Make up questions to determine intestinal diseases. Anti-epidemic measures when identifying a patient with acute bacterial intestinal infection (hereinafter referred to as ABI), gastroenterocolitis, dysentery, salmonellosis, intestinal infection of unknown etiology

Acute intestinal infection is a disease caused by microorganisms that have entered the human intestines. The causative agents of the disease are bacteria, viruses, protozoa or fungi. The source of infection is a sick person, an animal, everyday items and the environment, food, water.

Acute intestinal infections (AI) are characterized by indigestion, causing abdominal pain, diarrhea, vomiting and intoxication of the body. The disease is severe in children: the body quickly becomes dehydrated and has weak immunity.

Intestinal infections are dangerous during pregnancy: dehydration and intoxication of a woman’s body lead to miscarriage or provoke oxygen starvation of the fetus.

According to ICD 10, intestinal infections are in first place in the list, their codes are A00-A09. The most dangerous disease is cholera (ICD code 10 A00). The list of intestinal infections begins with this.

Intestinal infections are characterized by rapid spread. Transmission is by oral-fecal, nutritional and airborne routes. The infection is transmitted from person to person through unwashed hands, household items, poorly washed fruits and vegetables, and by water.

Pathogenic microorganisms are carried by insects (flies, cockroaches), sick farm animals, birds or rodents.

Pathogenic microorganisms choose the human intestine as their habitat.

Intestinal infectious diseases have similar clinical manifestations; etiology and epidemiology are different.

Intestinal infections, a list of which can be found in the medical literature, vary depending on the type of pathogen and the effect on the body. Medical reference books, books, magazines and online publications provide a list of OKIs describing the etiology, pathogenesis, clinical manifestations, methods of diagnosis and treatment.

Etiology of acute intestinal infections

Types of OKI:

Regardless of what types of microorganisms caused the disease, its symptoms are unpleasant, the treatment period is long, and the outcome is not always favorable.

Epidemiology of AEI

The reasons for the occurrence and spread of acute intestinal infections are that pathogenic microorganisms are quickly transmitted from a sick person or a carrier of infection.

Pathogenic microorganisms are resistant to environmental conditions, retain harmful qualities for a long time in the cold, and remain on objects with which an infected person has been in contact.

Pathogens leave the body infected with an intestinal infection along with feces and vomit and are transferred to surrounding household items, water, food with the help of hands, insects, and end up with sewage in water bodies. Transmission of the pathogen is “along the chain”, which leads to the emergence of an epidemic.

Classification of epidemics depending on the source of infection:

1. Water epidemics. Characterized by mass infection of people using a water source. When the use of water from the source or its disinfection is stopped, the epidemic subsides.
2. Food epidemics. As a result of eating foods that have not undergone heat treatment, or the ingestion of pathogenic microorganisms.
3. Household. A large number of sick children. Infections are transmitted through toys and household items.

Epidemics vary in intensity and seasonality.

Children who are unable to follow the rules of hygiene are susceptible to intestinal diseases.

If one child gets sick, the entire group of children is at risk.

Clinical picture of OKI

Intestinal infections are common diseases.

The clinic of all acute intestinal diseases is characterized by common manifestations:

The first symptoms of the disease appear 6-48 hours after infection.

Intestinal flu is the most common intestinal infection

Intestinal flu affects children from six months to two years. The nature of the disease is viral, the causative agent is rotavirus - a pathogenic microorganism that has a three-layer dense shell and a “wheel” shape.

Pathways and mechanism of infection with rotavirus

Rotavirus intestinal infection is transmitted by the fecal-oral route. Trillions of bacteria leave in the stool of an infected person, while a hundred units are enough to infect others. Rotaviruses are tenacious, resistant to low temperatures and remain on household items with which the patient or carrier of the virus has come into contact.

From these objects they are transferred through poorly washed hands into the oral cavity of a healthy person and settle on the mucous membranes of the stomach and intestines. In close contact, rotavirus is transmitted through the saliva of an infected person.

Rotavirus enters through unboiled water and food that is poorly washed or has not undergone sufficient heat treatment.

In the event of mass infection, a rotavirus epidemic occurs. An outbreak of the disease occurs in late autumn and winter. Foci of infection are in crowded places - kindergartens, schools, nursing homes, dormitories.

In order to prevent the mass spread of intestinal infections in schools, preschool institutions, groups, and enterprises, an “Operational Action Plan for the Prevention of Acute Intestinal Infections” is being drawn up.

Sources of infection

Sources of infection are sick adults and children who have already shown symptoms of the disease, or virus carriers - persons in whose body there is a virus, but there are no signs of the disease.

Rotavirus gets into the water supply system and water bodies with wastewater, where swimming leads to infection.

Incubation period and duration of the disease

The incubation period lasts up to six days.

The duration of illness for intestinal rotavirus infection is 2 weeks. The disease goes through two phases: acute and convalescent phase. The first phase lasts 7 days: the body fights the infection, the symptoms are severe. During the second phase, the body develops immunity, and gradual recovery begins.

Symptoms

Clinical manifestations of intestinal flu are similar to acute respiratory viral infections in the first days of the disease:

• temperature rise to 39 degrees;
• headache;
• sore throat and redness,
• runny nose, cough, headache;
• pain in the abdominal area;
• diarrhea;
• bouts of vomiting;
• lack of appetite;
• lethargy and weakness.

The absence of high temperature distinguishes food poisoning from intestinal infections caused by pathogenic bacteria or viruses.

A dangerous manifestation in the acute phase of the disease is dehydration. The patient must be given water.

Features of the course of the disease in adults and children

The three-layer shell makes rotaviruses invulnerable to the environment of the gastrointestinal tract and intestinal enzymes. During the course of the disease, the virus infects enterocytes - intestinal epithelial cells - and leads to their death, modifying the epithelium. Severe diarrhea and severe dehydration of the body occur; This is the pathogenesis of the disease.

Rotavirus in children

What is connected with the characteristics of the child’s body and immunity. OCI is a common disease among children from six months to two years.

Enterovirus and rotavirus infections often occur in childhood and are similar to each other. At first, parents confuse them with acute respiratory infections, as there is a jump in temperature, cough, watery eyes, and runny nose. Then vomiting and diarrhea follow.

For both enterovirus and rotavirus infections, the symptoms are high fever, diarrhea and vomiting, abdominal pain, lack of appetite, and weakness.

Unlike rotavirus, enterovirus affects, in addition to the gastrointestinal tract, the liver, heart and nervous system of the child and affects vision.

Dehydration and intoxication are manifestations of the disease. Dehydration of the body occurs so quickly that the child does not produce urine or tears. The pain disrupts the baby's sleep patterns.

Treatment boils down to drinking salted water or administering fluids intravenously.

Breastfed children are less susceptible to gastrointestinal infections due to the quality of mother's milk.

