Intestinal infection is acute. Types and methods of treating intestinal infection Diagnosis of intestinal infection

The general name intestinal infection refers to a whole group of infectious diseases of various origins. The causative agents of these diseases affect the digestive system. The characteristic features of each of them are body poisoning and dehydration. The infection penetrates the intestines and it is there that the pathogens localize and multiply.

The International Classification of Diseases assigned this group of pathologies code A00-A09. It includes diseases such as cholera, tuberculous enteritis, salmonellosis, amoebiasis, shegellosis, bacterial poisoning, and typhus. According to WHO, about 2 million people worldwide die every year from various forms of intestinal infection. Moreover, most of them are children under the age of 5 years. The peak incidence occurs in the summer period of the year.

Types of pathogens and routes of infection

There are other forms of intestinal infection caused by bacteria, but these are the most common. A bacterial gastric infection is provoked by microbes that can be opportunistic or purely pathogenic. The latter include the abdominal type bacillus and Vibrio cholerae. Their penetration into the human body always causes infectious poisoning.

Opportunistic pathogens are those microorganisms whose presence in small quantities is considered normal, i.e., in such a concentration they do not harm humans. But if for some reason reproduction occurs and there are too many of them, then they cause disease. Bacterial infection occurs through the fecal-oral or nutritional-household route. Infection often occurs when eating foods contaminated with germs and not following hygiene rules.

Gastrointestinal infections of viral etiology are divided into the following types:

• enterovirus;
• rotavirus
• coronavirus;
• norfolkvirus;
• reovirus.

A viral infection, penetrating the intestines, causes inflammation of its mucous membrane. A person who has suffered a viral intestinal infection remains infectious to others for one month after recovery. Viral infections of the stomach and intestines are in most cases transmitted by airborne droplets or household contact. Thus, infection can occur even through a kiss on the cheek of a child.

The simplest protozoan organisms are also the cause of the development of infectious diseases affecting the intestines and stomach. These include giardiasis, amoebiasis, schistosomiasis, and cryptosporidiosis. The protozoal form of intestinal infection is much less common than the bacterial or viral one. Infection usually occurs through water if water is swallowed while swimming in untested bodies of water.

Drinking unboiled water can also cause infection. Diseases caused by this pathogen are characterized by a long course. Infection with viral intestinal infections occurs through household and airborne transmission. Bacterial infections are transmitted by oral-fecal, household and airborne methods.

The source is a sick person. Microbial excretion occurs from the onset of the disease until complete recovery. The greatest risk of contracting gastrointestinal diseases is long-term storage of food. Intestinal infections are almost always enteral, that is, they enter the body through the mouth. Predisposing factors to infection are:

• ignoring the rules of personal hygiene;
• low stomach acidity;
• lack of access to clean water;
• living in unsatisfactory sanitary and hygienic conditions;
• intestinal dysbiosis.

The most common bacteria that cause intestinal diseases enter the human body as a result of consuming the following products:

• salmonella – poor heat treatment of meat and eggs;
• Staphylococcus aureus – mayonnaise and custards;
• Vibrio cholerae – contaminated water, including from open water bodies;
• E. coli – consumption of unboiled water or products washed with water from open reservoirs;
• parahemolytic vibrio - raw seafood.

Intestinal infection is caused by bacteria and viruses

Symptoms of intestinal infection

An intestinal infection, regardless of what pathogen caused the disease, is accompanied by severe intoxication and damage to the digestive organs. However, each type of disease has its own characteristics. After the causative agent of an intestinal infection enters the oral cavity, it is swallowed along with saliva and penetrates the stomach and then the intestines. But in the stomach they are not destroyed by hydrochloric acid, so they pass into the intestines and actively multiply, causing disease.

All types of pathology under consideration are characterized by one common and main symptom - diarrhea and loose stools. Other signs of intestinal infection such as nausea and vomiting, fever, abdominal cramps, and weakness do not always appear after infection. But the disease manifests itself in two types of syndromes: intestinal and intoxication. The severity of each of them varies depending on the type of pathogen.

The following classification is typical for intestinal syndrome:

• Colitic. Pain in the left lower abdomen, frequent urge to have bowel movements, stool contains an admixture of mucus and blood.
• Gastric. Intense pain in the stomach, nausea and vomiting after each meal, rare diarrhea.
• Enterocolitic. Severe abdominal pain, frequent bowel movements with mucus or loose stools.
• Gastroenteric. The pain is localized around the navel and in the stomach area, vomiting and frequent mushy stools appear, which then become foamy with a pungent odor.
• Enteriteric. They are characterized by only one symptom – frequent watery stools.
• Gastroenterocolitic. Vomiting and intense pain throughout the abdomen, painful bowel movements without relief, blood and mucus in the stool.

Intoxication syndrome is manifested by an increase in temperature above 37 degrees and general weakness. The patient complains of dizziness and headache, lack of appetite and nausea, and aches throughout the body. This infectious-toxic syndrome can last from 2 hours to several days. Due to excessive vomiting and diarrhea, the patient develops dehydration.

If left untreated, it can lead to death in a short period of time.

Diseases classified as intestinal infections

Symptoms of intestinal infection vary depending on the type of disease. In addition, how long each of them lasts is also determined by the type of pathogen. Depending on the duration of the infection, it can be acute and last less than 6 weeks, protracted - longer than 6 weeks, and chronic. The latter can last up to six months. Local manifestations of the disease also differ according to which organ of the gastrointestinal tract (GIT) is most affected.

The incubation period of dysentery lasts up to 1 week. The disease has an acute onset with a sharp rise in temperature to 40 degrees. Against the background of fever, convulsions and impaired consciousness cannot be ruled out. Associated symptoms of dysentery are as follows:

• severe weakness and weakness;
• lack of appetite;
• muscle and headache;
• sharp pain in the left iliac abdomen;
• intestinal spasms;
• false urge to defecate;
• inflammation of the anal sphincter;
• multiple intestinal lesions up to 20 times a day.

Stools are usually liquid and contain blood and mucus. In severe cases of the disease, intestinal bleeding may develop. Salmonellosis begins with a rise in temperature to 39 degrees and the appearance of nausea and vomiting. In most cases, the disease has similar symptoms to gastritis and gastroenterocolitis. She is characterized by copious and frequent stools.

In rare cases, respiratory and typhoid-like types of salmonellosis occur. In the first case, the symptoms are supplemented by signs similar to those of a cold. Infection with E. coli is called escherichiosis. Its main symptoms are profuse and prolonged vomiting, bloating, loss of appetite and weakness. The stool is frequent and has a yellow tint.

One of the most common types of intestinal infection, especially in children, is rotavirus infection. In most cases, it has a course of gastroenteritis or enteritis. The incubation period lasts from 1 to 3 days. Rotavirus has an acute onset, and the severity of symptoms becomes maximum by the end of the first day of illness

The infection is characterized by increased body temperature and general intoxication, nausea and vomiting, and copious foamy and watery stools. Rotavirus infection is often accompanied by catarrhal symptoms, such as runny nose, sore throat, swelling and redness of the pharynx, and cough. Usually cure occurs within a week after starting treatment.

No less common is staphylococcal intestinal infection. It can be primary or secondary. In the first case, the microbe enters the gastrointestinal tract through the mouth. The secondary type of disease is characterized by the fact that the pathogen is introduced into the gastrointestinal tract by blood flow from other foci of infection.

The disease is accompanied by dehydration and toxicosis, frequent bowel movements and vomiting. The stool has a watery, greenish consistency and may contain mucus. Often the infection has a course similar to a cold: a runny nose, low temperature and sore throat appear, then intestinal disorders occur.

There are many diseases that fall under the category of “intestinal infection”

Drug treatment

Medicines intended to treat intestinal infections are prescribed by a doctor on the basis of laboratory tests, through which the type of causative agent of the disease is identified. So, if the infection is viral in nature, then antiviral drugs are prescribed. If the source of the disease is bacteria, the patient is prescribed antibacterial tablets.

Since intestinal poisoning the most pronounced symptoms are intoxication and stool disturbances, first of all, they need to be eliminated. This is achieved by eliminating from the body of the diseased pathogenic agent that caused the disease. It is also necessary to normalize the water-electrolyte balance in the intestines and remove toxic substances from the body. To achieve the latter, it is necessary to treat the patient with sorbents.

Treatment of intestinal infection includes taking the following groups of drugs:

• antibiotics;
• antiviral agents;
• sorbents;
• medicines for diarrhea;
• enzymes;
• painkillers.

For intestinal infections of bacterial origin, antimicrobial agents from the group of fluoroquinolones, tetracyclines, amphenicolones or metronidazoles are prescribed. These may be Ofloxacin, Norfloxacin, Ciprofloxacin, Levomethicin, Doxycycline. All types of intestinal infections are accompanied by the formation of toxic substances as a result of the activity of pathogenic microorganisms.

Therefore, it is necessary to take medications to remove them from the gastrointestinal tract. For this purpose, sorbents are prescribed; they absorb harmful substances and remove them from the intestines unchanged. The most popular drug in this group is activated carbon. The recommended dose of the drug is 1 tablet per 10 kg of body weight. Also, in case of severe intoxication, Polysorb, Smecta or Enterosgel are prescribed.

To normalize stool and eliminate diarrhea, special medications are prescribed. Their names are as follows: Trimebutin, Loperamide, Stopdiar, Fthalazol, Nifuroxazide. Taking these drugs will have a positive effect on the functioning of the gastrointestinal tract. They help reduce intestinal tone and motility.

If, along with other symptoms, an intestinal infection is accompanied by severe pain, you can take painkillers. But this should be done only after the doctor’s approval, since taking them independently before being examined by a doctor can change the clinical picture, which will significantly complicate diagnosis. Usually, Spazmaton, No-shpa or Benalgin are prescribed to alleviate the condition.

After eliminating the acute symptoms of an intestinal infection, it is recommended to take enzymatic preparations to normalize and accelerate digestive processes. As such, Mezim forte, Pancreatin or Micrazim are most often prescribed. It is also necessary to restore the intestinal microflora; for this purpose, taking probiotics is provided. They are included in the complex treatment of intestinal infections in both adults and children.

In some cases of intestinal infection, emergency treatment may be required. The need for this arises when the patient experiences uncontrollable diarrhea more than 8 times a day. The nature of the stool is also important; it is watery and resembles rice water that is alarming. For such symptoms, it is recommended:

• put in a dropper with glucose and isotonic sodium chloride solution;
• Inject the lytic mixture intramuscularly;
• take steps to rehydrate;
• ensure the intake of adsorbents.

In case of food poisoning, gastric lavage and a cleansing enema are also performed. These procedures must be prescribed by the attending physician.

