Rectal spit in which disease. Dysentery. How often should stools be

02.07.2020

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.

Young children rarely get sick with 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. AT

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

the course of salmonellosis, escherichiosis caused by enteroinvasive Escherichia coli. A common feature 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, often of a 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 a high mortality rate.

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 relapse 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 in the 1st week are taken into account, 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 feels well, 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, loose stools up to

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, abundant 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.

AT general blood count, shifts occur only in 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.

AT 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, it is necessary to differentiate from salmonellosis, intestinal infections of 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, with 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 appear.

Diarrheal diseases or diarrhea - diseases with an increase in the number of bowel movements (more than 2 times / day) and liquefaction of the stool, up to severe dehydration - are found everywhere. Diarrhea is infectious and non-infectious; acute (7-10 days), protracted (up to 2 months) and chronic (3 months or more). Acute intestinal infections (AII) dominate among infectious diarrheas. In adults and, often, in children, acute intestinal infections of shigellosis etiology or shigellosis are more often diagnosed. Previously, and even today, along with shigellosis, there is an old name for diseases caused by shigella - dysentery.

Dysentery (shigellosis) is a long-known and ubiquitous human infectious disease caused by various types of bacteria of the genus Shigella (Shigella) from the family of enterobacteria (Enterobacteriaceae), occurring with symptoms of general intoxication and damage to the gastrointestinal tract, mainly the large intestine, in the form of colitis ( distal colitis).

Dysentery can be severe, complicated, protracted and chronic forms are observed. And today people are dying from shigellosis. With dysentery, special attention should be paid to decreed groups of people (food workers, etc.), since they can be the leading sources of shigellosis infection. This article discusses the etio-pathogenetic, clinical and diagnostic aspects of shigellosis infection (dysentery).

The causative agents of dysentery are four types of microorganisms of the genus Shigella: Sh. dysenteriae, Sh. flexneri, Sh. boydii, Sh. sonnei. In the international classification of shigella (ICD-10: A03.0 - A03.3), these 4 species belong, respectively, to subgroups A, B, C and D; have serovars and subserovars. Only Sh. Sonnei, in the absence of serovars and subserovars, have 3 enzymatic types. Shigella dysenteriae include sticks of Grigoriev-Shig, Stutzer-Schmitz, Large-Sachs and some others. The classification of shigella is presented below.

International classification of shigella:

Subgroup	View	Serovar	Podserovar
A	Sh. dysenteriae	1 - 12	―
B	Sh. flexneri	1	1a, 1b,
		2	2a, 2b,
		3	3a, 3b,
		4	4a, 4b,
		5	5a, 5b,
		6
		Xvar
		Y-var
C	Sh. boydii	1 - 18	―
D	Sh. sonnei	―	3 enzyme. type

Shigella are gram-negative rods, do not form spores and capsules, grow well on simple nutrient media. When they are destroyed, it releases endotoxin. It is this toxin that mainly determines the development of the intoxication syndrome in shigellosis. In addition, some Shigella are capable of producing toxins while alive - exotoxins(mainly Sh. dysenteriae). Among them are thermolabile and thermostable enterotoxins that enhance the secretion of fluid and salts into the intestinal lumen, and cytotoxin(damaging the membranes of epithelial cells). In addition, shigella Grigoriev-Shiga produce neurotoxin with a strong effect on the central nervous system.
Shigella are capable of producing toxins after adhering to and invading intestinal epithelial cells (mainly the colon). Pathogenicity in different types of microbes is different, it is exceptionally high in Shigella Grigoriev-Shiga, in other species it is much less. In the last decade in a number of regions of Russia, even where the milder Sonne dysentery dominated, the incidence of the more severe Flexner dysentery began to noticeably increase.
Shigella survive well in the external environment, which depends on temperature, humidity, pH of the environment, the number and type of microorganisms. Depending on the influence of these factors, their survival ranges from several days to months. Favorable environment for microorganisms are food products. Shigella Sonne in milk and dairy products, salads, vinaigrettes, minced meat, boiled fish, compotes and jelly can not only exist for a long time, but can also multiply. Shigella tolerate desiccation and low temperatures well, but quickly die under the influence of direct sunlight and when heated (at 100 ° C - almost instantly). Disinfectants (hypochloride, chloramine, etc.) at normal concentrations kill shigella in a few minutes.

