Rectal spitting is characteristic of. Dysentery symptoms

Distinguish between acute and chronic dysentery, as well as the bacteriocarrier of Shigella. Depending on the clinical manifestations of acute dysentery, colitis, gastroenterocolitic and gastroenteric variants are distinguished, and an erased course is also possible. Incubation period with dysentery, the average is 2-3 days with fluctuations from several hours to 7 days.

The colitis variant of the disease begins suddenly or after a short prodromal period (malaise, weakness, chilling, discomfort in the abdomen). A combination of intoxication phenomena is characteristic (fever, chills, weakness, headache, tachycardia, hypotension) and colitis . Patients complain of cramping abdominal pain, which usually precedes defecation and is localized mainly in the left iliac region, diarrhea begins at the same time. . The chair is frequent, while the volume of feces decreases rapidly, an admixture of mucus and blood appears in the stools. At the height of the disease, the bowel movements may lose their fecal character and consist of a meager amount of mucus streaked with blood (the so-called rectal spit). Defecation in severe cases of the disease is accompanied by painful urges (tenesmus), false urges to defecate are characteristic. Palpation of the abdomen reveals pain, mainly in the left iliac region, spasm and induration of the sigmoid colon. The peak period of the disease lasts from 1-2 to 8-10 days.

The gastroenterocolitic variant differs from the colitis variant in a more acute course and the predominance of signs of gastroenteritis (nausea, vomiting, watery stools) in the first 1–2 days of illness, and then the appearance of signs of colitis or enterocolitis. The gastroenteric variant is clinically similar to food poisoning: against the background of intoxication, nausea, vomiting, pain and rumbling in the abdomen, and watery stools are noted.

With an erased course of dysentery, clinical manifestations are mild or absent, therefore, patients are often detected only by bacteriological examination of feces or sigmoidoscopy, in which the majority show inflammatory changes in the distal colon.

Chronic dysentery is very rare. After 2-5 months. after suffering acute dysentery, periodic exacerbations of the disease occur with mild symptoms of intoxication. Gradually, symptoms of damage to other parts of the gastrointestinal tract appear - nausea, vomiting, pain in the epigastric region and right hypochondrium, bloating, etc. Sometimes there is a long continuous course of the disease.

The severity of the course of the disease is determined on the basis of the severity of the temperature reaction and signs of intoxication, the frequency of stools and the nature of bowel movements, the intensity of abdominal pain. With mild dysentery, the temperature is subfebrile or normal, symptoms of damage to the nervous and cardiovascular systems are absent or mild. Pain in the abdomen is minor, often diffuse. Bowel movements usually do not lose their fecal character, defecation occurs no more than 10 times a day, tenesmus and false urge to defecate may not be. With a moderate course, signs of intoxication are expressed, as a rule, there is an increase in temperature, cramping abdominal pain, bowel movements usually lose their fecal character, defecation occurs 10-25 times a day, tenesmus and false urge to defecate are observed. In severe cases, the phenomena of intoxication, colitis are pronounced, the frequency of defecation is several dozen times a day; toxic shock, severe dehydration may develop , toxic hepatitis or pancreatitis; secondary infection is possible. Very rare complications are peritonitis and intestinal obstruction.

Description

The causative agent of dysentery is the following types of bacteria from the genus Shigella: Shigella dysenteriae (the obsolete name is Shigella Grigorieva - Shigi), Sh. flexneri (Flexner's shigella), Sh. boydii (Boyd's shigella) and Sh. sonnei (Shigella Sonne). Sh. dysenteriae, which produce a strong exotoxin, the smallest is Shigella Sonne. In economically developed countries, among the causative agents of dysentery, Sonne shigella prevails, followed by Flexner shigella. An important feature of Shigella, especially the Sonne species, is the ability to stay and multiply in food products, primarily dairy products, for a long time.

Dysentery is a typical intestinal infection with a fecal-oral mechanism of pathogen transmission. The source of the infectious agent is patients who excrete it with feces. With dysentery caused by Sh. dysenteriae, the contact-household route of transmission of the infectious agent dominates, with Flexner's dysentery - water, with Sonne's dysentery - food. The incidence is recorded throughout the year with the highest level in the summer-autumn period.

Characterized by violations of all functions of the gastrointestinal tract, the development of intestinal dysbacteriosis from the first days of the disease and the long-term preservation of these changes in the period of convalescence (from several weeks to several months or more). The abuse of antibiotics in the acute period of the disease, the insufficient use of pathogenetic therapy, the violation of the diet in the period of convalescence, the presence of concomitant chronic diseases are the main reasons that contribute to the protracted course of the disease and the formation of chronic post-infectious pathology of the digestive system. Approximately 1/3 of convalescents develop postdysenteric enterocolitis in the coming months after the disappearance of the clinical manifestations of the disease.

Immunity is short-lived and type-specific. In this regard, there are frequent cases of re-infection when infected with a pathogen belonging to a different serotype.

Diagnostics

The diagnosis is made on the basis of the clinical picture, epidemiological history and laboratory results. In the blood of patients, an increase in the number of leukocytes and a shift of the leukocyte formula to the left may be noted. Most important method laboratory confirmation of the diagnosis is a bacteriological examination of the patient's feces. In order to increase the effectiveness of this method, it is necessary to follow the basic rules for taking feces (before the start of etiotropic therapy, preferably with lumps of mucus).

To confirm the diagnosis of chronic dysentery, it is necessary to isolate Shigella from the patient's feces of the same species (serotype) as in the acute period of the disease.

To detect specific antibodies in the blood serum of patients, an indirect hemagglutination reaction with dysenteric diagnosticums is used. A distinct increase in antibody titers in acute dysentery in dynamics can be detected from the 5th-8th day of illness, followed by their increase by the 15th-20th day. An indicative method of diagnosis can serve as an allergic intradermal test with dysentery. Sigmoidoscopy plays an important role in diagnosis. .

Treatment

Patients with dysentery are hospitalized according to clinical (severe and moderate course) and epidemiological indications (employees of food facilities, children's institutions and the water supply system, people living in hostels, etc.). In the acute period of the disease, it is necessary to follow a diet. Food should be mechanically and chemically gentle, milk and products that irritate the mucous membrane of the gastrointestinal tract (spices, alcoholic beverages, fatty, spicy foods, etc.) are excluded.

To prevent the contraction of the period of convalescence, it is very important to limit the use of antibacterial drugs, especially broad-spectrum antibiotics. They should be prescribed only for severe colitis or gastroenterocolitic variants at the height of the disease until severe diarrhea stops.