Due to the high infant mortality rate due to intestinal infections, pediatrics pays special attention to the prevention, diagnosis and treatment of acute intestinal infections in children.

Today, there are manuals and scientific articles devoted to the problems of child nutrition, methods of feeding them safely, treatment methods and the development of the immune system.

Rotavirus in adults

Features of the manifestation of intestinal flu in adults are that the course of the disease occurs with less pronounced symptoms. This is due to the protection of the adult organism - the acidic environment of the stomach and the content of immunoglobulin A in the secretion produced by intestinal enterocytes.

The manifestation of the disease in an adult is intestinal disorder. A person is a carrier of infection, not suspecting that an intestinal disease is hidden behind the mild symptoms.

Rotavirus in pregnant women

Does not pose a danger to the fetus. Dehydration of a woman’s body provokes oxygen starvation of the fetus. Therefore, it is important to prevent dehydration and maintain bed rest at the first signs of intestinal flu. Preventive measures and hygiene will help reduce the risk of intestinal infection.

Diagnosis of rotavirus infection

Identification of signs of disease - through examination of the patient and conversation. Data on body temperature is recorded, blood pressure is measured, and the abdominal area is palpated. They conduct examinations of the patient’s urine, feces and blood, and examine the mucous membranes of the rectum.

Differential diagnostics – for salmonellosis, cholera, dysentery, food toxic infections.

Determining the virus based on the analysis of RSC or RTHA in the first days is impossible: antibodies are produced in an adult after a few days, in a newborn - after a few months. The diagnosis is confirmed based on the epidemiological situation and seasonality.

Features of care for patients with acute intestinal infections in a hospital setting

In severe cases of illness or when it is not possible to isolate the patient at home, a patient with intestinal infections is admitted to a hospital.

During the treatment process, care for patients with acute intestinal infectious diseases is important.

Prevention of complications of intestinal infections is an integral part of nursing care on the patient’s path to recovery.

Nursing interventions provide:

• isolation of the admitted patient from those recovering;
• control over regular wet cleaning with bleach in the patient’s room and ventilation of the room;
• feces disinfection;
• support for rehydration regime;
• control of diet and hygiene;
• control of body temperature, pressure, condition of mucous membranes and skin.

Care must be taken to care for patients with severe symptoms (fever, delirium, clouding of consciousness) and for children.

In practice, all registered OCIs are usually divided into three main groups:

• diseases caused by an unknown pathogen (about 70% of cases);
• acute intestinal infections caused by an identified pathogen (about 20%);
• bacterial dysentery (about 10%).

The fact that 70% of cases of AEI occur in diseases with an unknown pathogen can be considered a consequence of the “syndromic” principle of diagnosis, generally accepted for AEI, which is fully justified in diseases that are not of an epidemic nature. In fact, with sporadic acute intestinal infections (and they are the majority), the similarity of the clinical picture and course of diseases of various etiologies makes it possible not to waste time on accurately identifying the causative agent, since this does not significantly affect the choice of treatment strategy and tactics. In case of epidemic acute intestinal infections, the earliest possible isolation and identification of the causative agent of the disease, on the contrary, becomes the most important task, which, unfortunately, requires a significant investment of time and the presence of a well-equipped laboratory.

It is important that the most extensive group of acute intestinal infections of unknown etiology also includes the majority of so-called foodborne toxic infections (PTI) - this group consists of approximately 20 etiologically different, but pathogenetically and clinically similar diseases that do not pose an epidemic danger.

In more than half of the cases, the etiology of acute intestinal infections cannot be established either clinically or laboratory. This task, as well as the choice of pathogenetic treatment, especially cannot be solved (and is not posed) at the stage of prehospital care. The efforts of the emergency medical technician (EMS) should be aimed at:

• correction of severe violations of the vital functions of the patient’s body;
• differentiation of infectious, therapeutic or surgical genesis of the disease;
• deciding on the need to hospitalize a patient for specialized treatment or anti-epidemic measures.

Clinical picture of OKI

OKI - diseases of various etiologies and semiotics - combine a common method for all these conditions, predominantly fecal-oral, of transmission of the pathogen and the development as a result of this characteristic symptom complex of acute diarrhea ().

At the same time, the severity of diarrhea syndrome, as well as the severity of the general condition, possible outcomes and treatment strategy for the disease are determined by the causative agent of the infection. Despite the relativity of syndromic preclinical diagnosis of acute intestinal infections, it is possible to identify the signs that are most characteristic of diarrhea of ​​various etiologies. Thus, bacterial diarrhea (BD) is distinguished by a more severe clinical course and a more unfavorable prognosis compared to viral diarrhea, since the pathophysiological mechanisms of BD are damage to the mucous membrane of the gastrointestinal tract by bacterial enterotoxins or as a result of invasion of microorganisms into epithelial cells. The incubation period for BD can last from 6-8 hours to 7-10 days, but most often it is about 3 days. The shortest incubation period is for coccal infections and salmonellosis. The onset of BD is accompanied by severe intoxication, a significant deterioration in general health, dehydration, headache, fever up to 38-39°C, nausea and vomiting. When the infection generalizes, symptoms of irritation of the meninges, muscle and osteoarticular pain may appear. BD is always accompanied by painful tenesmus and cramping severe pain in the abdomen, and in dysentery it leads to bloody stools. Often, men with BD develop Reiter's syndrome (arthritis, conjunctivitis, urethritis). In the acute phase of the disease, specific symptoms of a particular BD pathogen also appear. The prognosis of BD is always alarming, and with a clinically defined course, the disease in all cases requires hospitalization and epidemiological assessment.

PTI also belongs to BD, as it is caused by opportunistic bacteria and in some cases has a group, explosive nature. However, in the vast majority of cases, IPT occurs sporadically with the development of acute gastritis, gastroenteritis or gastroenterocolitis, with varying degrees of dehydration and intoxication and have a favorable prognosis.

With diarrhea of ​​viral etiology (VD), the integrity of the mucous membrane of the gastrointestinal tract in most cases is not impaired and the colon is rarely involved in the process. The incubation period is usually shorter than with epidemic BD. Acute viral gastroenteritis, although accompanied by fever and a disturbance in the general condition of the patient, rarely leads to severe intoxication, the development of a pronounced inflammatory reaction and dehydration of the patient's body. Significant differential criteria for VD include the absence of severe abdominal pain in these diseases, watery rather than mucopurulent and bloody stool. VD is often accompanied by acute respiratory disease, especially in children. The duration of VD rarely exceeds 3 days, and in general the disease has a favorable prognosis. Patients with a relatively mild course of VD do not require hospitalization.

In the modern classification of ACI, the so-called special forms of the disease are distinguished:

• traveler's diarrhea;
• diarrhea in homosexual men;
• diarrhea in HIV-infected people;
• antibiotic-associated diarrhea;
• syndrome of bacterial overgrowth in the gastrointestinal tract.