Intestinal infection requires complex treatment

Complications, prognosis and prevention

Any intestinal infection is fraught with the development of severe complications. The most common of these is dehydration. This occurs due to excessive vomiting and diarrhea, causing water and salts to leave the body. For a person, a loss of 10% of the total fluid volume is critical. This may result in coma and death. But such a prognosis is typical for a severe case of the disease and lack of treatment.

The following signs will indicate possible dehydration:

• lack of urination for more than 6 hours;
• dry tongue;
• dry skin;
• rapid pulse;
• lowering blood pressure;
• the skin takes on a grayish tint.

When assessing the degree of dehydration, you should not rely on the sign of thirst, since this symptom is not always present. Another form of complication of intestinal infection is infectious-toxic shock. This condition is provoked by the predominance of toxic substances in high concentrations in the blood. It can develop at the onset of the disease against the background of a rise in body temperature to high levels.

Often in children, intestinal infection is complicated by the development of pneumonia, which is the result of moderate dehydration when the fluid lost by the body is not sufficiently replenished. Acute renal failure often occurs against the background of intoxication of the body. Early diagnosis of the disease and adequate treatment contributes to the complete cure of the patient without the development of severe complications.

But it must be borne in mind that after suffering an intestinal infection, a person’s immunity is weakened and is susceptible to other viruses and infections. Therefore, it wouldn't hurt to take extra precautions. In this regard, you should not overcool and expose yourself to various nervous shocks. Typically, the acute period of the disease passes 3–4 days after the start of treatment.

But if no improvement is observed during this time, you should re-seek medical help and be examined to identify more dangerous infections. Particular attention should be paid to the well-being of children under one year of age. If they have severe diarrhea and vomit even from a sip of water, they should immediately consult a doctor.

Thoroughly washing fruits with clean water will prevent intestinal infections.

Intestinal infection is considered a disease of dirty hands and therefore one of the main ways to prevent it is to maintain personal hygiene. In addition, to prevent it, doctors recommend a number of simple rules:

• frequent hand washing with soap, especially after using the toilet and before eating;
• maintaining cleanliness of cutlery and bathrooms;
• wash fruits and vegetables thoroughly before eating;
• sufficient heat treatment of meat, milk and eggs;
• compliance with rules and shelf life of products.

If there is already a sick person in the family, the question arises of what to do. To reduce the likelihood of infection, healthy family members need to: use individual cutlery, wear a bandage when in contact with a sick person, clean with disinfecting solutions, disinfect the patient’s dishes and belongings.

I. Intestinal symptoms

1. Diarrhea. True diarrhea means the passage of copious loose or liquid feces several times a day.

The origin of diarrhea is varied. Acceleration of intestinal passage due to irritation of motor nerves, impaired absorption of water, dilution of intestinal contents by transudate from the blood or inflammatory exudate play a role in their occurrence. These factors act separately or simultaneously. With functional dyspepsia, there is no exudation.

Each of the factors described does not necessarily lead to diarrhea. Thus, the acceleration of passage in the small intestines may be accompanied by a slowdown in the thick intestines, which leads to increased absorption of water and thickening of stool. The release of water or exudate in spastically contracted intestinal loops will also not cause diarrhea, but only a false urge to defecate.

2. Constipation. The main factor determining the nature and consistency of stool is the motor function of the intestine, and any deviations from the norm are in one way or another associated with various forms of intestinal dyskinesia.

Constipation is characterized by retention of stool longer than the normal daily period, and stool is either completely absent or insufficient, with only the terminal part of the intestine being emptied. The urge to defecate may be completely absent or occur repeatedly, several times a day, not accompanied by complete emptying of the intestines.

The consistency of stool during constipation ranges from hard to watery. Fecal plugs, thickened from prolonged retention in the intestinal loops, especially in the ampulla of the rectum, become the direct cause of constipation. In some cases, patients are forced to release the ampoule with their hands, kneading and removing fecal lumps piece by piece.

The consistency of stool alone does not determine the pattern of constipation. The essence of this disorder is the retention of feces and incomplete cleansing of the distal intestine. Slow excretion of feces may be accompanied by some change in its consistency. Thus, retention in the distal colon leads to abundant absorption of water with the formation of hard fecal plugs, or “stones.” The delay in the cecum is associated with increased fermentation processes, dilution of feces and the development of gases. The consequence of such typhlostasis will be either an abundant release of liquid and mushy fermentative masses, i.e., a state of fermentative diarrhea, or an increased urge to defecate with scanty release of liquid feces from spastically contracted distal intestinal loops, i.e., the so-called state of constipative diarrhea. In this regard, the alternation of diarrhea and constipation in chronic colitis is understandable.

Changes in diarrhea and constipation are the most common symptom of colitis of various etiologies. Delayed stool inevitably alternates with increased excretion of liquid feces. It is important to try to determine the leading symptom against which functional disorders are compensated. Thus, against the background of prolonged constipation, diarrhea is a consequence of mechanical and chemical irritation of the intestines by stagnant feces. The feedback will also be understandable if we take into account that the empty intestine, which has just been cleared of its contents, ceases to receive impulses to defecate, especially since the next exacerbation of diarrhea entails a transition to a strictly gentle diet.

Thus, the alternation of diarrhea and blockage occurs as if in a vicious circle. It can be broken only with the help of careful therapeutic measures, mainly dietary ones.

3. False or constipative diarrhea, characterized by repeated urges to defecate with the release of scanty feces of any consistency: solid lumps in the form of sheep feces or liquid masses due to dilution with exudate, water or fermentation products. Patients themselves usually do not understand the essence of dyspepsia, mistakenly interpreting any increased frequency of urges as diarrhea, while in these cases we are talking about a special type of constipation.

4. False urges can be companions of both diarrhea and constipation. They arise from irritation of the motor nerves of the distal parts of the large intestine, mainly in the sigmoid or rectum, felt either in the left groin or in the anus. While simulating a normal urge, they are, however, not realized due to the absence of a fecal column in the rectum. False urges may be accompanied by the discharge of gases, liquid secretions, mucus or blood (with proctitis) or remain empty.

5. Tenesmus- a type of false urge, but with the obligatory discharge of mucous-bloody films (like “spitting”) and mainly with painful colic. Tenesmus is especially characteristic of the acute stage of dysentery. In mucomembranous colitis, tenesmus is accompanied by the discharge of large films of mucus in the form of ribbons with bloody streaks, which patients mistake for segments of a tapeworm (mucous colic, colica mucosa).

6. Pain in the intestinal area are a common symptom of intestinal diseases, both organic and functional. Unlike stomach pains, they are not associated with meals, but mainly with stool, appearing with the urge to defecate or after it. Pain may occur immediately after stool, accompanied by a feeling of incomplete release or a repeated urge to defecate. Only with transeversitis does pain occur after eating due to the pressure of a full stomach on the irritated transverse colon. The nature of the pain varies. In some cases, there is a feeling of distension and fullness in the abdomen, in others - cramping pain. The most common type is intestinal colic, especially painful when it is not accompanied by bowel movements. In addition to the above-mentioned mucous colic with the discharge of mucus films, so-called gas colic is characteristic, caused by increased formation and delayed passage of gases.

The mechanism of intestinal pain is associated with a number of moments: stretching of the intestinal loops along with their abdominal covering, irritation of the nerve endings in the intestinal wall, tension and twisting of the mesentery of the small intestines along with the nerves passing through it. In this case, painful stimuli are transmitted from the visceral nerves and plexuses through the connecting sympathetic branches to the posterior spinal roots, rising centripetally to the brain and then centrifugally projecting onto the abdominal wall. Painful stimuli emanating from the distal intestinal loops are directly transmitted to the spinal cord along the spinal nerves.

The main role in the mechanism of development of intestinal pain is played by intestinal motility: tone, peristalsis, rocking movements, stretching and spasms of intestinal loops. Expanding pain during intestinal obstruction is associated with stenotic peristalsis in a sealed segment of the intestine. Appendicular pain is either colicky in nature (appendicular colic) or associated with irritation of the peritoneum (acute attack with fever and hyperleukocytosis). With colitis, pain depends on stretching and peristaltic contractions of the inflamed intestinal wall; with enteritis, it depends on irritation of the mesenteric nerves. In diseases of the rectum and anus, pain occurs directly from irritation of the anal nerves. With mesenteric lymphadenitis, pain is the most constant symptom, depending on irritation of the mesenteric nerves or compression of them by inflamed lymph nodes.

It should be noted that in some cases, organic intestinal diseases, even the most severe ones (cancer), can occur for a long time without any pain, which makes their recognition difficult.

7. Proctodynia- pain in the rectum and anus, a feeling “as if sitting on an awl.” If these unpleasant sensations are associated with the act of defecation, then they are caused by an inflammatory process in the anus (sphincteritis, proctitis, fissure, hemorrhoids). Regardless of defecation, similar sensations can be purely functional in nature, being caused by painful spasm of the rectal muscles and hyperesthesia of the anal nerves.

8. Language. Old doctors attached great importance to the appearance of the patient’s tongue, considering it a “mirror of the stomach.” It is more correct to talk about the “gut mirror”, the condition of which is often reflected in the appearance of the tongue. Normally, the entire surface of the tongue is moist, uniformly pink in color, with pronounced papillae, sometimes slightly coated at the root. Pathological changes are expressed in dryness, grayish-yellow or brown plaque, deep furrows that give the tongue the appearance of a “geographic map”, cracks and ulcers (with glossitis). Thick plaque is usually observed with constipation with prolonged fecal retention or during an acute period of intestinal infection. Dryness and brown coloration are a sign of severe dehydration due to vomiting and diarrhea. With sprue, pellagra and dystrophic colitis, atrophy of the papillae resembles Genter's tongue in Biermer's anemia. The condition of the tongue changes rapidly, serving as one of the indicators in the dynamics of intestinal diseases.

9. Flatulence. The amount of intestinal gases (methane, nitrogen, hydrogen sulfide, carbon dioxide) in an adult with mixed food reaches 1 liter. Gaseous products are formed mainly during the breakdown of plant fiber by intestinal bacteria. The main sources of gas formation are legumes, vegetables, cabbage, mushrooms, bread, potatoes, and from animal products - fresh milk. The release of gases per day with a rational diet occurs in an amount of approximately 200 ml (measured using a gas outlet tube). With an abundant intake of beans and soybeans as the main source of proteins, it increases to 2600 ml, and with increased peristalsis even more. On the contrary, with sluggish peristalsis, the reabsorption of gases into the blood increases.