It is necessary to carry out pathogenetic therapy: detoxification (drinking plenty of water, in severe cases - intravenous administration water-electrolyte solutions, 5% glucose solution, hemodez, etc.), maintaining hemodynamics, prescribing anti-inflammatory and desensitizing agents.

Patients with a bacteriologically confirmed diagnosis of acute dysentery and patients with chronic dysentery are subject to dispensary observation in the office of infectious diseases of the polyclinic.

The prognosis for timely treatment in the vast majority of cases is favorable.

Prevention

Prevention is provided by general sanitary measures for the improvement of settlements, supplying the population with good-quality water and food, and hygienic education of the population. It is necessary to strengthen sanitary control over the implementation of the rules for collecting milk, its processing, transportation and sale, over preparation, storage and terms of sale. food products. Water from open water sources should be consumed only after boiling.

Anti-epidemic measures in the focus of infection include early active detection of patients, their isolation (at home or in a hospital), current and final disinfection . Persons who have contacted patients are sent for bacteriological examination of feces; put them under medical supervision for 7 days. Those who have had dysentery are discharged from the hospital no earlier than 3 days after clinical recovery, normalization of the stool and a single negative result of bacteriological examination of feces, carried out no earlier than 2 days after the end of etiotropic treatment. Persons hospitalized for epidemiological indications are discharged after a double bacteriological examination of feces with a negative result. They, as well as all convalescents with a bacteriologically confirmed diagnosis, are subject to dispensary observation for 3 months.

Medical Encyclopedia of the Russian Academy of Medical Sciences

prolonged bacteriocarrier and high lethality. Sonne shigellosis often proceeds as food poisoning with rapid positive dynamics, a smooth course, and low mortality.

The disease usually begins acutely with fever, malaise, sometimes vomiting, abdominal pain, frequent stools. In the first days of the disease, the stool has a fecal character, liquid, green or dark brown with an admixture of mucus or streaks of blood. In the following days, the stool loses its fecal character, takes the form of a "rectal spit" (scanty, mucous, sometimes with an admixture of blood in the form of dots or veins).

Characterized by a spastic condition of the large intestine (especially the sigmoid colon), tenesmus, compliance or gaping of the anus, prolapse of the rectal mucosa. Objectively, there is dryness and lining of the tongue, the stomach is retracted, painful on palpation along the colon,

the distal parts of the large intestine are spasmodic.

The mild form of shigellosis is characterized by the absence or mild symptoms of intoxication (subfebrile temperature, loss of appetite, slight lethargy). Stool up to 8 times a day, liquid or mushy with an admixture of a small amount of mucus. The compacted sigmoid colon is palpated.

In the moderate form of dysentery, the symptoms of intoxication are moderately expressed (increase in body temperature up to 39 ° C for 2-3

days, headache, loss of appetite, possible vomiting). Concerned about cramping pains in the abdomen, tenesmus. The chair becomes more frequent up to 15 times a day,

quickly loses its fecal character, contains a large amount of cloudy mucus, greenery, streaks of blood. The sigmoid colon is spasmodic.

Compliance or gaping of the anus is determined.

The severe form of the disease is characterized by the rapid development of toxicosis (body temperature 39.5 ° C and above, repeated vomiting, convulsions are possible). There is a violation of the function of vital organs and systems. Stool up to 40-60 times, scanty, without feces, like "rectal spitting". There are cramping pains in the abdomen, pronounced tenesmus.

The anus gapes, turbid mucus, stained with blood, flows from it. In the toxic form - hyper or hypothermia, convulsions, loss of consciousness,

decrease in cardiovascular activity, coma.

Children early age seldom suffer from dysentery. In the case of its development, the pathological process extends to the small intestine and more often manifests itself in the form of enterocolitis: the abdomen is swollen, the liver is often enlarged,

the stool is liquid with pathological impurities, the admixture of blood is less common, instead of tenesmus, their equivalents are observed (crying and reddening of the face during defecation, knotting of the legs, compliance of the anus). The course of the disease is longer. Much more often develops exsicosis, dysbacteriosis.

Complications of dysentery can be infectious-toxic shock, acute renal failure, hemolytic-uremic syndrome,

intestinal bleeding, peritonitis, intestinal perforation, intussusception, prolapse of the rectal mucosa, fissures and erosion of the anus,

intestinal dysbiosis.

In the case of mild and moderate dysentery in the blood, there may be moderate leukocytosis with a mild shift to the left and a moderate increase in ESR. In severe dysentery, high leukocytosis is noted (20-30x109 / l)

with a shift of the leukocyte formula to the left to young forms. In neutrophils, toxic granularity is found, in the blood - aneosinophilia. IN

the first days of the disease, due to thickening of the blood, a normal or even increased number of erythrocytes is noted, and then anemia develops.

Erased and mild forms of dysentery are characterized by the presence of mucus, leukocytes (2-15 in the field of view), single erythrocytes in the coprogram. In moderate and severe forms, mucus is detected in the feces in the form of strands filled with fresh leukocytes (neutrophils) and erythrocytes. Neutral fats, fatty acids,

digestible and non-digestible fiber, extracellular and intracellular starch.

Bacteriological examination is carried out in all patients with suspected or clinically diagnosed "Dysentery", "Enterocolitis of unknown etiology" three times with an interval of 6-8 hours.

The diagnostic titer in RA for Sonne dysentery is considered to be

1:100, and in children under 3 years old - 1:50, Flexner 1:100-1:20. Nonspecific and cross-reactions are possible. In weakened children, the production of antibodies is often reduced. Negative RA results do not rule out the diagnosis of dysentery. RNGA allows to detect anti-shigella antibodies, the minimum diagnostic titer is 1:160.

Differential diagnosis is carried out with colitis of another etiology, giardiasis, rectal polyps, intestinal intussusception. Differentiate dysentery more often with a colitis variant

course of salmonellosis, escherichiosis caused by enteroinvasive coli. common property of these diseases is a combination of fever, symptoms of intoxication and signs of damage to the large intestine.

More pronounced and prolonged (up to 10 or more days) fever is observed with salmonellosis. With dysentery, it persists for 2-3 days, and with escherichiosis, subfebrile body temperature is more often observed for a short time. This corresponds to the duration of general intoxication. Infectious-toxic shock can develop both with dysentery and with salmonellosis, but in the latter case it develops more often. Unlike salmonellosis and escherichiosis, dysentery is not characterized by the development of dehydration.

The level of damage to the gastrointestinal tract differs more significantly. With dysentery, as a rule, the large intestine is affected, which is manifested by the symptoms of distal colitis, with salmonellosis - all departments - gastroenterocolitis, with escherichiosis - the small intestine - enteritis.