Of the special forms of ACI, only one of the variants of antibiotic-associated diarrhea is important for the practice of an emergency physician - pseudomembranous colitis. This disease develops during or significantly after taking antibacterial drugs and is associated with colonization of the intestine by the opportunistic microorganism clostridium difficile. Pseudomembranous colitis occurs with high fever, bloody diarrhea, abdominal pain and is accompanied by significant intoxication with all possible complications of acute profuse diarrhea. If pseudomembranous colitis is suspected, the patient should be hospitalized in an infectious diseases hospital.

Preclinical and differential diagnosis of OD

A comprehensive study of the history of the present disease is the first step in examining patients who have characteristic signs of acute intestinal infection ().

In patients it is necessary to find out:

• when and how the disease began (for example, sudden or gradual development of the disease, the presence of an incubation or prodromal period);
• the nature of the stool (watery, bloody, mixed with mucus or pus, fatty, etc.);
• stool frequency, quantity and pain of bowel movements;
• the presence of symptoms of dysentery (fever, tenesmus, blood and/or pus in the stool).

In a conversation with the patient, it is very important to establish the presence and, what is especially important, the development of subjective and objective manifestations of dehydration (thirst, tachycardia, orthostatic reactions, decreased diuresis, lethargy and disturbances of consciousness, convulsions, decreased skin turgor) and intoxication (headache, nausea, vomiting, muscle pain).

In addition, in all cases it is necessary to identify possible risk factors for DCI: travel to countries with an epidemic situation unfavorable for infectious diarrhea; occupation; recent consumption of unsafe foods (for example, undercooked meats, raw eggs or shellfish, unpasteurized milk and juices); swimming in contaminated bodies of water or drinking water from them (for example, water from a lake or river); staying in rural areas, visiting “children’s” zoos, contact with wild or domestic animals; being surrounded by patients with similar symptoms; regular or recent use of medications (antibiotics, antacids, antidiarrheals); the presence of medical factors predisposing to the development of infectious diarrhea (HIV, taking immunosuppressants, a history of gastrectomy, early childhood or old age); addiction to anal sex; belonging to decreed groups of the population (food workers, teachers of child care institutions).

At the prehospital stage, AEI must be differentiated from a number of acute non-infectious diseases of surgical, therapeutic, gynecological and other profiles. The only purpose of the differential diagnosis in this case is to choose the direction of hospitalization of the patient. The main criteria for differential diagnosis are reflected in our proposed algorithm for prehospital medical care (Fig. 2).

The prevalence of misdiagnosis of DCI is illustrated by data from DuPont H. L. (1997). The analysis data provided by the author of more than 50 thousand cases of hospitalization of patients with ACI state that in 7.4% of cases this diagnosis was established for diseases such as acute appendicitis, acute cholecystopancreatitis, strangulating intestinal obstruction, thrombosis of mesenteric vessels, myocardial infarction, lobar pneumonia, decompensation of diabetes mellitus, hypertensive crisis. On the contrary, the above diseases were misdiagnosed in patients with ACI in 11.1% of cases.

Prehospital therapy for OD

The greatest threat to patients with ACI is the development of dehydration and associated arterial hypotension against the background of intoxication, which provokes a drop in blood pressure and dysfunction of the central nervous system. The scope of prehospital therapy for acute intestinal infections is based on monitoring the vital functions of the patient’s body: the state of consciousness and external respiration function, the level of blood pressure and hydration of the patient. If the emergency medical team is appropriately equipped, therapy for clinically significant hypovolemic and infectious-toxic arterial hypotension should be carried out under the control of central venous pressure. In accordance with standard recommendations, therapy at this stage is aimed at:

• to restore heart rhythm;
• to optimize the volume of circulating blood;
• to eliminate hypoxia and normalize acid-base balance;
• for inotropic/vasopressor therapy.

To eliminate hypoxia, the patient is prescribed oxygen therapy with a gas mixture with a 35% oxygen content.

Rehydration of the patient begins with the diagnosis of dehydration, the severity of which can vary from I to IV degrees ().

With dehydration of degrees I and II (85-95% of patients with ACI), replenishment of fluid loss can and should be done orally. WHO recommends the following solutions for oral rehydration: 3.5 g NaCl, 2.5 g NaHCO 3 (or 2.9 g sodium citrate), 1.5 g KCl and 20 g glucose or its polymers (for example, 40 g sucrose , or 4 tablespoons of sugar, or 50-60 g of boiled rice, corn, sorghum, millet, wheat or potatoes) per 1 liter of water. This produces a solution containing approximately 90 mmol Na, 20 mmol K, 80 mmol Cl, 30 mmol HCO3 and 111 mmol glucose. You can successfully use any of the ready-made solutions for oral rehydration (citroglucosalan, rehydron, gastrolit). The amount of liquid drunk should be 1.5 times greater than its loss through feces and urine. Compensation for dehydration is accompanied by an obvious decrease in thirst, normalization of diuresis and improvement in the general condition of the patient.

Dehydration of degrees III and IV, severe nausea or vomiting, as well as the unconscious state of the patient require emergency infusion therapy. For intravenous rehydration, polyionic crystalloid solutions are used: trisol, quartasol, chlosol, acesol. Less effective is the administration of monoionic solutions (saline sodium chloride solution, 5% glucose solution), as well as unbalanced polyionic solutions (Ringer's solution, mafusol, lactasol). Colloidal solutions (hemodez, rheopolyglucin, refortan) are administered only in cases of persistent hypotension, after restoration of the volume of circulating blood as a whole. In severe cases, the infusion of water-electrolyte mixtures begins at a volume rate of 70-90 ml/min, in case of moderate severity of the patient's condition - at a volume rate of 60-80 ml/min. In some cases, the required infusion rate is ensured by simultaneous infusion into 2-3 veins. After stabilization of blood pressure, the infusion rate is reduced to 10-20 ml/min. To prevent the progression of dehydration, the development of hemodynamic failure, pulmonary edema, pneumonia, disseminated intravascular coagulation syndrome and acute renal failure, the volume of fluid administered after stabilization of the patient's condition can be 50-120 ml per 1 kg of weight.

Prescribing antibacterial therapy for moderate and severe acute intestinal infections at the preclinical stage is not only not part of the tasks of the emergency physician, but is also categorically contraindicated, since it can significantly worsen the patient’s condition and complicate laboratory verification of the causative agent of the disease. The increasing threat of infections caused by antibiotic-resistant strains of microorganisms, the presence of undesirable reactions when using antimicrobial drugs, superinfection associated with the eradication of normal microflora by antibacterial agents, and the possibility of induction of certain virulence factors in enteropathogens by antibiotics (for example, induction by fluoroquinolones of the phage responsible for the production of Shigella toxin ), force you to carefully weigh the pros and cons when deciding on antimicrobial therapy and prescribe it only after an accurate diagnosis of the causative agent of acute intestinal infections. In connection with the above, antibacterial drugs are especially not recommended for the gastroenteric variant of OD of any severity, for a mild, erased course of the colitis variant and during the period of convalescence for any form of intestinal disease.

