetite, single vomiting).The frequency of the stool does not exceed 5 times a day; the bowel movements do not lose any staining character, liquid or mushy, with an admixture of a small amount of mucus;blood in the feces is usually absent and only in some patients in some portions is found in the form of thin veins in mucus. Palpable spasmodic or compacted sigmoid colon. Abdominal pain is absent or occurs only with defecation. Characteristic phenomena of sphincteritis and compliance of the anus.

    In the study of internal organs in most patients, abnormalities are not determined.

    Coprological examination allows detecting mucus, fresh leukocytes in the first days of the disease, from the 3rd day dramatically changed, very rare erythrocytes are rarely found.

    With rectomanoscopy, the catarrhal, catarrhal-follicular proctosigmoiditis is not clearly expressed.

    Medium-severe form of acute shigellosis .The moderate form in the general structure of shigellosis in children is about 40% and is characterized by the presence of mild symptoms of intoxication and developed colitis syndrome.

    The disease begins acutely, with an increase in body temperature to 38-39 ° C.Normalization of temperature is observed after 2-3 days. In the early days of the disease, vomiting is possible. The child refuses food, sleeps badly, complains of headache and abdominal pain, weakness.

    The chair is quickened up to 10 times a day, quickly loses its stained character, becomes lean, with a lot of turbid mucus, greens and blood streaks. Characteristic cramping pains in the abdomen, tenesmus, false desires. The abdomen in most children is slightly tense, painful on palpation, especially in the left ileal region. The sigmoid colon is spasmodic and painful on palpation. Deflection or compliance of the anus is determined.

    From the side of the cardiovascular system, some patients suffer from a slight muffling of heart sounds, sometimes a slight decrease in blood pressure.

    On the 3-4th day of the disease, a slight increase in the size of the liver is possible, its edge is rounded, palpation painless.

    The duration of the disease is an average of 3 weeks.

    When coprological examination of feces, mucus is detected and a large number of fresh unchanged leukocytes, individual red blood cells.

    Rektomanoskopii reveals pronounced catarrhal-hemorrhagic or follicular proctosigmoiditis, in some - erosive proctosigmoiditis.

    Clinic of severe shigellosis, proceeding with prevalence of local symptoms. This form of shigellosis begins acutely, with the temperature rising to 39 ° C and higher and rapidly passing symptoms of toxicosis. Since the first days of the disease, the symptoms of the defeat of the large intestine are prevalent. The chair is frequent, more than 10-15 times, lean, without stool - "rectal spitting"( mucus, greens, pus, blood).There are constant cramping pains in the abdomen, pronounced tenesmus. Possible paralysis of the sphincter of the anus, anus gaping, from it emerges turbid mucus, dyed with blood. The sigmoid colon is spasmodic, painful on palpation, sometimes symptoms of irritation of the peritoneum( "local peritonitis") can be determined in the left ileal region.

    Early changes appear on the part of the cardiovascular system: lowering blood pressure, muffled heart tones. The size of the liver increases, and sometimes the spleen.

    When a scatological examination reveals slime in the form of strands, filled with fresh leukocytes, red blood cells.

    Clinic of acute shigellosis, which proceeds with a predominance of symptoms of toxicosis. This form of shigellosis is more common in children older than a year, usually on the pathway of infection.

    The onset of the disease is acute. An increase in body temperature to 39-40 ° C is accompanied by chills. Often there is a neurotoxicosis characterized by impaired consciousness, seizures or convulsive readiness, positive meningeal symptoms, multiple vomiting. The possibility of an infectious-toxic shock with a sharp drop in blood pressure, hypothermia, pallor of the skin is not ruled out.

    The colitis syndrome is formed only after a few hours or even at the end of the day from the onset of the disease, its severity may be different.

    In the coprogram, leukocytes, erythrocytes, mucus are found in large numbers.

    Diagnostic criteria of transient bacteriocarrier Shigella. Shigellosis bacteriocarrier is very rare( 1-3%).

    The infectious process does not develop.

    Usually 1-2 days after infection of the child shigella stand out with feces, the chair remains decorated. There are no any coprological changes, there are no anti-Sigilella antibodies in the blood serum of the child. Rectoromanoscopy also does not show a pathological process in the large intestine.