Some of the gases are absorbed into the blood, the rest are released during bowel movements or pass away on their own. Pathological bloating of the intestine can be caused by increased formation of gases with an abundance of swelling foods in food, impaired absorption due to inflammation of the intestinal mucosa (with enterocolitis) or venous stagnation in the abdominal cavity (with circulatory disorders) and, finally, with mechanical or spastic delay in the passage of gases.

Under normal conditions, the presence of a certain amount of gases maintains the tone and peristalsis of the intestinal loops. Excessive flatulence (flatus) causes characteristic disorders: a feeling of fullness, bloating, sharp pain, gas colic, displacement of the diaphragm and heart, neurovascular reactions in the form of headaches, dizziness and even attacks of angina ("gastrocardiac syndrome").

Increased absorption of gases in the intestines causes a very unpleasant sensation of bad breath (foetor ex ore), often taking on the character of a painful obsessive state due to increased suspiciousness. Such subjects, usually pronounced neuropaths, avoid society, dooming themselves to loneliness due to an exaggerated fear of contaminating the air with fetid gases.

10. Peristaltic restlessness, rumbling, moving in the intestines is associated with nervous irritation of the intestinal muscles. The most common cause is functional neurosis. But such symptoms may be the initial expression of intestinal obstruction due to stenosis, strangulation or implantation. Particularly characteristic of stenosis is periodic tension of an isolated intestinal loop (Wal's symptom), sometimes changing its location, as well as the sound characteristic of a stream of liquid passing through a narrow opening.

11. Nausea- a common symptom of various intestinal diseases: acute enterocolitis, constipation, helminthic infestation. The mechanism of nausea is complex and not always uniform. Most often, nausea is an expression of spasm of the small intestines in the area of ​​the plica duodeno-jejunalis or jejunal loops. Reflex irritation of the stomach, reaching pylorospasm and antiperistalsis, causes vomiting and belching. The latter often has a rotten odor due to intestinal gases.

The source of nausea and vomiting is often identified only in parallel with the recognition and treatment of its root cause, for example, cholecystitis or acute enterocolitis: along with the elimination of the underlying disease, nausea also disappears. Sometimes a simple cleansing enema is enough to relieve nausea.

12. Anorexia. A loss of appetite is a symptom of a variety of diseases of many organs and systems or a general infection. A change in this complex unconditioned reflex indicates irritation or inhibition of food centers emanating from various parts of the body, often outside the digestive tract. At the same time, diseases of the latter (anacidic gastritis, colitis) can occur with normal appetite. Anorexia is always an aggravating symptom. With it, the processes of digestion and absorption of food are weak, the amount of food is limited; sometimes there is a feeling of disgust for food. Anorexia can be an indicator of a severe general illness, toxicosis or neurosis. A change in appetite very often serves as a subtle dynamic sign, signaling a turn in the course of the disease.

II Changes from other systems

Stomach. A decrease in the secretory function of the stomach up to complete achylia is a common occurrence in various intestinal diseases. Ahilia appears either as a consequence of an intestinal infection, or as a predisposing moment for it. In both cases, it aggravates the course of colitis.

Less commonly observed is an increase in gastric acidity and secretion of reflex origin due to primary colitis. The presence of hunger pain and pyloric spasm can simulate peptic ulcer disease. When carrying out complex therapy, it is always necessary to take into account the state of gastric secretion.

Liver and bile ducts. As an “internal filter”, the liver and biliary tract system is easily affected by any intestinal infection and infestation, most often with colibacillosis, giardiasis, amebiasis, ascariasis, typhoid fever and paratyphoid fever. In mild cases, the matter is limited to cholecystitis; in more severe cases, cholangitis and hepatitis develop (with ulcerative colitis). Amoebic colitis causes liver abscesses. Hence the need for all chronic intestinal diseases to examine not only bile pigments in urine and blood, but also duodenal contents and liver functions. In addition, disorders of digestion and absorption of food affect bile secretion and metabolic functions of the liver, which worsens the course of colitis.

The pancreas, like the bile ducts, is often the entry point for intestinal infections. For intestinal diseases, it is necessary to examine duodenal enzymes, diastasis in urine and blood, and trypsin content in feces. When performing scatological analyses, it is necessary to take into account the symptoms of pancreatic insufficiency (fat, muscle, connective tissue), especially with fatty diarrhea, which makes one think about chronic pancreatitis.

The cardiovascular system. The close relationship between digestive and cardiovascular disorders is manifested by a number of symptoms, which can be schematically divided into two groups depending on the underlying disease of one or another system. Reflex disorders of the heart and blood vessels in primary intestinal diseases seem especially important. These include heart displacement due to flatulence and constipation, shortness of breath, palpitations and heart pain after eating. Persistent diarrhea leads to dehydration, hypotension and even collapse. Prolonged constipation can cause vascular reactions in the form of headaches and cold extremities. Dystrophic diarrhea with endogenous vitamin deficiency, myocardial dystrophy, and hypoproteinemic edema have a particularly serious impact on the cardiovascular system.

Urinary tract. Cystitis and pyelitis can be associated with infectious colitis, especially in the presence of colibacillosis and putrefactive dyspepsia. Toxic nephrosis, usually of a volatile nature, is observed less frequently. Uremic diarrhea often occurs under the guise of severe ulcerative colitis.

Nervous system. With any intestinal disorders, there are certain symptoms from the nervous system: headaches (with constipation and intestinal intoxication), sleep and memory disorders, weakness, fatigue, irritability, decreased ability to work. The connection between fermentation and putrefactive processes and alternations between excitement and depression is denied by most authors.

Reflex, metabolic and dyspeptic factors are involved in the pathogenesis of neurointestinal connections. Damages to the nervous system are especially pronounced with secondary (endogenous) vitamin deficiencies, in particular with a deficiency of B complex vitamins. The most severe lesions of the nervous system are observed with pellagroid diarrhea.

Urine. A diagnostic role is also played by an increase in the amount of urobilin and bilirubin in the urine (with the involvement of the liver and biliary tract in intestinal pathology), indican (with putrefactive forms of colitis and high intestinal obstruction), the presence of pathological formed elements (with concomitant pyelocystitis), protein and casts ( with nephritis). Oliguria and anuria can occur after profuse diarrhea, polyuria - with dystrophic conditions, pollakiuria - with intestinal dyskinesias.

Blood. Changes in red blood in the form of hypochromic anemia are not uncommon with all kinds of severe colitis and enteritis. Anemia, even pernicious-like, may be the first symptom of stomach and intestinal cancer. Posthemorrhagic anemia complicates all kinds of intestinal bleeding (with ulcerative colitis, hemorrhoids, cancer, etc.).

Biochemical parameters. In addition to the above, the following data are important: residual blood nitrogen (for uremic colitis), calcium content in the blood (for sprue and other forms of fatty diarrhea), vitamins A, B 1 and C (for secondary vitamin deficiencies), prothrombin (for hemorrhagic diathesis and jaundice ), plasma proteins (for dystrophic colitis and vitamin deficiency).

Main functional intestinal syndromes

1. Intestinal dyskinesia

Disorder of intestinal motor function accompanies all kinds of organic diseases (colitis, tumors, obstruction), but can also be of a purely functional nature. Clarification of the pathogenesis of these dyskinesias is therefore crucial in recognizing any intestinal disease.

As an independent disease or syndrome, dyskinesia appears only in the picture of habitual constipation. However, its significance in intestinal pathology is not limited to this, since it usually complicates the course of the most common intestinal disease - chronic enterocolitis of any etiology. At the same time, dyskinesia as an early or intermediate stage prepares for a number of later complications and can contribute to the development of more serious diseases: the example of dyskinesia shows the transition of a functional disorder into organic suffering and back.

The causes of dyskinesia are disorders of intestinal innervation, impaired coordination in the autonomic and central nervous systems, and distortions of unconditioned and conditioned reflexes. A special place is occupied by reflex intestinal dyskinesias due to diseases of other organs, for example, cholecystitis and peptic ulcers. In this case, intestinal spasms are supported by viscero-visceral reflexes emanating from pathological foci of irritation (biliary tract, gastroduodenal zone).

The clinical picture of intestinal dyskinesia boils down to subjective feelings of fullness, heaviness in the abdomen, false urges, a feeling of incomplete release after defecation, and intestinal colic. Dyskinetic constipation also causes a number of general disorders: headaches, cold extremities, fatigue and weakness, decreased ability to work, and depression.

Various forms of intestinal dyskinesia. False diarrhea with repeated discharge of scanty liquid feces due to retention in the large intestine with irritation of its wall.

Discharge of feces of varying consistency:

A) first mushy, then dense; b) first a fecal plug, then mushy feces; c) rapid fecal eruptions associated with hypersecretion or hyperkinesia; d) left-sided (more often) or right-sided (less often) constipation.

2. Intestinal dyspepsia

This term usually refers to intestinal digestive disorders of a functional nature that are not associated with organic diseases of the intestinal tract. Dividing them into separate groups according to etiological principles, we can only offer a working scheme, since the line between functional and organic disorders is blurred, and also because functional disorders (dysfunctions) constitute an integral element of any intestinal disease. Nevertheless, such a working scheme is necessary to understand the etiology of individual clinical forms and develop appropriate therapy.

Gastrogenic dyspepsia. Disorders of the gastric phase of digestion easily lead to disorders of the intestinal phase. The most common form of such gastrogenic disorders is Achilles diarrhea, associated with accelerated gastric evacuation and irritation of the small intestine by abundant, poorly prepared stomach contents. In the initial stage of decompensated gastric achylia, diarrhea is quickly cured with hydrochloric acid or artificial gastric juice. In the future, diarrhea can be supported by secondary enterocolitis, when the gastrogenic factor in pathogenesis fades into the background, giving way to the infectious-inflammatory factor. These secondary enterocolitis give almost the same picture as simple gastrogenic dyspepsia (an abundance of digestible plant fiber and poorly digested muscle fibers), but require different therapy (see below). Coprologically, they differ from dyspepsia by the presence of mucus.

Pancreatic dyspepsia. This form of diarrhea is characterized by: lenteria, creatorrhea and steatorrhea with a predominance of neutral fats. In advanced cases, the feces have a large volume, an oily appearance and quickly harden in the air. Pancreatic dyspepsia is by no means necessary for gastric achylia. Treatment boils down to using a diet limiting fats and rough meats and prescribing pancreatin with bismuth, tannalbin or purified chalk.

Hepatic dyspepsia, that is, indigestion due to insufficiency of liver or bile duct function can affect the functioning of the stomach, intestines or the entire gastrointestinal tract. In the gastric form of hepatic dyspepsia, there are diopeptic symptoms reminiscent of gastritis (heaviness after eating, rapid feeling of fullness, bitter taste in the mouth, anorexia, nausea, belching), especially pronounced after eating fatty foods. The intestinal form is characterized by diarrhea that occurs early in the morning (an “alarm clock” symptom) or after eating fatty foods. Fat intolerance is associated with insufficient supply of bile acids to the intestines, especially with jaundice. Saponified fats and fatty acid crystals predominate in feces.