The source of infection and the reservoir of the pathogen is only a person(patients with acute and chronic dysentery, as well as convalescents and bacteria carriers that excrete shigella into the environment with feces). Patients with mild, obliterated and subclinical forms of the disease pose a great epidemiological danger. In epidemiological terms, patients with acute dysentery (especially in an erased form) are the most dangerous.
Transmission of dysentery pathogens to a susceptible person occurs through fecal-oral mechanism, which sold by food, water and contact household routes. At the same time, food products, water, the hands of the patient, household items, soil, flies become factors in the transmission of shigella. The leading route of transmission of infection in Grigoriev-Shiga dysentery is contact-household, Flexner - water, Sonne - food. All age groups are affected, but children aged 1–2 years and up to 6 years are more often affected.
Dysentery is characterized by summer-autumn seasonality. Post-infection immunity is short-lived, species- and type-specific. After the disease, immunity to dysentery is determined by the local tissue response to circulating endotoxin in the blood.

Having got, in one way or another, through the mouth into the human gastrointestinal tract, Shigella overcome the acid barrier of the stomach, enter the small intestine, and then the large intestine, where they penetrate the intestinal wall. In a hot climate (when a person consumes a large amount of liquid), as well as with low acidity of gastric juice, the process of passing Shigella through the stomach is greatly facilitated. The entry of Shigella into the body is accompanied by the death of some of the microbes in the stomach and intestines, not only due to the influence of gastric and other digestive juices, but also under the influence of secretory immunoglobulins, as well as the antagonistic action of the intestinal microflora.
In the development of the pathological process in dysentery, the entry of Shigella toxins into the blood is of paramount importance - toxinemia, other factors determining pathogenesis are secondary: ● microbial and ● allergic. The occurrence, development and outcomes of the disease are determined by other factors. Environmental factors affect the immune state of the body of an infected person, determine the characteristics of the pathogen and the action of epidemiological factors, and the forms and outcomes of the shigellosis process generally depend on this.

The disease can occur only with the penetration of shigella from the intestinal lumen into the thickness of the tissues. The penetration and reproduction of dysenteric microbes in the intestinal epithelium can only be considered as the beginning of a pathological process. Some Shigella are able to reach their own intestinal mucosal layer. Only when toxins enter the bloodstream, the disease manifests itself.. The vital activity of Shigella in the small intestine is accompanied by the production of entero- and cytotoxins, and their destruction is accompanied by the release of endotoxins. Symptoms of intoxication and pain in the mesogastrium that occur in the initial period of the disease are largely due to the action of endotoxin, pyrogens and biogenic amines.
Increased secretion of fluid and salts into the lumen of the small intestine leads to the development of diarrheal syndrome(secretory diarrhea). The stool during this period of the disease is plentiful, contains a large amount of liquid. The development of diarrhea usually includes several mechanisms simultaneously (impaired motility, secretion and absorption of intestinal contents), including intestinal dysbacteriosis, malabsorption syndrome and an allergic factor (mainly of microbial and food origin). In parallel with these processes, Shigella invasion into colonic epithelial cells with development typical of dysentery colitis(Inflammatory diarrhea occurs and dominates).