Salmonellosis (ICD A02)

Allocate typical and atypical forms of salmonellosis. Typical forms include gastrointestinal, typhoid and septic. By severity, mild, moderate, severe salmonellosis is possible. Along the course, acute, protracted and chronic are distinguished. The most severe forms are observed, as a rule, with salmonellosis caused by

S.typhimurium, S.choleraesuis. Salmonellosis caused by S.typhimurium,

infants are more commonly affected. Clinically, the disease is characterized by the development of enterocolitis, hemocolitis, toxicosis, exsicosis and generalized forms. This salmonellosis is characterized by nosocomial infection. With salmonellosis caused by S.enteritidis, there is a mild or moderate course with a quick recovery, bacteriocarrier is more often observed with salmonellosis caused by S.heidelberg, S.derby. With typhoid form, S.heidelbarg is usually found, with purulent meningitis - S.hartneri.

In most patients, the onset is acute. One of the most common symptoms is fever permanent type usually lasting more than one week. Signs of toxicosis are noted, neurotoxicosis may develop. Seizures may develop as if

nervous system with a toxin, and in the event of salmonella meningitis, meningoencephalitis.

The gastrointestinal form of salmonellosis can occur with a clinic of gastritis, enteritis, colitis, and more often gastroenterocolitis. During the examination, pallor, adynamia, dry tongue of the child attract attention. The abdomen is swollen, painful around the navel, growls, enlarged liver and spleen are palpated. Vomiting can be of toxic or gastric origin. The stool is watery, frothy, with an admixture of green mucus, often streaked with blood with a fetid odor, reminiscent of swamp mud.

With a mild form of the disease, the condition suffers slightly.

Body temperature rises to 38 ° C, single vomiting, minor abdominal pain are possible. The stool is mushy or liquid, without pathological impurities, up to 5 times a day.

In the moderate form, lethargy, pallor of the skin, loss of appetite, abdominal pain, and repeated vomiting are noted. Body temperature of 38.0-39.5 °C persists for 4-5 days. Stool profuse, watery,

frothy, fetid with mucus, greenery, sometimes streaked with blood, up to 10 times a day.

A severe form of salmonellosis begins violently. It is characterized by high fever (up to 39-40 ° C). Lethargy, drowsiness,

uncontrollable vomiting. Stool more than 10 times a day, green, offensive, mixed with mucus and blood. Severe toxicosis, exsicosis develop,

infectious-toxic shock, disseminated intravascular coagulation syndrome, acute renal failure.

The typhoid form is more often observed in older children. The disease begins with symptoms characteristic of the gastrointestinal form. However, in the usual terms of recovery, the patient's condition does not improve, but acquires features characteristic of typhoid fever. High fever of the wrong type lasts 10-14 days or more. Symptoms of damage to the nervous system are growing: headache, lethargy, delirium, hallucinations. The skin is pale. At the height of severity in the chest and abdomen, a scanty roseolous rash is noted. Bradycardia develops, systolic murmur is detected, blood pressure decreases. Tongue thickly coated, with imprints of teeth. Belly swollen

large liver and spleen. The chair is liquid, green, with pathological impurities. Sometimes the chair is delayed. In other cases

the disease may begin with symptoms of intoxication, and dyspeptic syndrome is mild or absent.

The septic form, as a rule, is observed in children with reduced immunity. The "risk group" includes newborns, premature infants, who have undergone various intrauterine infections, as well as children

weakened by background and other comorbidities. The septic form of salmonellosis may begin with symptoms of gastroenteritis, and in some cases without signs of damage to the gastrointestinal tract. Secondary septic lesions often develop in the lungs, brain,

bones, joints. Sometimes there is septic endocarditis. The septic form of salmonellosis is characterized by a long severe course and high level lethality.

Complications of salmonellosis are toxic shock, DIC, hemolytic-uremic syndrome, myocarditis, intestinal dysbacteriosis.

In the general blood test, due to thickening, erythrocytosis is possible, the number of leukocytes can increase up to 60-70x109 / l, neutrophilia (up to

90%) with a shift of the leukocyte formula to the left to young, but leukopenia is often observed, combined with aneosinophilia, neutropenia,

relative lymphocytosis. ESR is accelerated.

The coprogram changes depending on the localization of the infectious process in the gastrointestinal tract and the degree of functional disorders. In the presence of a pathological process in the small intestine, there are no signs of intestinal inflammation, but a lot of neutral fat, starch and muscle fibers are found.

With the predominance of colitis in the coprogram, a large amount of mucus, leukocytes, and erythrocytes are detected. In severe salmonellosis, these changes are more pronounced.

The material for bacteriological examination is blood,

feces, vomit, urine, washings of the stomach and intestines, bile, pus, exudate from inflammatory foci, food debris, washings from dishes. Feces for sowing are taken immediately after defecation (the last portions are better, as they come from the upper intestines and contain more pathogens).

Studies are carried out three times from the onset of the disease and always in case of exacerbation or recurrence of the disease. Positive blood culture always indicates the presence of the disease, and positive copro-, urine-,

biliculture can be of diagnostic value only in combination with clinical symptoms, as it can be positive in bacteriocarriers.

From serological reactions, RA, RNGA, RSK are usually used. The minimum diagnostic titer of RA is 1:200, RNGA - 1:160, RSK -

1:80. Diagnostic increase in antibody titer by 4 or more times. In young children, titers from 1:10 to 1:20 are taken into account at the 1st week, and from 1:40

up to 1:80 at 2-3 weeks of illness.

Salmonellosis should be differentiated from inflammatory infectious diarrhea of ​​another etiology, food poisoning, non-infectious diarrhea.

Escherichiosis (ICD A04)

Depending on the presence of pathogenicity factors, escherichiosis is divided into 4 groups: 1. Enteropathogenic Escherichia coli (EPEC) have antigenic affinity for Salmonella, cause focal inflammation mainly of the small intestine. Enteropathogenic Escherichia include about 30 serovars. The most common of them are O 111, O 55, O 26, O 44, O 125, O 127, O119.

Diseases caused by enteropathogenic Escherichia coli occur mainly in young children and are manifested by diarrhea with symptoms of intoxication and the possible development of a septic process. The onset of the disease is acute or gradual. Sometimes the temperature in the first days is normal. Subsequently, appetite decreases, vomiting appears (persistent, but not frequent).

By the 4th-5th day of illness, the child's condition worsens: lethargy, adynamia increase, facial features become sharper, a large fontanel and eyeballs sink. Pallor of the skin, "marbling", periorbital cyanosis, dry mucous membranes are noted. Increased signs of hypovolemia.