In other cases, constipation is observed, explained by a lack of stimulating effect of bile acids on the intestines, as well as reflex colospasm. Constipation, in turn, further inhibits the process of bile entering the intestines (vicious circle).

The functional and reflex nature of hepatic dyspepsia is caused by primary damage to the liver or biliary tract. The diagnosis of hepatic dyspepsia is also supported by the beneficial effect of pathogenetic therapy aimed at sparing the diseased organ and carefully stimulating its function - choleretic drugs (Carlsbad salt for constipation, holosas for diarrhea), methenamine, thermal procedures, a diet limited in fats and fried foods.

Fermentative dyspepsia develops due to excessive consumption of carbohydrates. The relative lack of amylolytic enzymes leads to the fact that excess carbohydrates are not digested or are broken down only partially, with the formation of abundant fermentation products, mainly in the cecum and ascending colon. Fermentation processes are further enhanced in the presence of gastric achylia due to a lack of hydrochloric acid, which breaks down the protein shell of carbohydrate products (amilorhexis).

The clinical picture of fermentative dyspepsia is severe only in early childhood. Often this disease leads to dystrophy. In adults, diarrhea with the release of foamy feces, bloating, and mild pain is observed. Feces are sharply acidic, contain a lot of starch grains, digested fiber and fermentative flora (yeast, clostridia, spirilla), but without any admixture of mucus and blood, as is the case with the fermentative form of colitis. The intestinal loops are sharply distended with gases, spastic in places, but slightly painful. Hepatic dullness is covered by the swollen ascending colon, the diaphragm is elevated. The heart acquires a horizontal position, which can cause attacks of shortness of breath, palpitations and discomfort in the heart area (especially in a lying position), which is relieved by sitting and walking. General nutrition suffers little, since the absorption of proteins and fats in the small intestines is not impaired.

The course of the disease is usually completely benign. With a diet limited in carbohydrates and plant fiber, improvement occurs quickly, and in the initial stages, recovery occurs. Prolonged forms are characterized by relapses at the slightest violation of the diet. An aggravating factor is gastric achylia, which reduces the process of aminorexis. Changes in intestinal flora and general weakening of the body open the gates to secondary infection, which easily leads to the development of chronic enterocolitis, with a more persistent course.

Putrid dyspepsia. The onset of this digestive disorder is associated with excessive supply of food proteins, mainly meat, or poor digestion of them. The abundant formation of putrefactive products of incomplete protein breakdown (indole, skatole, tryptophan, toxamines, etc.) causes a number of dyspeptic symptoms: headaches, vasospasms with cold extremities and pallor, hypochromic anemia. Feces are usually scanty, liquid or mushy, putrid odor, grayish-brown in color, sharply alkaline, with a rich content of muscle fibers and connective tissue.

Perversions of chemistry and intestinal flops with this form are more complex than with fermentation. In these cases, it is more difficult to normalize the bacterial flora and chemistry with the help of a contrasting (carbohydrate-fat) diet. Excess carbohydrates easily leads to irritation of the intestinal loops and the release into the intestinal lumen, first of a watery transudate, and then of an inflammatory exudate rich in protein. As a result, a vicious circle is created with a progressive increase in putrefactive processes and dyspeptic symptoms.

To break this vicious circle, it is necessary to radically unload the intestines from pathological decay products and at the same time sterilize it with laxatives and a short course of treatment with sulfonamides (10.0 for 2-3 days). It is also recommended to prescribe an apple fasting diet.

Nervous dyspepsia. This form of intestinal dyspepsia will be discussed in more detail in the chapter on intestinal neuroses. Its characteristic feature is the absence of pronounced colitis, and most importantly, the neurogenic cause of dyspeptic disorders. Neurovisceral connections in some cases are caused by reflex effects of neighboring organs (liver, gall bladder, stomach), in others - by the central nervous system, irritation of the cortex or subcortical centers. In the latter case, intestinal dysfunction in the form of diarrhea, constipation, distension, false urges, colic, etc. is directly related to negative emotions - fear, melancholy, obsessive thoughts, memories, “associations” (conditioned reflexes). Rapid diarrhea is especially typical

under the influence of obsessive thoughts or fear (the so-called bear disease). The sudden release of liquid stool without admixture of inflammatory elements is caused by a long peristaltic wave from the pylorus to the anus, which bypasses all physiological brakes of the ileocecal valve and kinks of the colon. The reason for such diarrhea is either an acute emotional experience, or conditioned reflex irritations of a more complex nature, for example, memories of similar experiences, unfavorable external conditions (being in an environment that excludes the possibility of using the restroom).

A correct interpretation of the nature of nervous dyspepsia, and therefore targeted therapy, is possible only in the light of corticovisceral pathology.

Afternoon diarrhea

A) Biliary diarrhea in the form of crises of sharp pain with a violent urge to defecate and the release of dark yellow or green feces with an abundant content of bile pigments. The equivalent of these diarrhea are “bile crises” with profuse vomiting of bile up to several liters (own observations). The causes of crises are a visceral reflex due to increased nervous excitability. It is based on latent cholecystitis. The discharge of bile stool causes a burning sensation in the anus. b) With colitis, the afternoon urge to defecate occurs from irritation of the transverse intestine from a full stomach. The nature of feces corresponds to the initial place of urge, from where long peristaltic waves come, which reach the rectum. The cause of afternoon diarrhea lies in an increase in intestinal and general nervous excitability.

3. Dystrophy

In contrast to early childhood dystrophy with its debilitating diarrhea, which is a specific nosological unit, dystrophy in adults is an intermediate, passing stage or complication of various intestinal diseases, for example, a very common consequence of severe colitis. Here we will consider only the role of dystrophy as one of the syndromes of intestinal pathology.

General nutritional disorders can develop with any intestinal disease, organic and functional, accompanied by impaired absorption of food in the small intestine. The causes of resorptive disorders may be the accelerated passage of food and atrophy of the wall of the small intestine due to prolonged inflammation (in severe enteritis), emptying of the lymphatic vessels of the mesentery (in tuberculosis or the so-called Whipple's lipodystrophy), but even outside such severe diseases, absorption processes can be disrupted by sharp acceleration of passage in the small intestines of a purely neurogenic nature.

Loss or sharp limitation of absorption in the small intestines naturally leads to a deficiency of the most important nutrients in the body, primarily proteins and fats. This deficiency is inevitable even when, after an accelerated passage through the small intestines, the food gruel lingers in the large intestine, where it thickens after the absorption of water. The consequence of hypoproteinemia is “protein-free” edema due to disruption of oncotic balance. At the same time, hypolipemia and hypoglycemia occur, as well as a deficiency of essential vitamins in the blood and tissues.

Debilitating diarrhea leads to dehydration of the body and thickening of the blood, which changes all biochemical parameters towards their increase: the numbers of hemoglobin and plasma proteins may be higher than normal, but the oncotic balance is maintained. However, this “dry” form of dystrophy is even more severe than the edematous one, giving, in addition to symptoms of protein, fat and vitamin deficiency, a picture of tissue dehydration with changes in neuromuscular functions: convulsions, paralysis, often depressive psychosis and multiple vitamin deficiency, in particular pellagroid type.

Suppression of all digestive functions, weight loss and general disruption of trophism can lead to irreversible changes in the nervous system. A sharp drop in resistance opens the gates to any infection (pneumonia, dysentery, tuberculosis, erysipelas), from which the patient can die.

Fortunately, these severe, irreversible cases under normal nutritional conditions are a rare exception. Much more common are erased, vaguely expressed forms, which, however, have a similar structure of pathogenesis. Here it is only important to emphasize the importance of the dystrophic factor, which complicates any intestinal disease and leaves its mark on the course of the disease. Of particular importance is the relationship between dystrophy and infection, which comes into play secondarily, giving rise to a new phase of the disease or even a new disease, for example, bacterial dysentery, which joins primary functional dyspepsia or dystrophy. Thus, dystrophy can serve as a connecting link between the functional and organic stages of the pathological process.

4. Intestinal autointoxication

Although most of the symptoms attributed to intestinal intoxication depend on other factors - nervous, vascular, allergic, infectious, the possibility of true self-poisoning with intestinal digestive insufficiency is beyond doubt. Thus, during putrefactive processes in the intestines, a number of toxic products are formed, mainly of protein origin: toxamines (histamine, etc.), ammonia, phenols (from tyrosine), indole and skatole (from tryptophan), sulfides and hydrogen sulfide (from cystine).

During fermentation processes, organic acids can have harmful effects:

A) hemolytic effect, b) decalcifying effect due to increased loss of calcium salts, c) acidotic effect due to increased formation of acetone, d) oxalemia due to the formation of oxalic acid from carbohydrates with the help of Escherichia coli (in the cecum).

During putrefactive and fermentative processes, a combination of several harmful factors usually occurs. It is possible to distinguish putrefactive dyspepsia from fermentative dyspepsia, in addition to scatological signs, on the basis of indicanuria, especially pronounced in putrefactive dyspepsia.

Thus, the listed functional syndromes - dyskinesia, dyspepsia, dystrophy and intoxication - are common accompaniments of most intestinal diseases. Appearing either separately or collectively, these syndromes characterize the clinical picture of the entire disease and determine the choice of pathogenetic therapy.

Chronic enteritis and enterocolitis

1. Chronic enteritis

Let us begin a systematic presentation of intestinal diseases with lesions of the small intestine, since diseases of the duodenum (peptic ulcer, duodenitis, diverticulosis, etc.) are closely related to the pathology of the stomach and should be considered when describing diseases of the latter.

The general conditions of the pathology of the small intestine arise from the functional characteristics of this segment of the intestinal tube.

Motor function is determined by two border zones: proximally - the border with the gastroduodenal zone (plica duodenojejunalis), distally - the ileocecal valve. Both of these border areas are active interoreceptors, sources of abundant reflex connections. Thus, gastric contents, entering the jejunum, send the first peristaltic wave, which, if the nervous system is overexcited, can reach the anus, causing immediate diarrhea. Rapid evacuation of the stomach, in addition, gives rise to hypoglycemic reactions due to accelerated absorption of carbohydrates, and is also accompanied by a special “small intestinal shock”. Hypoglycemia and shock complicate numerous diseases of different organs and are directly related to the upper part of the small intestine.

No less important is the absorption process, which is easily disrupted by lesions of the above department. It is clear that any somewhat serious enteritis entails symptoms of a deficiency of nutrients needed by the body, in contrast to colitis, when even severe ulcerative lesions do not threaten absorption processes. Therefore, the transition of the inflammatory process from the large intestine to the small intestine, especially to its upper sections, is always a serious complication.