Empirical prescription of antibiotics is possible in cases of mild to moderate acute intestinal infections of any etiology, as well as in travelers' diarrhea, the most likely causative agent of which is enterotoxigenic strains of E. coli or other bacterial pathogens. In this case, adults are prescribed fluoroquinolones, and children are prescribed co-trimoxazole, the use of which can reduce the duration of the disease from 3-5 to 1-2 days. For this category of patients, who, as a rule, do not require hospitalization, it is possible to recommend outpatient use of intestinal antiseptics: ercefuril, intetrix or enterosediva in standard doses for 5-7 days, as well as non-antimicrobial drugs that alleviate diarrhea ().

Just as dangerous as antibiotics in terms of worsening intoxication is the use of strong antidiarrheal drugs (imodium) and antinausea drugs (cerucal, torecan) during acute intestinal infections of any clinical course.

Of particular importance in acute intestinal infections is the correction of intestinal microbiocenosis with probiotics, carried out at various stages of treatment: in the acute period - in order to competitively displace pathogenic microflora, in convalescents - to ensure rehabilitation processes. Early, no later than the second day of illness, administration of bifidumbacterin forte in loading doses (50 doses 3 times every 2 hours on the first day of treatment) followed by maintenance doses (30 doses per day, according to indications - up to 6 days) is very effective.

The IV generation probiotic Bifidumbacterin Forte provides high local colonization of the intestinal mucosa, elimination of pathogenic and opportunistic microflora. A positive clinical effect for moderate salmonellosis was noted after 1-2 days, for severe salmonellosis and dysentery - by the end of the course. Of the probiotics prepared on the basis of microorganisms of the genus Bacillus, the drug of choice is biosporin, prescribed 2 doses 2-3 times a day for 5-7 days. The drug has a pronounced antibacterial, antitoxic and immunomodulatory effect, induces the synthesis of endogenous interferon, stimulates the activity of blood leukocytes and the synthesis of immunoglobulins. If enteric syndrome predominates, enterol obtained from Saccharomycetes Boulardii is recommended. It is prescribed 250 mg 2 times a day for 5 days. During the period of convalescence, along with traditional pathogenetic agents (stimulants of repair, general and local immune response), it is advisable to use preparations of obligate flora, optimally Bifidumbacterin forte, which has a stabilizing effect on the intestinal microbiocenosis and homeostatic processes.

Despite the expansion of capabilities for pathogen verification and a large selection of etiopathogenetic therapy methods that have appeared in the doctor’s arsenal over the past 20 years, acute intestinal infections today are still associated with high mortality. Thus, according to N.D. Yushchuk, with PTI and salmonellosis the mortality rate is about 0.1%, and with dysentery - 1.4%, while the cause of 20% of deaths in bacterial dysentery and 44.4% of deaths in all cases The remaining ACI is infectious-toxic shock. The reasons for such a high mortality rate probably lie in an inadequate assessment of the prognosis and severity of the patient’s condition with ACI and the failure to provide him with emergency care at the prehospital stage, including for reasons of insufficient instrumental, medicinal and information support. We would like to hope that our proposed simple algorithm for prehospital medical care for OD (Fig. 2) will prove useful for practicing doctors and their patients.

Literature

1. DuPont H. L. // Am. J. Gastroenterol. 1997; 92: 1962-75.
2. Kehl K. S., Havens P., Behnke C. E., Acheson D. W. // J. Clin. Microbiol. 1997; 35:2051-4.
3. Lobzin Yu. V., Korvyakova E. R., Litusov N. V., Zakharenko S. M. Modern pharmacotherapy of acute intestinal infections. VTP Center of the Ministry of Defense of the Russian Federation.
4. Mc Qbaid K. R. Diarrhea. Current medical diagnosis and treatment. 38th ed. Appleton & Lange, 1999, p. 546.
5. Springis D. et al. Emergency therapy. Geotar, Medicine, 2000. P. 30.
6. Yushchuk N.D., Brodov L.E. Principles of diagnosis and treatment of acute intestinal infections // Attending Physician. 1999. No. 7. P. 40.

Table 1. Typical clinical manifestations of acute intestinal infections

• Acute profuse diarrhea
• Dehydration
• Intoxication
• Abdominal pain
• Fever
• Blood in stool

Intestinal infections are one of the most common diseases in the world. Their prevalence among the population is extremely high, both in the children's age group and in adults. When we talk about intestinal infection, we mean acute intestinal disease.

Acute intestinal infections (AI) are a group of acute human infectious diseases caused by various infectious agents (mainly bacteria), with a nutritional mechanism of infection, manifested by fever and intestinal syndrome with the possible development of dehydration and severe course in children and the elderly.
The incidence of intestinal infections in the world, and in particular in Russia, is quite high. Every year more than 500 million people get sick on the planet. The incidence rate in Russia reaches 400 or more cases per 100 thousand population. The structure of childhood morbidity and mortality suggests that acute intestinal diseases are in third place.

Causes of intestinal infections

The digestive tract consists of the oral cavity, pharynx, esophagus, stomach, small intestine (including the duodenum, jejunum, ileum), and large intestine. In the saliva of the oral cavity there is a substance - lysozyme, which has a bacteriostatic effect. This is the first protective barrier. The mucous membrane of the stomach has glands that produce gastric juice (consisting of hydrochloric acid and pepsin). Hydrochloric acid is the second barrier for pathogenic microorganisms that can die in it (however, this does not always happen). The mucous membrane of the small intestine is covered with numerous villi that participate in parietal digestion and perform protective and transport functions. In addition, the intestinal mucosa contains secretory immunoglobulin - IgA, which plays a role in the immunity of the human body.

The microflora inhabiting the intestines is divided into obligate (mandatory for presence in the intestines), which includes bifidobacteria, lactobacilli, E. coli, bacteroides, fusobacteria, peptococci. Obligate flora makes up 95-98% of all representatives. The function of obligate flora is protective due to competitive presence and participation in digestive processes. Another group of microorganisms inhabiting the intestines is called facultative (additional) flora, which includes staphylococci, fungi, opportunistic microorganisms (Klebsiella, streptococci, Proteus, Pseudomonas aeruginosa, clostridia and others). Additional flora can also participate in the digestion process through the production of certain enzymes, however, opportunistic flora with a certain growth can cause the development of intestinal syndrome. All other flora that enters from the outside is called pathogenic and causes an acute intestinal infection.

What pathogens can cause acute intestinal infection?