The predominance of damage to the distal colon may be due to a relatively long accumulation of intestinal contents, toxins and bacteria in it, as well as intestinal dysbacteriosis and malabsorption. Under these conditions, there massive invasion of the pathogen into colonocytes. Shigella invasion of the colon mucosa leads to uneven damage to epitheliocytes with the appearance of superficial microerosions. The severe course of the disease is accompanied by a pronounced infiltration of the mucosa by neutrophils and the possibility of developing abscesses in the crypts. In most infected individuals, the main part of shigella is retained by phagocytic cells at the level of the basement membrane, but in severe cases, pathogens can spread in significant numbers no further than the submucosa and mesenteric lymph nodes. Most microorganisms are phagocytosed by neutrophils and macrophages at the basement membrane level. Thus, dysentery can be considered as "localized infection". Sometimes occurring short-term bacteremia has no pathogenetic significance and does not change the idea of dysentery as a localized infection. Shigella and their toxins, when phagocytes and mucosal cells are damaged, contribute to release of biologically active substances(histamine, serotonin, kinins, prostaglandins), which disrupt the microcirculation in the intestinal wall, increase the intensity of inflammation and exacerbate disorders of the motor, secretory and absorption functions of the intestine.

Violation of the innervation of the intestine and inflammatory changes in its mucosa are clinically manifested by sharp spastic pains in a stomach. Spasms and uneven contractions of individual segments of the intestine lead to a delay in the contents of the intestine in its upper sections. In typical and severe cases of dysentery, this explains the scanty stool of a stool-free nature, consisting of an inflammatory exudate. Convulsive contraction of the muscles of the sigmoid and rectum causes painful false urges for defecation and tenesmus(burning sensation or soreness in the anus and a feeling of an unfinished act of defecation). Along with damaging factors, adaptive and compensatory mechanisms are activated that ensure sanogenesis and overcome infection. The intensity of pathogenetic mechanisms and sanogenesis, along with the type of pathogen, determine the nature and severity of the course of dysentery.

In severe cases of the disease, especially in children, the resulting phenomena of toxicosis and exicosis lead to the development of acute vascular insufficiency and the possibility of death. The most severe course with pronounced toxicosis and colitis syndrome is characterized by Grigoriev-Shiga and Flexner dysentery. Shigella Sonne can cause gastroenteritis, which has many similarities with toxic infections. In some cases, dysentery takes a protracted or chronic course. This is facilitated by immunodeficiency states, unfavorable premorbid background, concomitant diseases, advanced and senile age.
During sigmoidoscopy in a patient with dysentery, inflammatory changes in the distal colon are most pronounced and well detected: from acute catarrhal inflammation to fibrinous-necrotic and even ulcerative process. In the vast majority of patients, ulcers heal completely in the process of recovery.

CLINIC.

Incubation period ranges from 1 to 7 days (usually 2-3 days). According to the duration of the course of dysentery, acute, protracted and chronic variants, as well as bacteriocarrier, are distinguished. The severity of the course and the variant of dysentery depend both on the ways and factors of infection, and on the number of microbes that have entered the body, as well as on the state of the body's immune forces, the presence and nature of concomitant diseases and conditions (especially helminthic invasions).
Clinical classification of dysentery (results of studies by leading clinicians (Guide to infectious diseases. Edited by Prof. Yu.V. Lobzin and Prof. A.P. Kazantsev. - St. Petersburg: TIT "Kometa", 1996, 720 pages) is presented Below In this classification (Reference book of the family doctor. Infectious diseases. Lobzin Yu. V., Finogeev Yu. P., Zakharenko S. M. - St. the course of acute dysentery and 3 possible variants of bacteriocarrier (with convalescent bacteriocarrier, individual clinical symptoms of the transferred manifest form are often found).

Clinical classification of dysentery.

1. Acute dysentery(1-4 weeks): ■ colitis; ■ gastroenterocolitic; ■ gastroenteric; ■ erased.
2. Protracted dysentery(up to 3 months).
3. Chronic dysentery(3 months - 2 years).
4. Bacteriocarrier:■ transient, ■ subclinical, ■ convalescent.