Secretory disorders of the small intestine play a lesser role in the overall digestive process due to the pronounced replacement role of pancreatic enzymes. However, with diffuse enteritis, both secretory and resorption processes suffer, and therefore, the trophism of the body.

Inflammatory diseases of the small intestines rarely occur in isolated form. Much more often we deal with enterocolitis. However, the involvement of the small intestine shows very clear signs. The predominance of pathology of the small intestine, even with enterocolitis, leaves a clear imprint on the entire clinical picture. However, in some cases, the clinical picture of enteritis is limited to individual symptoms, constituting only one of the components of the general disease.

Examples include giardiasis enterocolitis and mesenteric lymphadenitis. Irritations of the small intestine regularly accompany diseases such as anacid gastritis, cholecystitis, and diseases of the operated stomach.

But enteritis can also appear as an independent disease, most often in one of the following two forms.

1. Jejunal diarrhea are characterized by a violent urge to stool soon after eating (similar to Achilles or Giardiasis). The stools have a greenish color, a liquid mushy consistency, contain mucus closely mixed with feces, and abundant remains of saponified fats (crystals, lumps, needles of fatty acids). Excess fat can even make stool look discolored. This form is described as "soap dyspepsia" (Porges). Characteristic is a state of severe general weakness with a feeling of heat, trembling of the hands and dizziness, up to collapse, occurring immediately after a bowel movement and reminiscent of a hypoglycemic coma. The mechanism of this “small intestinal shock” has been explained in various ways. Some authors associate it with hypoglycemia due to the accelerated passage of food through the small intestines and rapid absorption of carbohydrates, which, with general nervous instability, causes these symptoms. Others attribute the main role to hyperemia in the region of the celiac nerve with reflex hypotension. This explanation seems to us more likely when we are talking about diseases of the small intestine, while hypoglycemia is more characteristic of a number of gastric syndromes, for example, with achylia and after gastrectomy.

2. Chronic enteritis can drag on for many years. The onset of the disease often dates back to childhood. The course is usually mild, not progressive, but with a tendency to transition to enterocolitis.

Causes

Chronic infections play a role, including tuberculosis, stomach diseases (anacidic gastritis, condition after gastric surgery), chronic intoxication (lead), overload with bulky and fatty foods. Infection in the small intestine can be maintained by changes in the bacterial flora (“dysbacteria”), when a decrease in the gastrointestinal barrier and an alkaline reaction of inflammatory secretions contribute to the introduction and development of bacteria that acquire increased pathogenicity. This fact has been proven experimentally by the intestinal cartridge method.

Main symptoms

Rumbling and transfusion in the abdomen, bloating, pain soon after starting to eat, simulating early pain in high-lying stomach ulcers. Insufficient attention is paid to the symptom of vasomotor shock after stool or food. The reason for the latter may lie in a violation of the barrier function of the epithelium of the small intestines as a regulator of the rhythm of food absorption. Diarrhea may be absent for a long time. The acceleration of passage through the small intestine is compensated by a slower passage through the large intestine, where feces have time to fully form, and starch and fiber are digested by bacteria and enzymes. Absorption disorders are manifested by abundant fat residues in the stool, which, with a large amount of fat taken, has a light color. This steatorrhea must be distinguished from other similar disorders (with pancreatitis, mesenteric tuberculosis, sprue).

Of the objective symptoms, first of all, one should note a painful zone of skin hyperesthesia in the region of the rectus abdominis muscle and posteriorly along the left paravertebral line from the last thoracic to the first lumbar vertebra (Porges). The pain point to the left of the navel coincides with that of a peptic ulcer of the small intestine. With regional ileitis, the pain point is in the ileocecal region, at the site of infiltration. With mesenteric lymphadenitis, the pain zones correspond to the course of the mesentery (Sternberg's symptom).

Laboratory symptoms

The characteristic scatological picture boils down to the presence of formed feces, closely mixed with mucus, greenish or light yellow in color, with a high content of saponified fats. Gastric secretion is often reduced to zero. Liver function tests complicated by severe hepatitis are pathological. There is an increased content of indican in the urine, as in putrefactive dyspepsia.

X-ray shows an acceleration of passage through the small intestine: after 2-3 hours, barium enters the large intestine. Sometimes, with fluoroscopy, after 2-3 hours, barium is in the stomach and large intestine, while the small intestines are empty. In other cases, there are levels of fluid in the loops of the small intestines with gas bubbles above them.

Complications. Most often, the pathological process moves to the large intestine, causing a banal picture of enterocolitis. Violation of absorption processes naturally leads to dystrophy, vitamin deficiencies and anemia. Damage to the intestinal epithelium maintains chronic intoxication, which causes a number of toxic and allergic symptoms: urticaria, eczema, Quincke's edema. In the future, the disease may be complicated by cholecystitis, hepatic colic, hypochromic anemia, glossitis, aphthous stomatitis, and anaphylactic diarrhea. Damage to the vessels of the abdominal cavity with the development of thrombophlebitic splenomegaly is also possible. As is known, the history of patients with this disease of the spleen contains indications of either abdominal trauma or chronic intestinal infections.

When differentiating enteritis from other diseases, intestinal tuberculosis, mesenteric lymphadenitis, sprue, and chronic appendicitis should be excluded.

Acute enteritis can be caused by any intestinal infection, possibly a virus or even simple cooling, judging by the literature.

Treatment involves split meals in small portions, slow eating and separate intake of solid food and liquid in order to slow down the evacuation and absorption of food. Coarse vegetable fiber and fatty bulky dishes are prohibited. Meat is recommended in large quantities (up to 200 g per day) minced or softly boiled. For constipation, raw juices, compote, and yogurt are prescribed.

Sample menu. Breakfast: soft-boiled egg, cocoa with water, toasted white (or gray) bread with butter. Lunch: meat broth or pureed vegetable soup with rice, meat cutlet, chicken or boiled lean fish with vegetable puree, fruit jelly. Early dinner: rice porridge on water with butter or cheesecakes. Before bed, tea, crackers, cookies.

For diarrhea, take an infusion of dry herbs (chamomile, mint, dill, clover) 1/4 cup 3-4 times a day.

Regional (terminal) ileitis (Crohn's disease)

In 1932, Krohn, Gunzburg and Oppenheimer first described 13 cases of severe enteritis with diarrhea, abdominal pain, exhaustion, anemia, fever, infiltrate in the ileocecal region, complicated by stenosis and fistulas. Half of the patients had scars after appendectomy. Later, similar changes (granulomas) were described in the large intestine and even in the stomach.

Pathological anatomy. Most often, the terminal loop of the ileum is affected, from where the process continues in the proximal direction, less often caudally, moving to the colon, capturing the loops of the intestine that are richest in lymphatic elements. The affected segments are thickened, rigid, the serous membrane is covered with fat and fibrinous effusion. The adjacent mesentery is swollen, thickened, and the lymph nodes are enlarged. The process of the cecum is embedded in the commissures. There are perforations of the intestine into the mesentery, with the formation of fistulas. On resected intestinal loops, the wall is sharply thickened, the lumen is narrowed, there are ulcers, necrosis and mucosal hyperplasia. Histologically, nonspecific hyperplasia of the lymphatic tissue of the submucosal layer is noted. In the lymph nodes there are giant cells without caseation and Koch's bacilli. This lymphogranulomatous process is almost indistinguishable from tuberculosis.

It was hypothesized that this disease develops due to tuberculosis of the intestine by bovine bacilli with good resistance of the macroorganism, with blockage of the lymphatic vessels and secondary infection. Anatomical similarities with Beck's sarcoidosis were also pointed out.

It was experimentally proven that it is possible to reproduce a similar process in the dog’s intestines by introducing irritating substances (fine sand, talc) into the mesentery and lymph nodes, which clog the milky ducts. Subsequent intravenous administration of bacteria enhanced the development of the process.

The etiology and pathogenesis boil down to a combination of an unknown infection with blockage of the lymphatic vessels.

The history often indicates appendicitis and bacterial dysentery, as well as poor nutritional conditions.

Crohn's disease, also known as regional ileitis, is a chronic inflammation of the intestinal wall, most commonly the final part of the small intestine or colon. Inflammation affects the deep layers of the intestinal walls, and ulcers and abscesses can form. Ulcers can completely destroy the wall, creating abnormal passages (fistulas) into other parts of the intestine, other organs such as the bladder or the skin. Deep fissures may also develop in and around the anus. Inflammation can lead to thickening of the intestinal wall and eventually complete blockage of the intestine. Symptoms of Crohn's disease appear in the form of attacks that alternate with periods of normal well-being. Some people have only one or two attacks and then recover; For others, attacks recur throughout their lives.

Causes

. The cause of Crohn's disease is unknown. . Hereditary factors apparently play some role in the development of this disease. . According to some theories, the causes of the disease may be: viral or bacterial infectious diseases, autoimmune diseases, food allergies or lymphatic stagnation. Prevention. There is currently no known way to prevent Crohn's disease, but there are various treatments that relieve symptoms.

Symptoms

1) ulcerative colitis syndrome with diarrhea and discharge of mucus and pus without obvious blood. The colon is affected only up to the descending loop, the sigmoid and rectum remain intact. However, in the future the process spreads caudally, so the operation must be performed before the onset of a late stage; 2) small intestinal obstruction syndrome; 3) pseudoappendicitis; 4) intestinal colic; 5) neurotic reactions. . Attacks of pain or cramping, usually around the belly button or lower right side of the abdomen. . Constant watery diarrhea. . Bleeding from the rectum or blood in the stool. . Anal fissures. . Nausea. . Fever. . Fatigue. . Loss of appetite and weight. . Complications in various organs and systems, such as joint pain due to arthritis, inflammation of the eyes and lesions on the skin.

Diagnostics

. A medical history and physical examination are necessary. . A blood test may be required. . An x-ray of the small intestine may be performed. . A barium enema may be given. Barium creates a clear image of the large intestine. . A rectosigmoidoscopy (to look at the lower part of the large intestine) or colonoscopy (to look at the entire colon and part of the small intestine) may be done. . A biopsy of the tissue lining the colon is usually performed during a rectosigmoidoscopy or colonoscopy to distinguish Crohn's disease from ulcerative colitis.