There are several types of intestinal infections depending on the etiology:

1. Intestinal bacterial infection: salmonellosis (Salmonellae enteritidis et spp.), dysentery (Shigellae sonnae et spp.), yersiniosis (Iersiniae spp.), escherichiosis (Esherihiae coli enteroinvasive strains), campylobacteriosis (enteritis caused by Campylobacter), acute intestinal infection caused by Pseudomonas aeruginosa ( Pseudomonas aeruginosa), clostridia (Clostridium), Klebsiellae (Klebsiellae), Proteus spp., staphylococcal food poisoning (Staphilococcus spp.), typhoid fever (Salmonellae typhi), cholera (Vibrio cholerae), botulism (botulinum toxin poisoning) and others .
2. AEI of viral etiology(rotaviruses, Norfolk group viruses, enteroviruses, coronaviruses, adenoviruses, reoviruses).
3. Fungal intestinal infections(usually fungi of the genus Candida).
4. Protozoal intestinal infections(giardiasis, amoebiasis).

Causes of intestinal infections

The source of infection is a patient with a clinically pronounced or erased form of intestinal infection, as well as a carrier. The contagious period is from the moment the first symptoms of the disease appear and the entire period of symptoms, and for a viral infection - up to 2 weeks after recovery. Patients release pathogens into the environment with feces, vomit, and less often with urine.

The mechanism of infection is nutritional (that is, through the mouth). The routes of infection are fecal-oral (food or water), household, and for some viral infections - airborne. Most pathogens of acute intestinal infection are highly resistant in the external environment and retain their pathogenic properties well in the cold (in the refrigerator, for example). Transmission factors are food products (water, milk, eggs, cakes, meat, depending on the type of intestinal infection), household items (dishes, towels, dirty hands, toys, door handles), swimming in open water. The main role in the spread of infection is given to compliance or non-compliance with personal hygiene standards (washing hands after using the toilet, caring for the sick, before eating, disinfecting household items, allocating personal utensils and towels to the sick person, reducing contact to a minimum).

Susceptibility to intestinal infections is universal, regardless of age and gender. The most susceptible to intestinal pathogens are children and the elderly, people with diseases of the stomach and intestines, and people suffering from alcoholism.

Factors predisposing to the development of intestinal infection in children: bottle-fed children, premature babies; violation of the rules for introducing complementary foods without the necessary heat treatment; warm season (usually summer); various types of immunodeficiencies in children; pathology of the nervous system in the perinatal period.

Immunity after an infection is unstable and strictly type-specific.

General symptoms of acute intestinal infections

The incubation period (from the moment the pathogen enters until the first signs of the disease appear) lasts from 6 hours to 2 days, rarely longer.

Almost any intestinal infection is characterized by the development of 2 main syndromes, but to varying degrees of severity:

1. Infectious-toxic syndrome(ITS), which is manifested by a temperature ranging from subfebrile numbers (37º and above) to febrile fever (38º and above). In some infections there is no temperature at all (for example, cholera), and the absence of temperature or a slight short-term rise is typical for food poisoning (staphylococcal, for example). Fever may be accompanied by symptoms of intoxication (weakness, dizziness, body aches, nausea, and sometimes vomiting due to high fever). Often, an infectious-toxic syndrome is the beginning of an acute intestinal infection, lasting until the appearance of the second syndrome from several hours to a day, rarely longer.

2. Intestinal syndrome. Manifestations of intestinal syndrome may be different, but there are similarities in symptoms. This syndrome can manifest itself as a syndrome of gastritis, gastroenteritis, enteritis, gastroenterocolitis, enterocolitis, colitis.

Gastritis syndrome is characterized by the appearance of pain in the stomach (epigastric region), constant nausea, vomiting after eating and drinking water, and even a sip of liquid can cause it. Vomiting can be repeated, bringing short-term relief. It is possible to liquefy the stool over a short period of time, sometimes once.

Gastroenteritis syndrome accompanied by abdominal pain in the stomach and umbilical region, vomiting, and the appearance of frequent stools, first of a mushy nature, and then with a watery component. Depending on the cause of the occurrence, the color of the stool may change (greenish with salmonellosis, light brown with escherichiosis, for example), as well as mucus and undigested food debris may appear.

Enteritis syndrome characterized by the appearance of only stool disorders in the form of frequent watery stools. The frequency depends on the type of pathogen and the degree of its infectious dose reaching a particular patient.

Gastroenterocolitis syndrome manifested by vomiting and frequent loose stools, abdominal pain becomes widespread and almost constant, defecation becomes painful and does not bring relief, often with blood and mucus in the stool. Some acts of defecation with scanty mucous discharge.

Enterocolitis syndrome characterized only by severe pain along the entire perimeter of the abdomen, frequent stool mixed with scanty discharge.

Colitis syndrome is manifested by fights in the lower abdomen, mainly on the left, acts of defecation are painful, the contents are scanty with an admixture of mucus and blood, false urge to stool, lack of relief at the end of defecation.

Syndromes such as gastroenteritis, gastroenterocolitis and enterocolitis are characteristic of salmonellosis, enterocolitis and colitis - for dysentery, escherichiosis is accompanied by the development of gastroenteritis, enteritis is the leading syndrome of cholera, gastritis syndrome can accompany food poisoning, but it can also be gastroenteritis, viral intestinal infections occur more often in form of gastroenteritis.

Features of acute intestinal infection in children

More severe course of acute intestinal infection,
rapid development of symptoms of dehydration,
a higher proportion of viral intestinal damage than in the adult age group.

When an acute intestinal infection occurs, a child quickly develops dehydration and desalination of the body, resulting in high mortality; In addition, even opportunistic microorganisms are characterized by the ability to cause a severe process in the intestines of children.

Complications of acute intestinal infections

1) Dehydration (dehydration)– pathological loss of water and salts in an unnatural way (vomiting, loose stools). There are 4 degrees of dehydration in adults:
- 1st degree (compensated) – loss of body weight up to 3% of the original; 2nd degree (transitional) – loss of body weight 4-6% of the original; 3rd degree (subcompensated) – 7-9% of the original; 4th degree (decompensated) – more than 10% loss of body weight from the initial one.

In children, grade 3: 1 degree (weight loss up to 5% of the original), 2 degree (6-9%), 3 degree (algid) - more than 10% loss of body weight from the original.

In addition to weight loss, concerns about dry skin and mucous membranes, thirst, decreased skin elasticity, and hemodynamic disturbances (increased heart rate, decreased blood pressure). Thirst does not always happen: if there is a salt-deficient type of dehydration (this happens more often with repeated vomiting), then there may not be thirst. If the water deficiency type of dehydration is present, then thirst is the main symptom.

2) One of the manifestations of fulminant dehydration: dehydration shock with possible death. There is severe dehydration and hemodynamic disorders (critical drop in blood pressure).

3) Infectious-toxic shock: occurs against a background of high temperature, often at the onset of the disease, and is accompanied by high toxinemia (high concentration of bacterial toxins in the blood), serious hemodynamic disturbances and possible death.

4) Pneumonia(pneumonia).
5) Acute renal failure.