According to the severity of the course, the colitis variant subdivided into mild, moderate and severe forms; gastroenterocolitic and gastroenteric- for mild and moderate with dehydration of I-II degree, as well as severe - with dehydration of III-IV degree. As noted, the last 2 forms, which are not very characteristic of dysentery, can occur with dehydration, which is not typical for it.

Dysentery often proceeds cyclically, there are 4 periods of the disease: - elementary, - peak period, - fading symptoms, - period recovery(with residual effects or chronicity).

COLITHIC OPTION- the most typical clinical manifestation of acute dysentery. It is characterized by two main syndromes:- intoxicating, - colitis. In most patients, the disease begins acutely with symptoms of intoxication: chills and fever, headache, loss of appetite. Body temperature quickly rises to maximum values (38-40oC) and remains at this level from several hours to 2-3 days, decreases mainly by the type of accelerated lysis. The disease can occur with low-grade fever or even with normal temperature. The nervous system is affected early. In most patients, weakness, weakness, apathy, depression, and headache appear from the very beginning.
The pulse is labile, sometimes the rhythm of heart contractions is disturbed, a decrease in arterial and venous pressure. Heart sounds are muffled, a systolic murmur may be heard at the apex. In severe cases, as a manifestation of intoxication, the development of infectious toxic shock (ITS) is possible.

In the classical course of this variant of the disease leading is colitis syndrome. Patients are disturbed at first by dull diffuse pains all over the abdomen. Soon they become cutting, cramping, localized in the lower abdomen, mainly in the left iliac region. The intensity and duration of pain depends on the form and severity of the disease. Abdominal pain usually precedes each bowel movement and builds up on it. The urge to defecate is often fruitless (false), accompanied by tenesmus - excruciating pulling pain in the rectum. On palpation of the abdomen, a spasmodic and tense large intestine (usually sigmoid) is determined. Often, palpation increases the spasm of the intestinal muscles and leads to the urge to defecate.