The abdomen is sharply swollen, peristalsis is weakened, oliguria, anuria develop. The chair is frequent, liquid, watery, yellow-orange or golden in color with an admixture of clear mucus, rarely streaked with blood.

With a mild form of the disease, the body temperature is normal or subfebrile, the child's health is not impaired, exsicosis does not develop, rare regurgitation is possible, the stool is mushy or liquid, without pathological impurities, up to 5 times a day.

The moderate form is characterized by fever up to 39 ° C, moderate intoxication (anxiety or lethargy, loss of appetite, pallor of the skin), persistent but infrequent vomiting, liquid stool before

10 times a day, exsicosis Ι - ΙΙ degree.

The severe form is accompanied by severe intoxication, severe intoxication, possibly the development of neurotoxicosis, repeated vomiting, frequent stools up to 15 or more times a day, exsicosis

ΙΙ - ΙΙΙ degree.

Enteroinvasive Escherichia coli include in their group O 124,

O 151 and a number of other strains. Diseases caused by this type of Escherichia are similar in clinical manifestations to shigellosis.

They are observed mainly in older children. The onset of the disease is acute with fever, weakness, headache,

vomiting, cramping abdominal pain. Intoxication is short-lived. Unlike dysentery, the stools are copious, with much mucus and streaks of blood, and tenesmus is usually absent. The duration of fever is 1-2 days, intestinal dysfunction - 5-7 days.

Enterotoxigenic Escherichia coli cause diseases similar to foodborne infections and mild cholera. This group includes strains O 78: H 11, O 78: H 12, O 6: B 16. In the clinical course, diarrhea is noted, often accompanied by severe cramping abdominal pain, nausea, and vomiting. An increase in body temperature and intoxication may be unexpressed. Stool watery, spitting,

without pathological impurities and odor. Enterotoxigenic escherichiosis proceeds benignly, the prognosis is favorable.

A feature of the clinical picture of escherichiosis caused by enterohemorrhagic Escherichia coli are pronounced signs of intoxication, severe cramping abdominal pain, profuse stools of the color of "meat slops", intense abdominal pain, the development of hemolytic-

uremic syndrome. Enterohemorrhagic escherichiosis often occurs in moderate and severe form with the development of acute renal failure and hemolytic-uremic syndrome.

Escherichiosis is characterized by an acute course. The duration of symptoms ranges from a few days to 1 month. We can talk about a protracted course if the process lasts more than 1 month,

when the possibility of superinfection is completely excluded and

reinfection. A protracted course is facilitated by the developing

intestinal dysbiosis.

IN general blood test shifts occur only with moderate and severe forms in the form of anemia, leukocytosis (up to 20x10 9 /l), neutrophilia, increased ESR, aneosinophilia. Anemia is often detected during the recovery period, since blood clotting is possible at the height of the disease.

IN the coprogram is determined by an insignificant admixture of mucus with a moderate amount of leukocytes, rarely - erythrocytes. As the disease progresses, a large amount of fat appears (more often fatty acids, less often neutral).

Bacteriological examination reveals Escherichia

certain serovars (for enterotoxigenic escherichiosis only if their growth is massive 106 or more per 1 g of feces). From

serological methods are used by RNGA. Diagnostic titer 1:80-1:100. An increase in antibody titers is important.

The spectrum of diseases with which the differential diagnosis of escherichiosis is carried out depends on the group of escherichia. diseases,

caused by enteropathogenic Escherichia, have to be differentiated from salmonellosis, intestinal infections staphylococcal etiology, caused by representatives of opportunistic enterobacteria, viruses. Escherichiosis is clinically difficult to differentiate from salmonellosis.

The diagnosis is decided after receiving the results of bacteriological and serological studies. Intestinal infection of staphylococcal etiology, as a rule, occurs secondarily, following staphylococcal infection of other localizations. Enterocolitis due to opportunistic

pathogenic flora, as a rule, occur in weakened children. The diagnosis is made on the basis of the isolation of pathogens of this group.

Differential diagnosis of enteroinvasive escherichiosis is carried out with mild forms of dysentery based on laboratory tests. Cholera is differentiated from enterotoxigenic escherichiosis based on the epidemiological situation and laboratory results.

Escherichiosis caused by enterohemorrhagic Escherichia coli,

differentiate with diseases accompanied by hemocolitis. Often, enterohemorrhagic escherichiosis is distinguished from hemolytic-

uremic syndrome, thrombocytopenic purpura, and systemic vasculitis.

Yersiniosis (ICD A04.6)

The disease is more common in the gastroenterocolitis form. Less often - in the appendicular or septic. The clinic of various forms and variants of the disease is characterized by a combination of several syndromes. Toxic syndrome is manifested by an increase in body temperature up to 38-40

o C, chills, myalgia. Dyspeptic - abdominal pain, nausea, diarrhea, vomiting. Catarrhal syndrome is characterized by sore throat,

hyperemia of the mucous membranes of the pharynx. Exanthematous - scarlatiniform and morbilliform rash. At the same time, symptoms of "hood", "socks", "gloves" are noted, when the rash is mainly localized on the face, neck, hands and feet. Often there are arthralgic (signs of joint inflammation) and hepatolienal syndromes.

Abdominal pain in the gastrointestinal form of yersiniosis can be severe enough to suggest acute appendicitis. They are more often localized in the iliac or paraumbilical region, but can also acquire a diffuse character. The stool is plentiful, liquid, brown-green in color, fetid, from 2-3 to 10-15 times a day, occasionally with mucus and blood.

Tongue dry, covered with white coating. The abdomen is moderately swollen. Soft. There is pain in the ileocecal and umbilical regions. The chair is usually normalized for 4-7 days of illness.

The criteria for the severity of yersiniosis are the severity and duration of toxicosis, the frequency and nature of the stool, the severity of the pain syndrome, the degree of enlargement of the liver, the intensity of the rash.

The appendicular form of yersiniosis begins acutely with an increase in body temperature to 38-39 ° C, the appearance of intoxication, the symptoms of acute appendicitis are clearly expressed - local pain in the ileocecal region, limited tension in the abdominal muscles, symptoms of peritoneal irritation. There may be short-term diarrhea or constipation, flying pains in the joints, catarrh of the upper respiratory tract.

The septic form occurs mainly in young children with reduced immunity. Drowsiness, weakness, anorexia, chills are noted. The fever becomes hectic in nature with daily fluctuations up to 2-3 ° C, the liver and spleen increase, jaundice is noted. On the 2nd-3rd day of illness, a characteristic rash appears. Septic

the form is characterized by severe symptoms and the possibility of death.