Differential diagnosis (non-infectious “masks” of intestinal infections)

At the stage of making a preliminary diagnosis of an acute intestinal infection, the doctor has to differentiate the intestinal infection from other conditions and diseases, the symptoms of which may also include vomiting and diarrhea (loose stools). An important role is played by a correctly collected medical history (medical history), in which it is necessary to describe in as much detail as possible the symptoms and the timing of their onset, the severity of complaints and their duration.

Gastroenteritis syndrome can accompany poisoning with mushrooms, heavy metal salts, and fish and shellfish poisons. Unlike infectious diarrhea, with the above poisonings there will be no ITS (infectious toxic syndrome) - neither fever nor symptoms of intoxication.

The syndrome of enterocolitis or colitis (with blood in the stool) occurs with UC (nonspecific ulcerative colitis), intestinal neoplasms, Crohn's disease, diverticular disease and others. Each of these conditions has other specific symptoms that characterize the disease. In particular, with Crohn's disease, diarrhea will be chronic, prolonged, cramping abdominal pain, weight loss, anemia. With UC - prolonged low-grade fever, prolonged diarrhea with blood, weight loss, pain in the lower left abdominal region, and others.

Most often, a practitioner must differentiate an acute intestinal infection from mushroom poisoning, ulcerative colitis, acute appendicitis, rectal cancer, thrombosis of mesenteric vessels, and acute intestinal obstruction.

If there is significant abdominal pain, especially in children, the first step should be to visit an emergency surgeon to rule out surgical pathology.

It is no secret that the appearance of frequent loose stools for most people is not a reason to see a doctor. Most try to use various drugs and methods to stop diarrhea and restore impaired health. At the same time, a simple (as it seems at first glance) intestinal infection can turn into a serious problem with long-term disability.

Symptoms that require you to see a doctor immediately:

1) early childhood (up to 3 years) and preschool age of the child;
2) elderly people (over 65 years old);
3) frequent loose stools more than 5 times a day in an adult;
4) repeated vomiting;
5) high fever with diarrhea and vomiting;
6) blood in the stool;
7) cramping pain in the abdomen of any localization;
8) severe weakness and thirst;
9) the presence of chronic concomitant diseases.

What absolutely should not be done if you suspect an acute intestinal infection:

If frequent loose stools appear, accompanied by abdominal pain and fever, then:

1) Painkillers should not be used. In the case of hidden symptoms of any surgical pathology (cholecystitis, appendicitis, intestinal obstruction and others), pain relief can complicate the diagnosis and delay the provision of timely specialized care.
2) You cannot independently use fixing agents (astringents) - such as immodium or loperamide, lopedium and others. In acute intestinal infection, the bulk of pathogen toxins are concentrated in the intestines, and the use of such drugs contributes to their accumulation, which will aggravate the patient’s condition. The course of intestinal infection will be favorable with timely emptying of intestinal contents along with pathogen toxins.
3) You cannot do enemas yourself, especially with hot water.
4) You cannot use heating procedures on the abdomen (a heating pad with hot water, for example), which certainly increases the inflammatory process, which will aggravate the patient’s condition.
5) If you have symptoms of an acute intestinal infection and suspect a surgical pathology, you should not hesitate and try to treat with improvised means (folk, homeopathic and others). The consequences of delaying seeking medical help can be very serious.

Laboratory diagnosis of acute intestinal infection

A preliminary diagnosis is made after a clinical and epidemiological examination, which includes contact with the patient, possible cases of intestinal infection among the immediate environment, consumption of poor quality products, products without water treatment and heat treatment, failure to comply with personal hygiene rules, as well as symptoms of the disease ( the onset of the disease, the main symptoms characteristic of a particular infection).

Already at this stage, an unmistakable diagnosis is possible (for example, in the case of the outbreak nature of the disease and the presence of similar patients in the infectious diseases clinic, in the presence of specific symptoms - blood in the stool, false urge to stool, temperature during dysentery, for example; copious watery stools without odor or impurities , without fever - with cholera), due to which in some cases, after collecting all materials for laboratory testing, specific treatment is prescribed already at the stage of preliminary diagnosis.

An experienced doctor, in the presence of obvious symptoms, may suspect a certain intestinal infection and prescribe adequate treatment.

The final diagnosis is made after laboratory confirmation:

1) Bacteriological methods (seeding materials for research on special media and growing bacterial colonies). Materials can be feces, vomit, gastric lavage, food debris, water samples. Preliminary sowing and the result can be issued on the 2nd-3rd day.
2) Serological methods (detection of specific antibodies in the blood) ELISA, RNGA - paired blood sera are necessarily taken with an interval of 10-14 days.
3) PCR diagnostics in biological fluids (for example, L-form salmonella). The result is issued on the same day.
Instrumental diagnostic methods: sigmoidoscopy, colonoscopy, irigoscopy.

Treatment for acute intestinal infection

1. Organizational and routine measures. All young children are subject to hospitalization
age with any severity of intestinal infection due to the risk of rapid development of dehydration syndrome. Adults are hospitalized for moderate and severe forms of acute intestinal infection, as well as when it is impossible to isolate the patient (living in small families with a shared toilet, dormitories, closed organized institutions - orphanages, etc.). For the entire period of fever, bed rest, then semi-bed rest until the loose stools stop.

Diet therapy (table No. 4 according to Pevzder). In the acute period of the disease - slimy soups, weak meat broths, pureed lean meat, boiled lean fish, scrambled eggs, cereals, white stale bread and crackers, dry uneaten cookies, baked apples without peel.
Excluded: milk, seasonings, spices, smoked meats, canned food, garlic, green onions, radishes, alcohol. They are transferred to the general table carefully and gradually over 3-4 weeks. Products such as milk and refractory fats are poorly digested for another 3 months.

2. Drug treatment of acute intestinal infection.

1) Rehydration therapy(replenishment of fluid loss and detoxification of the body). It is carried out for any acute intestinal infection in 2 stages: 1) elimination of symptoms of dehydration at the moment, 2) replenishment of ongoing losses.
You can take the liquid orally (drinking regimen in the absence of vomiting and the urge to do so), as well as parenterally (intravenous infusions of solutions). How to calculate the volume of oral rehydration at home with 1 degree of dehydration and outpatient treatment: this is 30 ml/kg of body weight per day in an adult, and 30-50 ml/kg/day in children. You need to drink the liquid in small portions every 5-10-15 minutes, warm. These are solutions of rehydron, citroglucosolan, enterodez. Intravenous rehydration is carried out only in a hospital setting under strict control of water-salt metabolism indicators.