Treatment

. For mild attacks, patients can take over-the-counter anti-diarrhea medications and pain relievers. . Anti-inflammatory drugs such as sulfasalazine or corticosteroids may be recommended. . Antibiotics may be prescribed to treat secondary viral illnesses. . Enemas containing corticosteroids or aspirin-like medications may be used to combat internal inflammation. . Immunosuppressants may be prescribed for long-term use to suppress autoimmune activity. . Measures such as dietary changes, vitamin or mineral supplements, or vitamin B12 injections may be used to replace nutrients lost due to poor absorption. . Surgery may be required to clear blockages, fistulas, or abscesses in the rectum or intestines. . With severe and prolonged development of the disease, the damaged part of the intestine can be removed. . See your doctor if you experience symptoms of Crohn's disease (especially pain in the lower right abdomen, which may indicate appendicitis). . Call your doctor if you have black or bloody stools, a swollen belly, or a fever. Crohn's disease, also known as regional ileitis, is a chronic inflammation

The disease is complicated by abscesses, perforations, fistulas, and stenoses.

The course is long-term, cyclical, with relapses of diarrhea, anemia, exhaustion, and fever. Diarrhea is allergic in nature, without the presence of certain food allergens.

An objective examination reveals infiltration in the terminal loop of the ileum, general exhaustion, edema, dermatitis, anemia, and leukocytosis. Radiological signs are: “string sign” in the area of ​​narrowed loops and a nipple-like filling defect in the cecum.

Regional ileitis must be differentiated from intestinal tuberculosis, lymphogranulomatosis, leukemia, lipodystrophy, and sarcomatosis.

Treatment in severe cases is only surgical (resection, bypass operations, opening of abscesses, suturing fistulas). Conservative treatment is possible only in the initial stages without dystrophy and stenosis, when the inflammatory process is still partially reversible. Treatment is the same as for chronic ulcerative colitis: blood and plasma transfusions, good nutrition, multivitamins, fresh yeast, large doses of calcium.

Pellarga and SPRU

Both diseases, in which one of the most severe symptoms is debilitating diarrhea, are considered vitamin deficiencies. Even if vitamin deficiency is not the only cause of diarrhea, it still plays a major etiological role.

Pellagra

In the etiology of pellagra, the main role is played by deficiency of nicotinic acid - exogenous, due to insufficient supply with food, or endogenous, due to poor absorption or increased destruction of this vitamin. Deficiency of vitamins C and B1 also plays a role.

The well-known triad of symptoms - diarrhea, dermatitis and dementia (the "three Ds") is not repeated so clearly in any other clinical syndrome. However, individual elements of the same clinical picture (“pellagroid”) are found in all types of severe eating disorders.

Diarrhea, which began as a consequence of vitamin deficiency, subsequently becomes the cause of progression of the disease (according to the mechanism of a vicious circle). Watery stools contain a lot of undigested food debris. Intestinal passage is accelerated throughout the entire tract. Skin changes (hyperkeratosis, hyperemia with transition to brown pigmentation, peeling, weeping blisters), as well as neuropsychic disorders, are the result of deep degenerative, often irreversible changes.

The most effective therapeutic agent is nicotinic acid, administered subcutaneously or intravenously in a 1% solution of 1-5 ml or orally 0.05-0.1 g two to three times a day. At the same time, ascorbic acid and thiamine in a 5% solution of 1-2 ml are injected in the same way.

Sprue

Sprue disease is known in two forms: tropical and endemic. Like pellagra, it manifests itself as a triad of clinical symptoms: diarrhea is combined with glossitis and anemia. The crimson-red tongue with smoothed papillae resembles Genter's tongue in Biermer's anemia. Diarrhea is accompanied by steatorrhea - abundant release of all fat fractions, mainly neutral fats, as in pancreatic insufficiency, but without simultaneous creatorrhoea.

Regular passage of fatty stools is described under the terms idiopathic steatorrhea, endemic (non-tropical) sprue, white diarrhea, Herter's disease or celiac disease of childhood. This disease should not be confused with various forms of symptomatic steatorrhea due to pancreatic disease or lipodystrophy (tuberculosis of the lacteal vessels, mesentery - Whipple's disease).

Pathological changes are expressed in lympho- and plasmacytic infiltration of the wall of the small intestines, atrophy, and less often in ulcerations of the mucous membrane and fibrosis of the submucosal membrane. The same changes, less pronounced, are also observed in the large intestine. The adrenal glands show some atrophy and a decrease in lipid content.

Along with essential forms of sprue, symptomatic, secondary ones due to mesenteric lymphosarcoma and Hirschsprung's disease are also noted.

The pathogenesis of sprue is not fully understood and, apparently, is not uniform. Biochemical disorders are reduced to a violation of the absorption of dietary fats and the phosphorylation process that occurs with the participation of hormones of the adrenal cortex. It is possible that a lack of secretion of bile acids by the liver plays a role. Recently, a certain role has been attributed to folic acid deficiency. The whole syndrome appears, therefore, as a hormonal and vitamin deficiency. However, some authors do not exclude the role of infection in the form of tuberculous lesions of the lymphatic system of the mesentery or typhoid fever suffered in early childhood.

The main etiological factor is considered to be inadequate food, one-sided, excessive carbohydrate nutrition, which, especially in hot climates, contributes to the development of fermentative dyspepsia. Endocrine insufficiency plays a role as a concomitant factor, in particular during pregnancy and lactation.

According to other authors, the main role in the etiology and pathogenesis of sprue belongs to a deficiency of external or internal Castle factor, as well as damage to the absorption capacity of the small intestines after severe infections (dysentery, typhoid fever, tuberculosis).

Fermentative (“gas”) dyspepsia leads in these patients to impaired absorption of fats, calcium, vitamins and antianemic substances in the affected small intestine. From here it is easy to explain all the main symptoms of the disease: fatty diarrhea, hypocalcemia with osteoporosis, anemia and a number of vitamin deficiencies (cheilosis, glossitis, hemeralopia, polyneuritis).

Symptoms

In the first place is diarrhea with the release of grayish-yellow pasty or liquid feces, an acrid or putrefactive odor. Feces contain 45-70% of ingested fat (instead of 6% during normal digestion), mainly in the form of fatty acids and soaps. The release of nitrogenous wastes is not increased. A regular symptom in the period of exacerbation is anemia, the nature of which is variable: in the period of exacerbation - hyperchromic-macrocytic, in the period of remission - hypochromic. With severe dehydration, anemia can be masked by thickening of the blood. Glossitis of the Genterov type, stomatitis and cheilosis are regular signs of vitamin deficiency. Less regular symptoms are polyneuritis of the beriberi type (I.A. Kassirsky) and funicular myelosis. With severe diarrhea, symptoms of deficiency of all other vitamins also appear.

Hypocalcemia is accompanied by symptoms of osteoporosis and muscle spasms with normal calcium levels in the urine. The basal metabolic rate is usually increased. Despite profuse diarrhea, there is polyuria with low specificity. weight of urine, refractory to pituitrin and adiurecrin, i.e. not of pituitary origin, but arising due to insufficient reabsorption in the tubules. The content of proteins, residual nitrogen, cholesterol and blood sugar is reduced. Liver function tests are normal. Rectoscopy does not reveal anything characteristic. An X-ray examination reveals smoothness of the contours of the small intestines, persistent barium retention in individual loops of the jejunum (“fake symptom”), spotty and pinnate relief, and sometimes a megacolon pattern. The patchiness of the relief apparently depends on the accumulation of small lumps of mucus in the small intestines, which can explain the disruption of absorption processes.

The disease usually lasts for many years. The first dysyeptic symptoms (diarrhea, bloating) are often noted in childhood. Women get sick more often than men. The course is always cyclical: long-term exacerbations are replaced by more or less light intervals, when all symptoms subside, even steatorrhea disappears against the background of a low-fat diet. Anemia does not go away completely, but becomes hypochromic.

The cyclical course of sprue is characterized by a change in symptoms during periods of exacerbations and remissions: the onset of remission may be accompanied by the appearance of glossitis, cheilosis and angular stomatitis. Glossitis is observed in 90% of cases and serves as a kind of transitional symptom (from relapse to remission and back). It is not curable by diet, niacin, or riboflavin, but may resolve spontaneously or with liver therapy. Anemia is also subject to dynamic fluctuations, passes with the onset of remission through the phases of macrocytic anemia, pure macrocytosis without anemia with a transition to (normalization of red blood. The outcome is often aplastic anemia.

One of the causes of anemia and cachexia is sodium deficiency, and to a lesser extent, chloride deficiency due to the loss of electrolytes in feces.

In the differential diagnosis, a number of related “diseases” should be taken into account. Lesions of the pancreas (severe pancreatitis, cystic fibrosis) occur with a normal nitrogen content in the stool, neutral fats predominate, urine diastasis is increased. Pancreatic cancer is characterized by severe pain and weight loss. Intestinal tuberculosis pulmonary history, lung damage and the presence of bacilli in the stool are important. With Addison's disease, skin pigmentation, hypotension, and a flattened sugar curve after exercise are observed. Tropical sprue occurs with persistent hyperchromic anemia, otherwise it is difficult to distinguish from endemic sprue and is treated with the same methods.

Pellagra does not cause hyperchromic anemia even in the period of exacerbation, but it is characterized by characteristic dermatitis and mental changes. Biermer anemia occurs with more pronounced hemolysis, normally colored stool, persistent gastric achylia, without cachexia. Among the changes in the nervous system, funicular myelosis is most often noted, and not polyneuritis, as with sprue.

Treatment. In the foreground is a diet aimed at influencing two main digestive disorders - steatorrhea and fermentative dyspepsia.

Some authors solve this problem by recommending a sharp restriction of carbohydrates and an increased supply of fats, which should replenish their loss in feces (10-15 eggs and 50 g of butter per day). However, most doctors put forward another principle of diet, which seems more justified: a sharp restriction of fats with a slightly reduced supply of carbohydrates, which, as experience shows, are better tolerated on a low-fat diet. Among carbohydrates, products with loose fiber (fruits, berries) are most recommended, while limiting starchy foods (bread, potatoes), which enhance fermentation processes in the intestines. During periods of exacerbation, sugar is sharply limited. It is necessary to increase the supply of proteins to 1.5-2 g per 1 kg of weight to combat fermentative dyspepsia and hypoproteinemia. Calcium is prescribed in large quantities both in the form of sour dairy products and as a medicine: intravenously 5% calcium chloride and orally gluconate and calcium carbonate. To increase its absorption, daily injections of 1 ml of parathyroidism are indicated.

The effect on anemia is achieved with the help of iron and vitamin B 12 supplements. Liver drugs are effective only when administered parenterally, in contrast to Biermer's anemia, when internal methods also help. Treatment of vitamin deficiency requires the use of all vitamins.