Complications of yersiniosis often occur at 2-3 weeks of illness.

The most common complications are peritonitis, myocarditis, urethritis, Reiter's syndrome.

In the general blood test, leukocytosis, neutrophilia, eosinophilia, monocytosis, an increase in ESR up to 20-40 mm/h or more are detected. It is possible to increase bilirubin in the blood, thymol test, aminotransferase activity. In the coprogram, mucus, leukocytes, single erythrocytes, moderate creatorrhea, steatorrhea, amylorrhea are detected. stool pH is higher

The diagnosis is confirmed bacteriologically (seeding rate 10-50%). Feces, urine, blood, areas of the resected intestine, lymph nodes, swabs from the pharynx, the contents of pustules can serve as material for research.

The agglutination reaction (RA) is set according to the Vidal type. A titer of 1:80 or more is considered diagnostic. For the reaction of indirect hemagglutination (RIHA)

diagnostic titer 1:160 and above.

With yersiniosis, differential diagnosis is carried out depending on the leading clinical syndrome. So, in the gastrointestinal form of the disease, it is necessary to exclude shigellosis,

salmonellosis, typhoid fever and enterocolitis of other etiologies. With the appendicular form, acute surgical pathology has to be excluded. The septic form requires differentiation from sepsis of another etiology. In the presence of exanthema, measles must be excluded,

rubella, scarlet fever, enterovirus infection.

Typhoid fever (ICD A01.0)

Typhoid fever is a disease with a predominantly gradual onset of the disease and a slow development of clinical symptoms. The initial period of the disease is characterized by a gradual increase in body temperature, malaise, myalgia, headaches and abdominal pain. In some patients, at the onset of the disease, there may be

"typhoid status" (stupor, hallucinations, delirium). By the end of 1 week, body temperature becomes constant, nosebleeds, cough, enlarged spleen, and abdominal pain may occur.

The human intestine is divided into two sections: thin and thick. Immediately after the stomach begins the small intestine. It carries out the main mechanisms of digestion of food and absorption of nutrients into the lymph or into the blood. IN normal condition It does not contain any micro-organisms neither harmful nor beneficial.

In most diseases of the gastrointestinal tract, when there is a violation of the function of enzymes, an environment appears in the small intestine that is suitable for the life of microbes. If pathogenic microbes get there, an infection is formed, accompanied by severe diarrhea (diarrhea), bloating and rumbling in the abdomen, and pain in the navel. If there are good for the large intestine, non-pathogenic microorganisms, then a feeling of discomfort and bloating develops.

The small intestine is followed by the large intestine. They are separated by a thin mucous membrane. Its main function is to prevent the return of contents from the large intestine back to the small intestine, and also to protect the small intestine from the entry of a large number of microorganisms living in the large intestine. At a small distance from the valve is a process of the caecum (large) intestine, which is known to everyone as the appendix (it is an organ of immunity).

The composition of the large intestine includes: blind, transverse and descending sigmoid and bypass, ascending colon. Finally comes the rectum. The large intestine in its structure is radically different from the small intestine, in addition, it performs completely different functions: food is not digested in it, but nutrients are not absorbed. But it absorbs water and contains about one and a half kilograms of all kinds of microorganisms, which are extremely important for the life of the body.

Colitis is an inflammatory disease of the mucosal (inner) lining of the large intestine. If the mucous membrane of the large and small intestine becomes inflamed at the same time, this disease is called enterocolitis.

Forms of colitis

Acute forms of colitis are characterized by violent and fast current, and chronic ones proceed sluggishly and for a long time. An acute inflammatory process in the colon is often accompanied by inflammation of the stomach (gastritis) and small intestine (enterocolitis).

Meet different types colitis:
infectious (they are caused by pathogens),
ulcerative (associated with the formation of ulcers on the walls of the intestine),
medicinal,
radiation,
ischemic (blood does not enter the intestines well), etc.

Causes of colitis

long-term use of certain antibiotics (for example, lincomycin) and others medicines(neuroleptics, laxatives, etc.);
intestinal infection (viruses, bacteria, fungi, protozoa - for example, salmonellosis, dysentery, etc.);
improper diet (monotonous diet, excessive amounts of flour and animal foods in the diet, abuse of spicy foods and alcoholic beverages);
violation of the blood supply to the intestine (occurs in the elderly);
exposure to radiation;
intestinal dysbacteriosis;
bad heredity;
food allergy;
poisoning with lead, arsenic, etc.;
worms;
overstrain (both mental and physical) and incorrect daily routine;
foci of infection in the pancreas and gallbladder;
reasons are unclear. For example, the reasons for such inflammatory diseases chronic bowel disease, such as Crohn's disease and ulcerative colitis.

The mechanism of development of colitis

At the heart of every case of colitis lies damage to the intestinal mucosa.

The most rapid course is characterized by colitis, the appearance of which is associated with an intestinal infection. The simplest (for example, amoeba), bacteria and other viruses and microbes, when they enter the intestinal mucosa, damage it. The process of inflammation begins. Edema appears on the intestinal wall, mucus secretion and peristalsis (contraction) of the intestine are disturbed. There are pains in the abdomen, painful urge to defecate, diarrhea (in some cases with mucus and blood). Substances secreted by bacteria enter the bloodstream, resulting in an increase in body temperature.

During chronic colitis the intestinal mucosa is damaged due to factors such as malnutrition, impaired blood supply to the intestinal wall, food allergies, and so on.

Manifestations of colitis and enterocolitis

The main symptom of every case of colitis is abdominal pain, which may also be accompanied by bloating and rumbling. Stool disorders are noted: diarrhea, constipation, unstable stool (when diarrhea is replaced by constipation and vice versa). The stool may contain blood and mucus. The patient notes weakness, lethargy, in difficult cases there is an increase in body temperature. The duration of acute colitis is from a couple of days to several weeks, chronic type colitis is longer.