2) Pathogenetic and syndromic therapy.
- Antidiarrheal drugs: enterosorbents (polyphepam, white coal, Filtrum, Lactofiltrum, Enterosgel and others), smecta, bactisubtil, Helac-Forte.
- Probiotics (linnex, acipol, acylak, bion3, bifidumbacterin forte, bifiform, bifistim and many others),
- Intestinal antiseptics (intetrix, enterol, entero-sediv, intestopan, enterofuril)
- Enzymes (pancreatin, creon, ermital, micrazim, mezim and others).
- Antibacterial drugs of the fluoroquinolone group only prescribed by a doctor!
- Probiotics (linnex, acipol, acylak, bion3, bifidumbacterin forte, bifiform, bifistim and many others).

Rehydration therapy should be carried out at the first symptoms of an intestinal infection, and treatment with enterosorbents should also be started at the first symptoms. Intestinal antiseptics and antibacterial agents will not help with a viral infection, but they can be prescribed by a doctor until a definitive diagnosis is confirmed or to prevent a secondary bacterial infection. On the third day of treatment with antibacterial agents, be sure to start taking probiotics to restore intestinal microflora.

Prognosis of acute intestinal infection

The outcomes can be both favorable (recovery) and unfavorable (formation of chronic forms, carriage). In the children's age group, in 25% of cases, the outcome of intestinal infection can be the formation of gastrointestinal tract pathology in the form of pancreatic dysfunction, biliary tract disorders, intestinal dysbiosis, and functional dyspepsia.

Prevention of acute intestinal infection comes down to the following measures:

1) compliance with personal hygiene rules;
2) drinking boiled or bottled water;
3) washing vegetables and fruits before consumption with running water, and for small children - with boiled water;
4) thorough heat treatment of the necessary food before consumption;
5) short-term storage of perishable foods in the refrigerator;
6) do not accumulate garbage;
7) monitor the cleanliness of the home and the sanitary maintenance of the toilet room and bathroom.

Infectious disease doctor N.I. Bykova

Only correct answers are given!!!

Typhoid fever tests

1. Define typhoid fever.

1. Acute infectious intestinal disease caused by typhoid bacillus, typical anthroponosis.

2. Name the causative agent of typhoid fever.

1 Typhoid bacillus (salmonella typhi).

1. Sick person.

2. Bacteria carrier.

4. Path of infection.

1. Enteral (food).

5. List the main pathogenetic points in the development of typhoid fever.

1. Bacteria enter the lower part of the small intestine and multiply with the development of inflammation.

2. The entry of bacteria through the lymphogenous route into the lymphatic apparatus of the small and large intestines with the development of inflammation.

3. Hematogenous generalization of infection.

4. Elimination of the pathogen with urine, feces, and bile.

5. Increased proliferation of infection in the bile ducts.

6. Bacteria enter the intestines with bile and develop a hyperergic reaction with the formation of necrosis.

6. Name the localization of local inflammatory changes in typhoid fever.

1. The mucous membrane of the small and large intestines (catarrhal inflammation).

2. Lymphatic apparatus of the small and large intestines - Peyer's patches, solitary follicles, regional lymph nodes (granulomatous inflammation leading to necrosis).

7. What stages are usually distinguished for typhoid fever?

1. Brain swelling stage.

2. Stage of necrosis.

3. Stage of ulcer formation.

4. Stage of clean ulcers.

5. Healing stage.

8. What morphological type of inflammation develops in the intestinal lymphoid apparatus during typhoid fever?

1. Productive granulomatous inflammation (formation of macrophage granulomas).

9. List the general changes in typhoid fever.

2. Formation of typhoid granulomas in different organs.

3. Hyperplastic processes in the lymphatic system.

4. Dystrophic changes in parenchymal organs.

10. Name the intestinal complications of typhoid fever.

2. Perforation of ulcers with the development of peritonitis.

11. Name the extraintestinal complications of typhoid fever.

1. Pneumonia.

2. Purulent perichondritis of the larynx.

3. Waxy necrosis of the rectus abdominis muscles.

4. Osteomyelitis.

5. Intramuscular abscesses.

6. Sepsis.

12. Indicate the most common causes of death in typhoid fever.

1. Intestinal bleeding.

2. Peritonitis.

3. Pneumonia.

4. Sepsis.

Salmonella

1. Define salmonellosis.

1 Infectious intestinal disease caused by Salmonella, related to anthroponoses.

2. Name the causative agents of salmonellosis.

1 Various types of salmonella (usually Salmonella typhimurium, Salmonella enteritidis, Salmonella cholerae suls, etc.).

3. Who is the source of infection for salmonellosis?

1. Sick animals (through infected meat, eggs).

2. Sick person.

3. Bacilli carrier.

4. Name the route of infection.

1 Food (enteral).

5. Name the main links in the pathogenesis of salmonellosis.

1. The pathogen enters the small intestine, multiplies with the development of inflammation.

2. Absorption of endotoxin with pyrogenic, cytotoxic, vasoparalytic effects.

3. Lymphogenous spread of the infection is possible.

4. Hematogenous spread of the infection is possible.

6. List the clinical and morphological forms of salmonellosis.

1. Intestinal (toxic) form.

2. Typhoid form.

3. Septic form.

7. What local morphological changes are characteristic of the intestinal form?

1 Exudative-alterative inflammation in the small intestine and stomach (acute gastroenteritis).

8. What general changes develop in the intestinal form?

1. General dehydration.

2. Dystrophic changes in parenchymal organs.

9. List the local changes characteristic of the typhoid form of salmonellosis.

1 Development of morphological changes similar to those observed in typhoid fever, but mild.

10. Name the changes characteristic of the septic form of salmonellosis.

1. Mild inflammation in the small intestine.

2. Hematogenous generalization of the pathogen with the development of foci of purulent inflammation in different organs.

11. Indicate the most common complications of salmonellosis.

1. Toxic-infectious shock.

2. Purulent complications.

3. Dysbacteriosis.

Yersiniosis tests

1. Define intestinal yersiniosis.

1 Acute infectious diseases characterized by damage to the stomach and intestines with a tendency to generalization and damage to various organs.