With manifest forms of shigellosis, the stool becomes more frequent up to 20-30 times a day or more. Usually a bowel movement does not bring relief. Despite multiple stools, the amount of feces excreted per day is small, rarely more than 0.5 - 1.0 liters. With frequent stools, stools lose their fecal character. In practice, the stool consists of thick transparent mucus, then an admixture of blood, and later pus (“rectal spit”) joins it. The stools may take the form of meat slops with suspended lumps of mucus.
With this course of the disease, the functions of all other parts of the digestive tract are disrupted. Salivation is inhibited (dry mouth occurs), the secretion of gastric juice changes (in most patients, its acidity decreases, up to achlorhydria), the proteolytic activity of gastric contents decreases, gastric motility is perverted. The functions of the small intestine are impaired (motility, secretion, membrane hydrolysis and resorption). In severe cases, there is a slight proteinuria, microhematuria, cylindruria.
The hemogram at the height of the disease is characterized by a slight increase in ESR, moderate leukocytosis, a shift to the left of the leukocyte formula, and monocytosis. The duration of the peak of the disease ranges from 1-2 to 8-9 days. Morphological recovery lags behind the clinical one by 2-3 weeks. Late hospitalization, inadequate therapy and an unfavorable premorbid background can lead to the transition of the disease to a chronic form or to the development of post-dysenteric conditions (asthenia, impaired motility, secretion and resorption of the gastrointestinal tract).
Mild colitis characterized by moderate or mild intoxication, begins acutely with a short-term rise in temperature to 37-38 ° C. In the first hours, weakness and a decrease in appetite are noted, later moderate pains in the abdomen appear. Chair from 3-5 to 10 times a day. The stools are semi-liquid or liquid, often with mucus and sometimes streaked with blood. Patients remain able-bodied and often self-medicate. The sigmoid colon, on palpation, rumbles, painful and spasmodic. Sigmoidoscopy can reveal catarrhal or catarrhal-hemorrhagic proctosigmoiditis and sphincteritis. More often the disease lasts 3-5 days and ends with recovery.
Colitis of moderate severity begins with chills, general "ache" and weakness. The temperature rises to 38-39°C and lasts 3-5, rarely 7-8 days. Anorexia, headache, nausea, sometimes vomiting, severe cramping abdominal pain, tenesmus are often observed. Diarrhea joins after 2 - 4 hours from the onset of the disease. Stool 10-20 times a day, bowel movements quickly lose their fecal character and consist of mucus stained with blood. They can be sparse (in the form of “rectal spit”) or more abundant and mucous. Hemocolitis is observed in 70-75% of patients. Acute phenomena gradually subside on the 3-5th day. In the feces, the amount of mucus and blood decreases, the stool normalizes, but the pathological coprogram remains. Rectoromanoscopy reveals catarrhal-erosive proctosigmoiditis. Clinical recovery occurs by the end of the 2nd week of the disease, but complete healing of the intestinal mucosa with normalization of the body occurs after 1.5 months.
Severe form of the colitis variant also begins acutely with a rapid manifestation of the disease. It is manifested by severe intoxication and an increase in temperature to 39 ° C and above. There may be fainting, delirium, nausea, vomiting. Pain in the abdomen is pronounced and accompanied by painful tenesmus and frequent urge to defecate. Stools from 20-25 to 50 times a day, scanty, stool-free, mucous-bloody, sometimes looks like meat slops. Patients are adynamic, lethargic, there is no appetite. The skin and mucous membranes are dry. The arterial pressure is lowered, constant tachycardia is observed. A collapse may develop on the first or second day. Tenesmus and spasms of the intestine can be replaced by its paresis, bloating, gaping of the anus and involuntary defecation. In the blood, leukocytosis or leukopenia with a shift of the leukocyte formula to the left and toxic granularity in leukocytes. Palpation of the abdomen reveals spasm, rumbling and soreness of the large intestine (or only the sigmoid colon), flatulence. Severe condition persists for 7-10 days.
With Sonne dysentery, catarrhal-hemorrhagic, catarrhal-erosive and, sometimes, ulcerative changes in the mucosa are determined by sigmoidoscopy. With Flexner's dysentery, fibrinous-necrotic, fibrinous-ulcerative and phlegmonous-necrotic lesions of the colon mucosa are detected. The illness lasts 3-6 weeks or more.

Individuals with immunodeficiency may not have a pronounced fever, but the damage to the colon is total!

GASTROENTEROCOLITIC VARIANT for dysentery is less characteristic and proceeds as a food poisoning with a short incubation and rapid onset of the disease. At the beginning of the disease, the main syndrome is gastroenteritis, which is combined with severe symptoms of intoxication. In the future, enterocolitis begins to dominate. Vomiting, profuse diarrhea, copious watery stools without blood and mucus, and diffuse abdominal pain are typical for the initial period. Later, the stool becomes less plentiful, an admixture of mucus and blood is found in it, and dysentery can already be assumed. When assessing the severity of this form of the disease, the degree of dehydration is taken into account.

GASTROENTERITIC OPTION observed rarely, close downstream to the initial period of gastroenterocolitic. The difference lies in the absence of symptoms of colitis in the later period of the disease (after the 2-3rd day of illness). The leading syndromes are gastroenteritis and dehydration. The shigellosis nature of this variant of dysentery is confirmed by the results of laboratory tests.

ERASED FLOW dysentery occurs in all variants of the disease. Manifested by minor abdominal pain and short-term (1-2 days) bowel dysfunction. The stools are semi-liquid, there is no blood in them, and mucus is often absent. The temperature may be subfebrile, but usually does not exceed the norm. Often, palpation of the abdomen is determined by increased sensitivity of the sigmoid colon. In the coprogram, the number of leukocytes exceeds 20 in the field of view. With sigmoidoscopy - catarrhal proctosigmoiditis. The diagnosis is established on the basis of clinical and anamnestic, epidemiological and timely laboratory studies.