Find out which part of the gastrointestinal tract is affected and the probable cause of this is possible if pay attention to the nature of the complaints.
enterocolitis: bloating, pain in the navel, diarrhea with a high content of foamy stools.
infections, severe dysbacteriosis: the color of the stool is green (especially with salmonellosis), the smell is fetid.
acute gastroenteritis: joining vomiting, nausea, pain in the stomach indicate that the stomach is also affected.
infection of the large intestine: diarrhea with a small admixture of softened stools, mucus, sometimes with blood streaks; pains are concentrated in the lower abdomen, usually on the left, the nature of the pain is spastic. Frequent urge to go to the toilet.
dysentery: when the terminal (distal) sections of the large intestine (rectum, sigmoid colon) are damaged, often there are false urges to defecate (tenesmus), "ordering" urges that cannot be restrained (imperative), frequent and painful urge to defecate, accompanied by the release of small portions of feces (the so-called "rectal spit"), which may contain pus, blood, mucus.
amoebiasis: the stool takes on the appearance of "raspberry jelly".
infectious lesions: they are characterized by general symptoms (pain in the head, feeling of weakness, weakness), often there is an increase in temperature (both slightly and pronounced).
dysbacteriosis, non-infectious colitis: regular constipation or alternating diarrhea and constipation, the stool looks like “sheep feces”.
ulcerative colitis: the stool contains blood impurities.
hemorrhoids, fissure, cancer: blood is found on the surface of the stool.
intestinal bleeding: liquid "tarry" dark-colored stools. In this case need to contact urgently ambulance! However, if the stool is dark in color but shaped, it is due to the food consumed and does not pose a health hazard.

Diagnostics

The problem of colitis is under the jurisdiction of gastroenterologists and coloproctologists. During the first visit, the doctor will listen to complaints, conduct an examination, and then prescribe additional examinations. First of all, you need to take a stool test, which will allow you to conclude how well the intestines work and whether there is an intestinal infection.

Methods that are also used to diagnose colitis:
sigmoidoscopy - an examination of the area of ​​​​the intestine (up to 30 cm), for this, a rectoscope is inserted through the anus - a special endoscopic apparatus;
irrigoscopy - examination of the intestine with an x-ray, before the procedure, the intestine is filled with a contrast agent;
colonoscopy - is carried out according to the same principle as sigmoidoscopy, however, a section of the intestine up to one meter long is examined.

All of these methods require careful preliminary preparation, the purpose of which is to cleanse the intestines. To clarify the diagnosis, the specialist can send the patient for an ultrasound of the abdominal organs.

Treatment

Every colitis is treated with special diet. Further treatment depends on the cause of the disease:
1. If the disease was caused by an intestinal infection, antibiotics may be prescribed. During intestinal infections, poisoning, self-administration of adsorbents is allowed ( lactofiltrum, Activated carbon ). After a little more than half an hour from the moment of taking adsorbents for infections, it is allowed to drink but-shpu(if there are spasms), intestinal antiseptics ( furazolidone).

Can have both antiseptic and adsorbing effect smecta And enterosgel. A very common mistake is self-administration of antibiotics, which often only exacerbate intestinal disorders, leading to dysbacteriosis. Antibiotics should be taken only as directed by a doctor. If diarrhea is profuse and vomiting is present, replenish fluids with saline solutions. Oralit, rehydron are suitable for use at home. It's good to always have them on hand. Prepare the solution in accordance with the instructions, and then drink a liter of the solution in small sips within an hour.
2. If the appearance of colitis is caused by prolonged use of drugs, the previously prescribed drugs are canceled or, if it is impossible to cancel, they are replaced by others.
3. If colitis occurs in a chronic form, intestinal motility regulators, antispasmodics are used (for example, no-shpa), antidiarrheals (such as imodium, loperamide) and anti-inflammatory (such as sulfasalazine) means, in difficult situations - glucocorticoid hormones.

In addition, psychotherapy, physiotherapy (thermal treatment) and spa treatment can be prescribed.

Complications of colitis

if the infection is severe, dehydration and poisoning may occur;
with ulcerative lesions - acute blood loss and;
in chronic colitis, there is a decrease in the quality of life (chronic poisoning of the body, as well as all sorts of its consequences);
chronic forms of colitis are risk factor for cancer at the same time, signs of colitis can appear directly with tumors.

Treatment of colitis with folk methods

In a glass of boiling water, brew one teaspoon of sage, centaury and chamomile. Take one tablespoon about 7-8 once a day with a break of two hours (the number of doses will depend on how much time a person spends in a dream). Usually after some time 1-3 months) the dose is reduced, and the intervals between doses of the drug are increased. Such a medicine cannot cause harm, so it can be used for a long time, which is fully consistent with the seriousness of the disease and the long-term treatment required.

By 3-4 drink onion juice one teaspoon before meals once a day (used for colitis and constipation with reduced intestinal motility).

Infusion of fennel, anise, buckthorn and licorice: mix anise fruits - 10 g, fennel fruits - 10 g, licorice root - 20 g, buckthorn root - 60 g. One tablespoon of this mixture is taken for one glass of boiling water. insist within 30 minutes, then strain. Take with intestinal atony in the morning and evening for a full glass.

If colitis is accompanied by constipation, the following remedy will be effective: dried apricots, figs, prunes - each 200 g, aloe leaf - 3 pcs., senna - 50 d. Grind all this, divide it into 20 equal parts, roll into balls. At night, eat one such ball.

If colitis occurs in a chronic form, you can make a collection of herbs that are available to you: mint leaf - 1, chamomile flowers - 6, valerian rhizomes - 1, hypericum herb - 1, sage leaf - 1, plantain leaf - 3, blueberry fruit - 4, cumin fruits - 1, herb mountaineer bird - 1, oregano herb - 1, shepherd's purse grass 1, yarrow herb - 1, motherwort herb - 1, nettle leaf - 1. Two tablespoons of this collection for an hour insist in a glass of boiling water. Drink half or a third of a glass after meals two to three times a day.

Bacillary dysentery, Shigellosis, dysenterya. A03.0, A03.1, A03.2, A03.3, A03.8

Version: Directory of Diseases MedElement

Shigellosis, unspecified (A03.9)

general information

Short description

shigellosis- acute infectious disease, caused by bacteria of the genus Shigella with a fecal-oral mechanism of transmission of the pathogen and characterized by a picture of distal colitis and intoxication.

Classification

The currently accepted classification of shigellosis takes into account the severity of the main syndromes, the nature of the course of the disease, and the type of pathogen.

Classification of forms and clinical variants of the infectious process in shigellosis

Form Clinical
option
The severity of the current Peculiarities
currents
Etiology
Spicy
shigellosis
colitis
Gastroentero-
colitis

Gastroenterology
tic

Lung;
medium heavy; heavy

HI degree; heavy with
dehydration III-IV degree
Lung; moderate with dehydration
HI degree; heavy with
dehydration III-IV degree
Erased, lingering Shigella of any
of the listed
species: Sonne,
Flexner, Boyd
Grigorieva-Shigi,
Large Saxa,
Stutzer-Schmitz
Chronic
shigellosis
- - recurrent,
continuous
shigellosis
bacteriocarrier
- -

subclinical,
reconvale-

cent


Etiology and pathogenesis

Shigellosis is caused by a number of biologically related microorganisms belonging to the Enterobacteriacea family and united in the genus Shigella.