    Diagnostic criteria of the subclinical form of shigellosis. Criteria for diagnosing the subclinical form of shigellosis are sowing from the excrements of the pathogen( more often Shigella Sonne) and the growth of anti-Sigilella antibodies in dynamics.

    Clinic of the erased form of acute shigellosis .The erased form of acute shigellosis is characterized by the absence of symptoms of general intoxication with mild and short-term bowel dysfunction. On examination, it is possible to detect a spasmodic, sometimes moderately painful sigmoid colon, a mushy stool, coated with a white tongue. Symptoms of lesions of the gastrointestinal tract are short-term( 1-2 days).

    With a rectomanoscopic examination, the catarrhal or catarrhal-follicular proctosigmoiditis is usually determined.

    Coprological examination reveals mucus in feces, a small amount of white blood cells.

    • the possibility of not only acute, but subacute, gradual onset of the disease, especially in children of the first months of life;

    • Distal colitis syndrome is mild, more frequent is the development of enterocolitis and enteritis;

    • the severity of the disease is due to violations of hemodynamics, water-electrolyte and protein exchanges;

    • admixtures of blood in feces are less common;

    • the course of the disease is longer, especially with Flexner shigellosis.

    For acute shigellosis in children older than one year, regardless of its clinical variant, in addition to the acute onset of the disease, there is a parallelism in the dynamics of the development of symptoms of intoxication and local syndrome, as well as rapid relief of general and local symptoms.

    Clinical features of acute shigellosis Sonne. When shigellosis Zon-not the duration of vomiting usually does not exceed one day, the temperature is one or two days, diarrhea is one week, the discharge of blood with feces is one to three days. The disease is more often characterized by the development of light and medium-heavy forms.

    Clinical features of acute shigellosis Flexner. In Shigellosis Flexner, the duration of all symptoms is longer and more pronounced local syndrome: more bowel movements, more marked signs of distal colitis and hemorrhagic syndrome, up to intestinal bleeding. The disease proceeds mainly in moderate and severe forms, the mild form is rarely recorded.

    Shigellosis Flexner is characterized by prolonged bacterial excretion, more than one or two weeks in 1/3 of patients( Talikova EV, 1998).

    Variants of Shigellosis. The course of shigellosis can be acute( up to 2 weeks), prolonged( up to 1 month), smooth and with complications. Chronic current is currently rare.

    The acute course of shigellosis with complete clinical recovery by the 7th-10th day is the most frequent outcome of the current course of the disease in children. Complete morphological and functional restoration of the intestine occurs only towards the end of the month from the onset of the disease( sometimes in 2-3 months), which must be taken into account when appointing a diet in the period of convalescence.

    Prolonged flow is observed in weakened children, patients with an unfavorable background( rickets, hypotrophy, IDS), in the presence of concomitant diseases, with irrational use of antibiotics and is due mainly to an inadequate response of local immunity, the impossibility of rapid elimination of the pathogen from the body.

    The development of chronic shigellosis is due to the presence of a large number of causes. First of all, it is burdened premorbid state, including functional inferiority of the gastrointestinal tract, intestinal dysbacteriosis, chronic diseases of the gastrointestinal tract and liver, as well as eating disorders, hypotrophy, rickets, exudative diathesis, artificial feeding. It is necessary to note concomitant acute diseases, inadequate therapy of shigellosis, disturbances in the patient's food regime during early convalescence, sensitization of the organism to a number of allergens. The immunodeficiency of the patient is of great importance in the process chronicization.

    Clinic of chronic shigellosis with recurrent course. Relapses of the disease appear after 2-3 weeks, sometimes - a month after the onset of clinical recovery and are characterized by the repetition of clinical signs of acute shigellosis and repeated sowing of the pathogen, pathological changes in the coprogram. The treatment cures the symptoms of the disease, but after a while they may appear again. More often relapses are connected with joining of ARVI, sore throat and other infections.

    With sigmoidoscopy, a catarrhal focal catarrhal, catarrhal-follicular or even catarrhal-erosive process is revealed.

    If a relapse occurs in the late period of the disease, differential diagnosis should be made with a new shigella infection.

    The new disease with acute shigellosis against the background of chronic differs from relapse with greater severity and severity of clinical manifestations. Bacteriological examination of the patient makes it possible to detect a shigella change or a change in the enzymatic type.