The effect of folic and folinic acid (10-15 times more effective than folic acid), as well as vitamin B 12, was studied mainly in tropical sprue. An increase in reticulocytosis and an improvement in the composition of red blood were noted in some patients treated during the period of remission. Folic acid potentiates the hematopoietic effect of vitamin B 12. Plasma transfusions help normalize blood protein levels. The use of pancreatin in doses up to 3.0 per day is indicated. Corticohormones and ultraviolet irradiation are recommended as general stimulants.

A complete cure for sprue is hardly possible. However, long-term remissions make it possible to restore relative working capacity for a long time. For illustration, we present excerpts from case histories.

The role of tuberculosis was reduced to the influence of a secondary aggravating factor, which was layered on the main background of vitamin deficiency. The factors of vitamin deficiency, dystrophy and secondary infection were closely intertwined, which made it difficult to identify the leading factor in pathogenesis and etiology, and only dynamic observation made it possible to clarify the sequence and relationship of individual elements of this complex nutritional disorder.

Chronic enterocolitis

This section of intestinal pathology presents the greatest difficulties in terms of nomenclature and classification. The terms “colitis” and “enterocolitis” refer primarily to inflammatory processes in the intestines, as opposed to purely functional conditions.

Naturally, the line between functional and organic suffering can be blurred in some cases, for example, when functional constipation is complicated by inflammatory reactions with the development of “constipative colitis.” The feedback relationship between functional disorders due to the primary organic process is also clear, i.e. colitis can occur with constipation, when both conditions mutually aggravate each other, according to the “vicious circle” mechanism. And yet, with all the closeness of organic and functional diseases, they can be studied separately in order to gain a clearer understanding of the pathogenesis of intestinal diseases.

An attempt by some authors to distinguish between two pathogenetic groups of colitis - infectious and alimentary - has not found wide recognition, since the first group can be considered as dysenteric, post-dysenteric, protozoal colitis, etc., and the second - as intestinal dyspepsia and dystrophic enterocolitis.

The widely used term “spastic colitis” is completely unsuitable from a clinical point of view. Under this mask, a variety of conditions are hidden: reflex colospasm due to certain diseases of the abdominal organs, vegetative reactions due to general neurosis, as well as any form of colitis accompanied by intestinal spasms. In each individual case, a detailed examination will be required to clarify the etiology. The diagnosis of “spastic colitis” is usually only a forced designation for all sorts of unclear intestinal diseases.

Syndromes of multiple bowel diseases

1) spastic syndrome with alternating constipation and diarrhea; 2) hyperkinetic syndrome with diarrhea and acceleration of the entire intestinal passage; 3) pain syndrome with normal or delayed stool, intestinal colic and severe pain in the intestinal tract; 4) toxic syndrome with symptoms of general intoxication (headaches, weakness, fatigue, sleep disturbances); 5) anemic syndrome due to intestinal bleeding and slow blood regeneration; 6) dystrophic syndrome due to severe enterocolitis with impaired absorption and utilization of food and multiple hypovitaminosis.

The listed syndromes, although not associated with a specific etiology, give a typical pathogenetic imprint of the disease and help in the choice of differentiated therapy.

The study of the causes of chronicity of colitis deserves great attention. Most chronic colitis develops from acute forms, and this transition occurs either directly, without visible recovery, or imperceptibly, after an intermediate hidden stage of apparent, false recovery. The latter forms are more difficult to recognize, their etiological roots can remain hidden for a long time.

But there are also forms with such an imperceptible tendency towards a gradual, persistent course that one gets the impression of primary chronic colitis, occurring like chronic appendicitis. This includes many cases of intestinal giardiasis and trichomoniasis, and possibly other chronic infections, even bacterial dysentery, when the onset of the disease is not specified by anamnesis, the disease proceeds cyclically with alternating exacerbations and remissions over a number of years.

The cause of chronicity can often be accurately determined. With bacterial dysentery, it usually consists of delayed recognition, late initiation of treatment and insufficient radicality and duration of therapy using too weak doses, which contribute to the development of sulfonamide-resistant strains of bacteria. In other cases, for example, with invasion by Giardia and amoebas, these protozoa become encysted and disappear from the intestinal lumen; they take refuge in the submucosa or deep pockets and become inaccessible to specific drugs.

Finally, in a number of cases, the chronicity of the lesion is supported by weak body resistance, vitamin deficiency, anemia, dystrophy, which delays the fight against invasion for a long time and interferes with recovery. Resistance to infection may precede or develop as a result of the disease itself. In such cases, specific therapy usually turns out to be powerless and must be replaced by general restorative means of influencing the macroorganism, for example, blood transfusions, glucose with vitamins, enhanced nutrition, and climatic treatment.

Pathomorphology of enterocolitis

The old division into “superficial” and “deep” colitis (in other terminology - severe, ulcerative, parietal) does not cover the entire amount of morphological changes occurring in the intestinal wall during enterocolitis. In addition, a morphological sign does not always serve as an indicator of the severity of the disease. Only in the most severe, irreversible forms of colitis (amoeba, tuberculosis, dysentery) do we deal with deep lesions of all layers of the intestinal tube, up to penetrating and perforated ulcers, fistulas, stenoses, reticulosis, granules, tumor-like infiltrates.

In acute and subacute processes, the most common are the usual inflammatory changes (swelling, hyperemia, increased secretion of mucus, easy soreness and bleeding). Inflammatory exudate may contain leukocytes, plasma cells, erythrocytes, deflated epithelial cells, and soluble protein. In clinical conditions, these inflammatory changes are detected using laboratory and rectoscopic studies and partly according to X-ray examination of the relief.

In chronic processes, deeper lesions (wall rigidity, adhesive adhesions, stenosis and deformation of intestinal loops) are established during life mainly by radiology. These intravital diagnostic methods make it possible, along with a physical examination of the abdomen, to monitor the dynamics of anatomical changes, which are partially reversible with treatment.

Autopsy data also indicate a wide variety of morphological changes in the intestinal wall during colitis. The anatomical process in some cases occurs diffusely, in the form of “pan colitis,” often spreading to the small intestines. In other cases, it is nested, focal in nature, localized in certain parts of the intestinal tube. A specific topography is characteristic of the infiltrative-ulcerative form of intestinal tuberculosis with its favorite localization in the cecum (tumor ileo-coecalis), with a tumor-like infiltrate and caseous decay. Regional ileitis produces similar gross morphological changes in the terminal ileum, but without the participation of bacillary factor.

The histomorphology of colitis is characterized by exceptional diversity, an abundance of cytological variants (proliferation of lymphocytic, plasmacytic, reticuloendothelial elements according to the type of reticulocytosis). Individual layers of the intestinal wall are also affected differently: from hypertrophic and polypous changes to complete atrophy, then the intestine turns into a thin-walled tube with almost complete disappearance of all parenchymal elements, by analogy with atrophic gastritis. Unlike the pathology of the stomach, when in chronic gastritis inflammatory processes alternate or are combined with degenerative restructuring of the epithelium, in colitis inflammatory changes predominate. It is noteworthy, however, that in a number of cases there is a striking discrepancy between the clinical picture of dystrophy and the nature of the anatomical process, when instead of the expected thinning of the intestinal wall, hypertrophy and swelling of the folds of the mucosa are detected. Thus, in patient 3., who died from dystrophic enterocolitis, the section revealed hypertrophy of the intestinal wall with the proliferation of reticular elements of the submucosal layer.

The main anatomical forms of enterocolitis (catarrhal, follicular, diphtheritic and ulcerative-necrotic) do not exhaust the variety of morphological changes in the intestinal wall. Tuberculosis is characterized by caseous decay, and amoebiasis is characterized by the formation of granulomas (“amoebas”) with the possibility of malignancy, which is not characteristic of bacterial dysentery.

Ulcerative processes in the intestines often reflect the specific etiology of the disease. Thus, ulcers in dysentery, amoebiasis, tuberculosis, lymphogranulomatosis and cancer, regional ileitis and ulcerative colitis have a morphological imprint characteristic of this etiological factor. But there are also uncharacteristic changes characteristic of any chronic inflammatory process.

In bacterial dysentery, three morphological stages are described: catarrhal-diphtheritic, ulcerative and regenerative. As with all anatomical processes, in the intestine, especially with ulcerative lesions, changes in the peripheral autonomic nervous system are of great importance.

There is no doubt that damage to nerve endings and plexuses (Auerbach's, Meissner's, solar, aortic) occurs not only in ulcerative forms, but also in all other severe intestinal diseases, and possibly in functional dyspepsia, dyskinesias and anatomical anomalies such as megacolon and dolichosigma , in which denervated areas of the distal colon are observed, explaining movement disorders during the expansion of intestinal loops.

Lesions of the peripheral nervous system best explain trophic, vascular and motor disorders in all forms of colitis and serve as a link between functional and organic diseases.

Lesions of the lymphatic vessels and mesenteric nodes are important, causing severe disorders of fat absorption. This applies to various forms of mesenteric lymphadenitis (tuberculous, etc.), so-called intestinal lipodystrophy (Whipple's disease), regional ileitis (Crohn's disease), celiac disease (Herter's disease), etc.

Acute diarrhea, frequent passage of watery stools, is not a disease, but rather a sign of an underlying medical condition. As food passes through the digestive system, water is absorbed through the walls of the large intestine. Diarrhea and dehydration occur when fluid is not absorbed but remains in the intestines and is excreted in the feces. Although diarrhea usually clears up without treatment within two or three days, any resulting dehydration is a serious problem (especially among infants and older adults) and needs to be treated quickly.

Causes

Food poisoning due to various causes, including viruses or bacteria. . Viral infection of non-food origin. . Reaction to certain foods (for example, citrus fruits or beans). . A large number of artificial sweeteners found in foods, chewing gum and other products. . Alcoholic drinks. . Certain medications, including medications for hypertension, heart disease, and some antibiotics. . Infectious diseases such as traveler's diarrhea, typhoid fever, amoebiasis and bacillary dysentery (shigellosis). . Emotional stress and anxiety.

Symptoms

. Watery stool. . Increased bowel frequency. . Cramps and pain in the abdomen. . Signs of dehydration in young children: drowsiness; indifference; tight skin; glassy eyes; dry, sticky mouth and tongue; constant crying. . Eat cooked foods and fruits that you can peel yourself. Local water or raw food may contain bacteria that cause diarrhea. . Find ways to relieve emotional stress and try to avoid stress.

Diagnostics

Diarrhea is easy to identify by its characteristic symptoms. . A laboratory stool test may be performed for persistent diarrhea. . A colonoscopy with a rectal biopsy can help diagnose diarrhea caused by viruses, bacteria, or inflammation.