According to modern classification, the genus Shigella is divided into four species:

Group A: Shigella Dysenteriae, 1 - Grigorieva-Shigi, Shigella Dysenteriae, 2 - Stutzer-Schmitz and Shigella Dysenteriae 3-7 - Large-Saksa;

Group B: Shigella Flexneri with subspecies Shigella Flexneri 6 - Newcastle; serovars 1-6, each of which is subdivided into subserovars a and b, as well as serovars 6, X and Y;

Group C: Shigella Boydi, serovars 1-18;

Group D: Shigella Sonnei.

Shigella are gram-negative non-motile rods, facultative aerobes. Stick Grigoriev-Shiga forms shigitoxin (exotoxin), other species contain thermolabile endotoxin - LPS. The smallest infecting dose is typical for Grigoriev-Shiga bacteria, the largest for Flexner bacteria and the highest for Sonne bacteria. Representatives of the last two species are the most stable in environment: on dishes and wet linen they can persist for months, in soil - up to 3 months, on food - several days, in water - up to 3 months. When heated to 60 ° C, they die after 10 minutes, when boiled - immediately, in disinfectant solutions - within a few minutes. Of the antibacterial drugs, the highest in vitro sensitivity was noted to fluoroquinolones (100%).

Pathogenesis

During the day (sometimes longer) shigella can be in the stomach. At the same time, some of them disintegrate here, releasing endotoxin. The remaining bacteria enter the small intestine, where they can linger for up to several days and even multiply. Further, shigella move into the lower intestine, where they also multiply and disintegrate in greater numbers than in the small intestine. The defining moment in the development of the infectious process in shigellosis is the ability of shigella to invade intracellularly. Of paramount importance among the defense mechanisms is the state natural factors resistance, especially local ones (lysozyme and (β-lysins of the mucous membrane of the distal colon). Together with humoral factors (bactericidal activity, lysozyme, serum complement), they react to the development of the infectious process throughout the disease.

The degree of non-specific resistance is genetically determined to a certain extent, but at the same time it depends on a number of factors: the age of the patient, nutritional value, concomitant diseases.


Epidemiology

The only source of the causative agent of shigellosis is a person sick with a manifest or erased form of the disease, as well as a bacterioexcretor. The greatest danger is posed by patients who, by the nature of their work, are associated with cooking, storing, transporting and selling food products. Shigellosis is spread by the fecal-oral transmission mechanism. This mechanism includes the transmission of the pathogen by contact-household, water, food. The disease is ubiquitous, but the incidence prevails in developing countries among the contingent of the population with unsatisfactory socio-economic and sanitary-hygienic status. For countries with temperate climate characterized by summer-autumn seasonality.

Population susceptibility to shigellosis is high in all age groups children are most often affected. After the transferred disease, a short type-specific immunity is formed.

Specific prophylaxis has not been developed. Measures of non-specific prevention consist in improving the sanitary culture of the population, disinfecting drinking water (chlorination, boiling, etc.), as well as observing the rules for the preparation, storage and sale of food products. Employees of food enterprises and persons equated to them are allowed to work only after a negative bacteriological analysis for shigellosis, and after a previous disease with shigellosis - after two negative test results taken no earlier than on the 3rd day after treatment, and the absence of clinical manifestations. In the case of a patient staying at home, current disinfection is carried out in the apartment. Persons who have been in contact with patients are placed under medical supervision for 7 days.

Clinical picture

Symptoms, course

The incubation period for acute shigellosis in most cases is limited to 2-5 days. The duration of the disease ranges from several days to 3 months, shigellosis lasting more than 3 months is regarded as chronic.

Clinical picture of the colitis variant of acute shigellosis

This variant of the course of the disease is diagnosed most often in clinical practice. With it, the characteristic signs of shigellosis are determined, especially in severe and moderate course. The disease, as a rule, begins acutely, in some patients it is possible to establish a short-term prodromal period, manifested by a short feeling of discomfort in the abdomen, slight chills, headache, and weakness. After the prodromal period (and more often against the background of complete health), characteristic symptoms of the disease appear. First of all, there are cramping pains in the lower abdomen, mainly in the left iliac region; sometimes the pain has a diffuse character, atypical localization (epigastric, umbilical, right iliac region). A feature of the pain syndrome is its reduction or short-term disappearance after defecation. The urge to defecate appears simultaneously with the pain or somewhat later. The stool is initially fecal, gradually the volume of feces decreases, an admixture of mucus and blood appears, the frequency of bowel movements increases. At the height of the disease, stools may lose their fecal character and look like a so-called rectal spit, i.e. composed of only a meager amount of mucus and blood. Defecation may be accompanied by tenesmus (drawing convulsive pain in the anus), often there are false urges. The admixture of blood is most often insignificant (in the form of blood points or streaks). On palpation of the abdomen, spasm is noted, less often - soreness of the sigmoid colon, sometimes flatulence. From the first day of the disease, signs of intoxication appear: fever, malaise, headache, dizziness. Possible cardiovascular disorders that are closely associated with the syndrome of intoxication (extrasystole, systolic murmur at the apex, muffled heart sounds, fluctuations in blood pressure, the presence of changes in the electrocardiogram, indicating diffuse changes in the myocardium of the left ventricle, overload of the right heart).

The duration of clinical symptoms in uncomplicated acute shigellosis is 5-10 days. In most patients, the temperature first normalizes and other signs of intoxication disappear, and then the stool normalizes. Abdominal pain persists for longer. The criterion for the severity of the course in patients with shigellosis is the severity of intoxication, lesions of the gastrointestinal tract, as well as the state of the cardiovascular, central nervous system and the nature of the lesion of the distal colon.

Gastroenterocolitic variant of acute shigellosis

The clinical features of this variant are that the onset of the disease resembles PTI, and at the height of the disease, the symptoms of colitis appear and come to the fore. The gastroenteric variant of acute shigellosis along the course corresponds to the initial period of the gastroenterocolitic variant. The difference lies in the fact that in later periods the symptoms of enterocolitis do not dominate and clinically this variant of the course is more similar to PTI. With sigmoidoscopy, less pronounced changes are usually observed.