BACTERIOLOGY. Fundamentally, bacterial excretion is interpreted as a form of dysentery with a subclinical course. At the same time, there is no intoxication and intestinal dysfunction. However, the detection of shigella and the use of the entire complex of modern diagnostic methods confirm the presence of an infectious process. Cases with no diarrhea during the examination period and in the previous 3 months with shigella excretion in feces are classified as subclinical bacterial excretion. Isolation of shigella after clinical recovery - convalescent bacterial excretion, a transient bacterial excretion- this is a single or repeated detection of Shigella in the feces without clinical and laboratory confirmation of the infectious process.

CHRONIC DYSENTERIA.

Chronic dysentery can be recurrent and continuously ongoing. The diagnosis is established if the disease lasts 3 months or more. Under the guise of chronic dysentery, a variety of diarrhea can be hidden: irritable bowel syndrome, ulcerative colitis, Crohn's disease, hologenic diarrhea, HIV infection with diarrhea, intestinal amoebiasis, some neoplasms, etc.

RECURRENT FORM occurs much more often than continuous and is characterized by alternating remissions and relapses of the disease. The duration of each new return of dysentery and light intervals are different. The symptoms of distal colitis predominate. Intestinal dysfunction is similar to mild or moderate acute dysentery, differing in persistence and duration. Systemic examination of the patient can reveal signs of involvement in the pathological process of the stomach, small intestine, pancreas, hepatobiliary system. The central (irritability, excitability, sleep disturbance, etc.) and autonomic nervous systems suffer differently (vagotonia is more often observed). With sigmoidoscopy during an exacerbation, the picture resembles the changes characteristic of acute dysentery, but their intensity in different areas is different; during the period of remission, a pale and atrophic mucosa with a pronounced vascular network is revealed. Functionality is preserved.

CONTINUOUS FORM. With it, there are practically no light gaps. When the patient feels constantly unwell, his condition gradually worsens. Deep digestive disorders, malnutrition, anemia develop, signs of hypovitaminosis and pronounced intestinal dysbacteriosis appear. Today, this form is rare, more often in the elderly and in old age, as well as in immunodeficiencies of various origins.

COMPLICATIONS.

Serious but rare complications include infectious-toxic shock (ITS), infectious-toxic + hypovolemic shock in children, infectious-toxic damage to the nervous system, peritonitis, pneumonia, which develop during the height of the disease and have a serious prognosis.
Complications of a general nature:- mono- and polyarthritis, - nephritis, - iridocyclitis, - toxic hepatitis, - collapse, - protein-free edema, - polyneuritis.
Complications from the gastrointestinal tract:- dysbacteriosis, - paraproctitis, - rectal fissures, - pericolitis - intestinal invagination, - hypo- and beriberi, - bleeding, - prolapse of the rectum.
Complications of secondary infection:- pneumonia, - pleurisy, - pyelonephritis, - otitis media, - sepsis, - urethritis, etc.

With modern dysentery, the nature, severity and frequency of these complications have been significantly reduced.

FORECAST in dysentery depends on the age of the patient, the severity of the disease, comorbidity, complications, timeliness and adequacy of treatment. The prognosis is severe in subgroup A dysentery, milder in Flexner's dysentery, and favorable in Sonne's dysentery.

DIAGNOSTICS.