2. What diseases belong to the group of intestinal yersiniosis?

1. Yersiniosis itself.

2. Pseudotuberculosis.

3. Name the causative agents of intestinal yersiniosis: A) yersiniosis, B) pseudotuberculosis.

1. Iersinia enterocolitica.

2. Iersinia pseudotuberculosis.

4. Who is the source of infection?

1. Animals (rodents, pets, birds, etc.).

2. Sick person (rarely).

3. Bacteria carrier (rarely).

5. What is the route of infection?

1 Usually nutritional.

6. Name the main links in the pathogenesis of yersiniosis.

1. Introduction of the pathogen into the intestinal wall with the development of enteritis.

2. Spread of the pathogen by the lymphogenous route to regional lymph nodes with the development of lymphadenitis.

3. Entry of the pathogen into the blood with the development of damage to internal organs and intoxication.

7. List the clinical and morphological forms of yersiniosis.

1. Abdominal (frequent).

2. Scarlatina-like.

3. Arthralgic.

4. Septic.

5. Other rare forms (anginal, with damage to the meninges, etc.).

8. Which parts of the gastrointestinal tract are affected in the abdominal form of yersiniosis?

1. Stomach.

2. Small intestine (ileum).

3. Large intestine (cecum).

4. Appendix.

5. Mesenteric lymph nodes.

9. What forms of abdominal yersiniosis are usually identified?

1. Gastroenterocolitis.

2. Terminal yelitis.

3. Appendicopathy.

4. Mesadenitis.

10. Name the main morphological changes in the intestinal wall during yersiniosis.

1. Exudative inflammation (catarrhal, catarrhal-necrotic).

2. Formation of ulcers.

3. Presence of characteristic granulomas.

11. Indicate the main morphological changes in the lymph nodes in yersiniosis.

1. Nonspecific inflammatory changes with infiltration of polymorphonuclear leukocytes.

2. Formation of granulomas.

3. Development of necrosis and purulent melting.

12. Give a morphological description of granuloma in yersiniosis: A) cellular composition, B) outcome.

A) 1. Macrophages.

2. Epithelioid cells.

3. Giant multinucleated Pirogov-Langhans cells.

B) 1. Outcome into necrosis and purulent inflammation.

13. Name the general changes in yersiniosis.

1. Development of vasculitis.

2. Development of arthritis.

3. Dystrophic changes in the liver (sometimes hepatitis).

4. Hyperplasia of the spleen.

14. What is the septic form of yersiniosis?

1 A form of yersiniosis, in which hematogenous generalization of the infection develops with the appearance of foci of inflammation in various organs (granulomas with suppuration).

15. List the most common complications of yersiniosis.

1. Perforation of ulcers with the development of peritonitis.

2. Pneumonia.

3. Myocarditis and other infectious and allergic complications.

16. What are the causes of death in yersiniosis?

1. Septic form (fatal in 50% of cases).

2. Intestinal complications (rare).

Dysentery tests

1. Define dysentery (shigellosis).

1 Intestinal infectious disease with predominant damage to the large intestine and symptoms of intoxication.

2. Name the causative agent of dysentery.

1 Group of Shigella (several species).

3. Path of infection.

1 Enteral.

4. Name the source of infection in dysentery.

1. Sick person.

2. Bacilli carrier.

5. List the main pathogenetic links of dysentery.

1. Penetration of Shigella into the intestinal epithelium with its damage (dystrophy, necrosis, desquamation).

2. Circulatory disorders (the result of the vasoparalytic effect of the toxin).

3. Dystrophy of nerve cells of the intestinal ganglia (the result of the neuroparalytic effect of the toxin).

4. Toxic damage to cells of the APUD system with increased release of histamine and serotonin.

5. Development of intestinal inflammation.

6. General toxic effect.

6. Damage to which parts of the intestine is most typical for dysentery?

2. Sigmoid colon.

7. List the classic stages of dysentery.

1. Catarrhal colitis.

2. Fibrinous colitis.

3. Ulcerative colitis.

4. Healing of ulcers.

8. Name the morphological types of colitis that can occur with dysentery in addition to the classical pattern.

1. Catarrhal colitis.

2. Follicular and follicular ulcerative colitis.

3. Gangrenous colitis.

4. Chronic ulcerative colitis.

5. Chronic atrophic colitis.

9. What general changes can develop with dysentery?

1. Moderate hyperplasia of the spleen.

2. Fatty degeneration of the liver and myocardium.

3. Necrotic nephrosis.

4. Calcareous metastases.

10. Name the main complications of acute dysentery: A) intestinal; B) extraintestinal.

A) 1. Perforation with the development of peritonitis, paraproctitis, intestinal phlegmon.

2. Intestinal bleeding.

3. Cicatricial stenosis of the intestine.

B) 1. Bronchopneumonia.

2. Pyelitis and pyelonephritis.

3. Serous arthritis.

4. Pylephlebic liver abscesses.

11. Indicate the main complications of chronic dysentery.

1. Amyloidosis.

2. Exhaustion.

12. List the distinctive features of dysentery in children.

1. Discrepancy between the severe clinical picture and unexpressed morphological changes in the intestine.

2. High frequency of damage to the small intestine.

3. Dominance of catarrhal dysentery.

4. High incidence of follicular and follicular ulcerative colitis.

5. In some cases, long, protracted recovery and poor regeneration.

13. Name the main features of the pathomorphosis of dysentery.

1. Predominance of light, erased forms.

2. Dominance of catarrhal colitis.

3. The presence of long-term carriage of bacteria.

Cholera

1. Define cholera.

1 An acute infectious disease primarily affecting the stomach and small intestine.

2. Name the causative agent of cholera.

1. Asiatic cholera vibrio (Koch vibrio).

2. Vibrio El Tor.

3. Who is the source of infection?

1. Sick person.

2. Vibrio carrier.

4. Path of infection

1. Enteral (usually water).

5. Name the main pathogenetic links in cholera.

1. Vibrio penetration into the small intestine and its reproduction with the release of exotoxin (cholerogen).

2. Secretion of a large amount of isotonic fluid by the intestinal epithelium under the influence of cholerogens.

3. Impaired reabsorption of fluid due to blockade of the enzymatic systems of the sodium-potassium pump by cholerogens.

4. Increased tissue and vascular permeability as a result of damage to cell and vascular membranes.

5. As a result, profuse diarrhea and dehydration.

6. What stages (periods) are distinguished in the development of cholera?

1. Cholera enteritis.

2. Cholera gastroenteritis.

3. Algic period.

7. What morphological type of inflammation is characteristic of cholera enteritis and gastroenteritis?

1 Serous (serous-hemorrhagic) inflammation.

8. List the morphological changes in the wall of the small intestine during the algid stage.

1. Severe plethora (there may be hemorrhages).

2. Severe swelling.

3. Necrosis and sloughing (desquamation) of the villous epithelium.

4. Infiltration of the mucous membrane with lymphocytes, plasma cells, neutrophils.

9. List the general changes in cholera.

1. Exicosis.

2. Dystrophic changes and necrosis of parenchymal organs (myocardium, kidneys, liver, etc.).

3. Signs of suppression of the immune system (atrophy of spleen follicles, lymph nodes).

10. What changes in the kidneys can develop during cholera?

1. Glomarulonephritis.

2. Necrotizing nephrosis.

11. Name specific complications of cholera.

1. Cholera typhoid.

2. Postcholera uremia.

12. Specify nonspecific complications of cholera.

1. Pneumonia.

2. Abscesses, phlegmons.

4. Sepsis.

13. What are the most common causes of death in cholera?

1. Dehydration.

2. Uremia.

3. Intoxication.

4. Nonspecific complications.

14. List the main features of the pathomorphosis of cholera.

1. Prevalence of mild forms.

2. Reducing mortality.

3. The rarity of dehydration.

4. Disappearance of typhoid cholera.