Erased course of acute shigellosis

It is characterized by short-term and unexpressed clinical symptoms (1-2-fold disorder of the stool, short-term abdominal pain), the absence of symptoms of intoxication. Such cases of the disease are diagnosed by determining sigmoidoscopy changes (usually catarrhal) and isolating shigella from feces. A protracted course of acute shigellosis is said when the main clinical symptoms do not disappear or resume after a short-term remission for 3 weeks - 3 months.

Bacteriocarrier

This form of the infectious process includes cases where there are no clinical symptoms at the time of the examination and in the previous 3 months, with sigmoidoscopy and the isolation of shigella from feces, no changes in the mucous membrane of the colon are detected. Bacteriocarrier can be convalescent (immediately after suffering acute shigellosis) and subclinical if shigella is isolated from individuals who do not have clinical manifestations and changes in the mucous membrane of the distal colon.

Chronic shigellosis

A chronic disease is registered in cases where the pathological process continues for more than 3 months. Chronic shigellosis according to the clinical course is divided into two forms - recurrent and continuous. With a relapsing form, periods of exacerbations are replaced by remission. Exacerbations are characterized by clinical symptoms characteristic of the colitis or gastroenterocolitic variant of acute shigellosis, but mild intoxication. With a continuous course, the colitis syndrome does not subside, hepatomegaly is noted. In chronic shigellosis, sigmoidoscopy also reveals moderate inflammatory and atrophic changes.

Features of shigellosis Grigoriev-Shigi

It proceeds mostly hard, characterized by an acute onset, intense cramping pain in the abdomen, chills, fever up to 40 ° C. Chair on the first day appearance resembles meat slop, then the volume of feces decreases, an admixture of blood and pus appears. Note tenesmus. In some cases, infectious TSS, sepsis with inoculation of the pathogen from the blood are observed, hemolytic-uremic syndrome may develop. Hypovolemic shock occurs with copious stools and early vomiting.

Diagnostics

Clinically, the diagnosis of shigellosis can only be established in cases of a typical colitis variant of the course of the disease. To clarify the diagnosis in cases not confirmed by laboratory, sigmoidoscopy is performed, which in all cases of shigellosis reveals a picture of colitis (catarrhal, hemorrhagic or erosive-ulcerative) with damage to the mucous membrane of the distal colon, often sphincteritis. Gastroenteric and gastroenterocolitic variants are diagnosed only in case of laboratory confirmation. The most reliable method of laboratory diagnosis of shigellosis is the isolation of coproculture of shigella. For the study, stool particles containing mucus and pus (but not blood) are taken, it is possible to take material from the rectum with a rectal tube. For inoculation, 20% bile broth, Kaufman's combined medium, and selenite broth are used. The results of bacteriological examination can be obtained no earlier than 3-4 days from the onset of the disease. Isolation of blood culture is important in Grigoriev-Shiga shigellosis. In some cases of gastroenteritis, presumably of shigellosis etiology, a bacteriological study of gastric lavage is performed. The diagnosis can also be confirmed by serological methods. Of these, the most common method is with standard erythrocyte diagnosticums. An increase in antibodies in paired sera taken at the end of the first week of illness and after 7-10 days, and a fourfold increase in titer are considered diagnostic. ELISA, RKA are also used, it is possible to use aggregation hemagglutination and RSK reactions. An auxiliary diagnostic method is a scatological study, in which an increased content of neutrophils, their accumulations, the presence of erythrocytes and mucus in a smear are detected.

From instrumental methods of primary importance are endoscopic (sigmoidoscopy and colonofibroscopy), which confirm the characteristic changes in the mucous membrane of the colon.

Ultrasound and radiological research methods are used for the purpose of differential diagnosis.

Differential Diagnosis

Most often performed with other diarrheal infections, acute surgical pathology of the abdominal organs, UC, tumors of the distal colon. The most relevant differential diagnosis with the diseases presented in the table:

sign Nosoform
acute shigellosis Salmonellosis with colitis syndrome acute appendicitis mesenteric
thrombosis
UC acute/subacute
form
distal cancer
thick
guts
Epidemic history Patient contact, use
neobezzara-
women's water
group character
disease, disorder
rules for storage and preparation
food, nutrition
in "Community"
- Possible overeating - -
Age, history
life
Any Any Any 60 years and older, coronary artery disease,
atherosclerosis
young, average, episodes
diarrhea with a tendency
to weighting
middle, senior,
blood in the stool
Development of the disease acute, at the same time
abdominal pain, diarrhea,
fever
acute, at the same time
abdominal pain, vomiting,
fever, then diarrhea
Acute, abdominal pain,
then vomiting, diarrhea,
fever
Acute, abdominal pain,
vomiting, diarrhea, fever
in 1-2 days
Acute, subacute, diarrhea,
fever
abdominal pain, diarrhea,
fever intermittent
Stomach ache Cramping in the left
iliac region
Cramping in
epigastrium, then shifted
to the bottom
belly
Constants get stronger
coughing, moving
in the right iliac
areas, sometimes in the lower
parts of the abdomen
spilled, mostly
left, cutting
Weakly expressed, spilled In the left half
abdomen, dull, unstable
Vomit Possible in the early days Constantly, repeatedly Possible at the beginning
1-2 times
Often, possible admixture
blood
Not typical Not typical
Chair Lean, with mucus and
blood, often
Abundant, green, with
pungent odor, sometimes
with mucus, frequent
mushy, without
impurities, up to 4-6 times
mushy, liquid,
with an admixture of aloe
blood
Abundant, frequent, liquid,
with blood ("meat
slops")
Liquid, with mucus,
blood and pus that
saved after
chair design
Tenesmus, false
urges
Characteristic not characteristic Not observed not characteristic not characteristic not characteristic
Stomach Soft, retracted swollen tense, local
pain, symptoms
peritoneal irritation
Bloated, diffuse soreness Swollen, painless Soft, sore
left
Sigma Spasmodic, painful painful Not changed Not changed slightly painful Dense, thickened,
motionless
Endoscopy Changes typical
for shigellosis
catarrhal,
catarrhal
hemorrhagic colitis
Norm ring-shaped hemorrhages,
necrosis
Severe swelling, bleeding
fibrin plaque,
erosion, ulcers
Tumor with necrosis
bleeding, peri-
focal inflammation

Salmonellosis presents difficulties for differential diagnosis in the presence of colitis syndrome, acute appendicitis - in atypical course (diarrhea, unusual localization of pain), mesenteric thrombosis - in the presence of blood in the stool, acute or subacute variants of UC - in cases with fever, a rapid increase in diarrhea and the appearance blood in feces, cancer of the distal colon - with an asymptomatic course of the disease, if diarrhea and intoxication develop due to infection of the tumor.