In typical cases, the diagnosis of dysentery is not difficult. The diagnosis is established on the basis of clinical ( inspection faeces), epidemiological, laboratory and instrumental studies. Bacteriological research remains leading, but the sowing rate of shigella ranges from 22 to 80% and depends on many factors (method, timing and frequency of material sampling, the nature of the nutrient medium, etc.).
Serological method also used to diagnose dysentery, but positive responses can be obtained from the 5th day of illness. The reaction of indirect hemagglutination (RIHA) with erythrocyte diagnosticum is used, the minimum diagnostic titer in RIHA is 1:200. An increase in antibody titers in this reaction is observed in the early stages of dysentery, and from the 4-5th week their titers decrease.
For express diagnostics epidemic outbreaks of dysentery, immunofluorescence reaction (RIF), RNGA with immunoglobulin (antibody) diagnosticums, enzyme immunoassay (ELISA), latex agglutination reaction (RLA), polymerase chain reaction (PCR) are used.
Coprogram- universally available and simple auxiliary method for diagnosing dysentery. When coprocytoscopy of the patient's feces, mucus, an accumulation of leukocytes with a predominance of neutrophils, erythrocytes and altered epithelial cells (various amounts) are naturally detected. Sigmoidoscopy, colonoscopy and others. expands diagnostic capabilities and allows you to monitor the progress of recovery.

DIFFERENTIAL DIAGNOSIS.

Shigellosis must be differentiated from salmonellosis, escherichiosis, food poisoning, intestinal yersiniosis, cholera, amoebiasis, balantidiasis, giardiasis, candidiasis, and some helminthiases. It should also be borne in mind poisoning with salts of heavy metals and fungi, uremic colitis, intestinal tuberculosis, chronic nonspecific enterocolitis, nonspecific ulcerative colitis.
Often there is a need to distinguish between shigellosis and acute surgical diseases (appendicitis, thrombosis of mesenteric vessels, intestinal obstruction, intestinal tumors), and also to distinguish it from acute gynecological pathology (ectopic pregnancy, adnexitis, pelvioperitonitis).
Attention should be paid to the features of dysentery in children, which affects the quality of its diagnosis and the nature of therapy. Based on research materials at NIIDI in St. Petersburg in young children the contact-household way of transmission of infection is predominantly realized, in older children- more often food (dairy products, often sour cream). The clinic of the initial period of dysentery depends on the age of the patient, the type of pathogen and the ways of infection.

In children older than 1 year, the manifest forms of the disease most often occur in 2 clinical variants:
I-th option - colitis, with varying degrees of toxicosis (weakness, headache, loss of appetite - in moderate forms and meningism, convulsions, twilight consciousness, hemodynamic disorders - in severe forms of the disease) and the development of distal colitis syndrome and a typical stool in the form of “rectal spitting” after a few hours ” with an admixture of cloudy mucus and streaks of blood. The maximum development of all symptoms is noted already on the 1st day of illness. There are no difficulties in diagnosing this form of dysentery. In the coprogram, a large number of leukocytes and erythrocytes are found, which can cover the entire field of view, and in the hemogram there is often a pronounced stab shift (up to 30% or more).
II-nd option - gastroenterocolitic. It occurs mainly in moderate and severe forms. The disease begins with repeated vomiting and severe intoxication (up to endotoxin shock), later exsicosis of I-II degree may also develop. Intestinal dysfunction appears after a few hours. The stool initially has an enteric character, only by the end of the first - second days the syndrome of distal colitis, typical for dysentery, develops (the volume of feces decreases, mucus and blood appear in them (often). Differential diagnosis of this clinical form in the first hours is difficult (it is necessary to keep in mind influenza , meningitis, food poisoning).
Regardless of the clinical variant, dysentery in children older than 1 year, in addition to the acute onset of the disease, is characterized by parallelism in the dynamics of the development of symptoms of intoxication and local syndrome, as well as the short duration of the disease.
In children of the 1st year of life, dysentery has its own characteristics, which should be taken into account in clinical diagnosis:
- The possibility of not only acute, but subacute and gradual onset of the disease, especially in children in the first months of life.
- The rarity of the colitis form of the disease with its characteristic syndrome of distal colitis, more often the development of enterocolitis and enteritis.
- The severity of the disease is not due to a neurotoxin, but to a violation of hemodynamics, water-mineral and protein metabolism.
- An admixture of blood in the stool appears less frequently than in older children, not always from the 1st day of illness.
- The course of the disease is longer (especially with Flexner's dysentery), without timely diagnosis and treatment leading to dystrophy.