    Conical signs of chronic shigellosis with continuous flow. The disease is characterized by constant dysfunction of the colonic intestine, spasm of the sigmoid colon, supple of the anus. As a result of violation of parietal digestion, hypotrophy, hypovitaminosis, anemia develop. Immunodeficiency state, allergosis, intestinal dysbiosis are formed. Asthenic or asthenovegetative syndromes are expressed.

    Coprological examination detects mucus, leukocytes in feces. With sigmoidoscopy, an erosive or ulcerative process in the large intestine is detected.

    This form of chronic shigellosis is currently rare.

    Features of the flow of mixed shigellosis-viral and shigellosis-bacterial infections. Possible development of shigellosis-bacterial associations( combination of shigella with pathogenic and opportunistic bacteria), shigellosis-virus mixed infections with rota-, entero-, adeno-, herpesviruses;Shigella with protozoa, Candida. Probably combinations of three pathogens.

    The development of mixed infections significantly increases the severity of acute shigellosis, increases the incidence of toxicosis, neurotoxicosis. Symptoms of intoxication persist for a longer time. The hemolytic character of the stool is observed in the patient for two weeks or more. In children with mixed infections, specific and nonspecific complications develop more often, and a prolonged bacterial release is formed. In addition, the addition of superinfection promotes the formation of protracted, and then chronic forms of shigellosis.

    • Dysentery differs from usual infectious diarrhea by the presence of blood.

    • Physical examination and medical history are necessary.

    • Stool samples are taken for examination under a microscope and for sowing a bacterial culture to confirm the presence of a dysentery rod.

    • A blood test can be taken to find abnormalities in ion concentrations or anemia.

    A reliable diagnostic method is bacteriological, based on the isolation of the pathogen.

    The material for research is feces containing pathological impurities( blood, pus, mucus), which are taken from the middle portions originating from the upper part of the rectus and sigmoid colon. Collection of feces can be made before defecation with a dry sterile loop( smear).The time between the collection of material and sowing should not exceed two hours. In case the time exceeds 2 hours, the material is placed in the enrichment medium or in a preservative.

    Urine and blood cultures are usually not produced due to the rarity of detection in them of the pathogen.

    At autopsy, except the intestine, it is mandatory to study the mesenteric glands and parenchymal organs. First, a piece of liver, spleen, gland tissues is selected, and then the intestine is opened.

    Serological methods( RNGA), as a rule, are additional, as they make it possible to justify the diagnosis retrospectively, with erased forms - to determine the type of pathogen. In acute course, agglutinins can be detected on the 3rd-4th day with a subsequent increase in titers 3-4 times or more. In chronic course - the increase in the titres of agglutinins is noted by the 20-30th day.

    Postinfectious agglutinins are stored in credits 1: 100 - 1: 200 to 6 months. The diagnostic titer of agglutinins is taken: with the Flexner pathogen for adults - 1: 200, for children - 1: 100, for children under 3 years - 1: 50;with the pathogen Grigoriev-Shiga, Zon-not, Newcastle - for adults 1: 100, for children - 1:50 and for children under 3 years - 1:25.

    The most promising method of diagnosis is ELISA, which allows determining the class-specific immune response.

    • Solutions of electrolytes( such as sodium and potassium) may be required to prevent dehydration. In severe cases, they can be used intravenously. Before meeting with your doctor, pre-dehydrate using drinks for athletes or a solution of one teaspoon of salt and four teaspoons of sugar per liter of water. It is important to prepare the solution correctly, because too much salt can increase dehydration. Drink half a liter every hour, while diarrhea persists.

    • Do not take over-the-counter anti-diarrhea drugs unless directed by a doctor. With the help of diarrhea, the body gets rid of the pathogens of infection.

    • Although the infectious disease generally goes by itself to limit its spread, antibiotics are often given. Medicines must be taken for the entire prescribed period.

    • To prevent the spread of infection, wash your hands often with warm water and soap, especially after emptying the bowels or before eating.(Because the dysentery has an incubation period of up to four days, you can be a carrier of the disease without knowing it.)

    • When traveling abroad or in areas with poor sanitation, drink only bottled or boiled water or other bottled drinks, eatonly cooked foods, as well as fruits that you can clean yourself.

    • Isolation from other people is necessary to prevent the spread of the disease.

    • Consult your doctor as soon as you notice signs of dysentery. The disease is dangerous and extremely quickly spreading, so you need to see a doctor as soon as possible.