Treatment

Prevent dehydration (especially important for older people and young children) by drinking a solution of one teaspoon of salt and four teaspoons of sugar in one liter of water. Measure accurately as too much salt can increase dehydration. Drink 0.5 liters of solution while diarrhea continues. . Do not take anti-diarrhea medications for the first few hours (diarrhea may be ridding your body of infection carriers or irritants). If work or other obligations require the use of anti-diarrhea medications, use one that contains loperamide (such as Imodium) or bismuth subsalicylate (Pepto-Bismol). . Reduce (or avoid) dairy, alcohol, and fiber-rich foods during your recovery. . For young children: While diarrhea persists, do not feed them milk. Instead, give them an electrolyte solution, which can be purchased at the pharmacy. If the diarrhea goes away within two days, start giving milk gradually over 24 hours. . Call your doctor if diarrhea persists for more than 48 hours or is accompanied by dizziness, severe cramping, a temperature higher than 38.3°C, or blood in the stool. . Contact your doctor if diarrhea occurs frequently. . Attention! Call a doctor immediately if a young child or elderly person shows signs of dehydration.

Prevention

Do not eat food if you think it has gone bad. . Avoid foods to which you are sensitive. . When traveling abroad, drink only bottled or boiled water.

Bacterial dysentery

Despite the long-known etiology, well-studied typical characteristics of different types of bacteria and rich epidemiological experience, bacterial dysentery continues to remain the focus of attention of doctors. The reasons for this interest are clear. Dysentery is still one of the most difficult infections to eradicate, since contact infections persist throughout the year almost everywhere. The complete elimination of dysentery is made difficult by the constant presence of small foci, mainly in the form of carriers and excretors of bacteria - people who are practically healthy, but have recently been ill or have not even been ill at all. In addition, a delay in recognizing and isolating patients with acute dysentery easily leads to dispersion of infection and epidemic outbreaks, which are much more difficult to eliminate than individual, sporadic cases. Dangerous epidemic foci are also maintained by unsanitary conditions, especially during the hot months of the year.

In the first days of the disease, positive cultures from mucous-bloody stools are observed in 85% of cases, from mucous stools - in 18%, and from stools uncharacteristic of dysentery - only in 9%.

Bacterial dysentery is a potentially dangerous and extremely easily transmitted infectious disease of the colon. Symptoms appear after an incubation period of one to four days and usually subside after 10 days. In severe cases, the illness can last up to six weeks, but in most cases the illness is mild. Dysentery is most common in children aged one to four years. It is common in overpopulated areas with poor sanitation and often occurs in epidemics; To stop the spread of the disease, sick people are isolated and quarantine is introduced in the area of ​​the epidemic.

Symptoms

Initially, watery diarrhea. It can progress to diarrhea with mucus and blood. . Tension during bowel movements, accompanied by pain in the rectum. . Abdominal pain; pain all over the body. . Nausea and vomiting. . Fever. . Rapid dehydration and weight loss (young children and older adults are especially susceptible to dehydration).

Treatment

Electrolyte solutions (such as sodium and potassium) may be needed to prevent dehydration. In severe cases, they can be used intravenously. Until you see your doctor, stay hydrated by using sports drinks or a solution of one teaspoon of salt and four teaspoons of sugar per liter of water. It is important to prepare the solution correctly as too much salt can increase dehydration. Drink half a liter every hour while diarrhea persists.

Do not take over-the-counter anti-diarrhea medications unless your doctor recommends them. With the help of diarrhea, the body gets rid of infectious agents.

Although the infection mostly goes away on its own, antibiotics are often given to limit its spread. Medicines must be taken for the entire prescribed period.

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

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

Prevention

To prevent the spread of infection, wash your hands frequently with warm water and soap, especially after bowel movements or before eating. (Because dysentery has an incubation period of up to four days, you could be a carrier of the disease without knowing it.) When traveling abroad or in areas with poor sanitation, drink only bottled or boiled water or other bottled drinks, and eat only cooked foods and fruits that you can peel yourself.

Symptoms

Typical bacterial dysentery begins acutely, after a short, often hidden prodromal period of general malaise (corresponding to the phase of absorption of toxins in the intestines). The initial symptom is diarrhea with the release of loose stools, soon followed by tenesmus with the discharge of mucous-bloody films and cramping abdominal pain. Tenesmus reaches a frequency of 20-40 or more per day. The severity of the disease is determined by high temperature, frequency of tenesmus, general condition of the patient, activation of previous diseases (malaria, tuberculosis, hidden septic lesions). An aggravating factor is the age of the patients: dysentery is especially dangerous and has the highest mortality rate in infancy and old age.

The pathogenesis of diarrhea in dysenteric colitis is toxic, similar to malarial colitis. Late and inconsistent damage to the small intestine is explained by local immunity of the small intestinal mucosa.

Immunity to dysentery is usually very unstable and only rarely lasts 2-3 years. Hence the frequency of relapses, reinfections and chronic forms of the disease. Relative immunity still apparently occurs, since healthy people have a positive agglutination reaction, the diagnostic value of which, however, is small.

The entire course of the disease can be divided into three periods (not counting the prodromal period). The first period, lasting 2-3 days, is characterized by symptoms of acute irritation of the nerve endings of the distal colon with the release of first liquid feces, and then films of mucus, blood and pus, with a high temperature reaction. Depending on the severity, this stage is also marked by a number of general toxic symptoms (headache, drowsiness, fatigue). It is especially pronounced when infected with Grigoriev-Shiga-Kruse bacilli, which form endotoxins. In mild and atypical cases, tenesmus disappears within a few hours or may be absent altogether, making diagnosis difficult.

In the second period, there is a subsidence of tenesmus, a drop in temperature, the disappearance of general intoxication, the appearance of loose stools due to additional damage to the small intestines and the removal of primary colopasm, which delayed the passage of feces. This enterocolitis is already commonplace, uncharacteristic and can drag on for 2-3 weeks. An aggravating factor is gastric achylia, which developed due to a dysentery infection or preceded it. During this period, symptoms from the liver and biliary tract, activated by intestinal infection, may appear. Dysentery bacteria in feces disappear when acute symptoms are eliminated, but can linger until complete clinical recovery in deep encysted foci of intestinal folds.

The third period is marked by early complications in the form of pyelocystitis, nephrosis, hepatitis, polyneuritis, polyarthritis or arthromyalpy, general dystrophy. Irritation of the thyroid gland and interstitial medulla sometimes causes prolonged tachycardia and sweating. Toxic reactions from various organs and systems can drag on for many months. Post-dysenteric arthritis and neuritis, as well as general nutritional disorders, are particularly persistent.

In severe forms, symptoms of dehydration (cholerine type) develop in the form of dry tongue and skin, convulsions, collapse, cold extremities, and hypotension. We also had to observe a picture of real meningitis, which subsided within (several days.

In recent years, the general “regime” of dysenteric diseases has changed significantly. The Grigoriev-Shiga forms have become very rare, inferior in frequency to the Sonne and Flekener forms. The clinical picture has also changed significantly, in which it is not the previous acute hemorrhagic forms with tenesmus and multiple ulcers on the colon mucosa that predominate, but milder, erased forms of the disease. Severe complications, especially from the joints and nervous system, are also much less common.

In the blood picture in the acute period, the most constant is the band shift of neutrophils, which is almost never found in food infections (salmonellosis). There is often a slightly increased leukocytosis (ie 12,000-15,000). An increase in the number of leukocytes to 70,000 is observed only in the toxic form, often simultaneously with erythrocytosis, due to irritation of the reticuloendothelium and blood thickening. Increased lymphocytosis is observed less often. The toxic form, in addition to leukocytosis, is characterized by the phenomena of nutritional dystrophy, necrosis of the intestinal wall and general sepsis from a secondary purulent infection.

Complications of dysentery affect numerous organs and systems. Otitis, iridocyclitis, polyarthritis, pericolitis, mesenteric lymphadenitis, pancreatitis, and less commonly myocarditis, encephalitis, and paraplegia are observed. In addition, there are complications due to secondary infection in the form of bronchitis, pneumonia, and pleurisy. Children often have stomatitis, gingivitis, mumps, pyelocystitis, and nephritis. Sepsis may develop due to pyogenic and anaerobic infections, especially after intestinal perforation.

Nowadays, thanks to timely and vigorous therapy, these complications have become very rare.

Many patients, after suffering from dysentery, experience achylia of the stomach, usually of a transient nature. However, in some cases it is replaced by persistent anacid gastritis.

Diagnostics

Dysentery differs from ordinary infectious diarrhea in the presence of blood. . A physical examination and medical history are necessary. . Stool samples are taken for examination under a microscope and for culture of bacteria to confirm the presence of dysentery bacillus. . A blood test may be taken to look for abnormalities in ion concentrations or to determine anemia.

Bacteriological diagnosis turns out to be positive on average only in 40-50% of cases of infection, despite technical improvements (Zhagar et al.), and in chronic dysentery even much less often. An increase in the percentage of positive answers is possible only with 3-5 repeated tests on the same patient. Therefore, it is quite correct to propose that any acute intestinal disease that occurs against the background of an epidemic outbreak be considered dysentery, regardless of a negative stool test.

Naturally, technical defects in bacteriological research (remoteness of laboratories and their overload, incorrect taking of substrate, lack of high-quality media, etc.) necessitate clarification of clinical diagnostics. In typical cases, this is not difficult: an acute onset, an increase in temperature and, most importantly, characteristic tenesmus with the release of muco-bloody films - a fairly typical picture, almost never encountered in acute colitis of other etiologies.

However, this acute stage can be so short-lived or erased that by the time you first contact a doctor, the disease already gives the impression of banal enterocolitis, especially if the disease is associated with food intoxication.

Such cases often give rise to diagnostic errors when acute dysentery is visible. In these patients, during the initial stool examination, no dysentery bacteria are found; the patients are discharged with a diagnosis of “food intoxication,” but upon secondary hospitalization, one or another type of dysentery bacteria is already detected.

All this gives grounds for infectious disease specialists to consider every case of acute enterocolitis as dysentery and to demand the immediate isolation of such patients in special departments, not only against the backdrop of summer epidemics, but also under normal conditions, all year round. This strict approach is justified from an epidemiological point of view. But it also has a downside: a certain percentage of non-dysenteric patients end up in infectious diseases departments, which does not exclude the danger of contact nosocomial infection. . This often forces the less conscious population to hide intestinal disease from the district doctor. An even greater danger of such a one-sided approach to the etiology of intestinal diseases is that it reveals a whole series of colitis of a different nature, especially protozoal and salmonella.

A further aggravating factor is the hot summer season with an abundance of flies that transmit infections from sewage to humans, contaminating food and drinking sources, with the danger of infection from increased consumption of raw water and cold drinks, and contamination of food with dusty hands. It is clear that the fight against dysentery comes down mainly to issues of housing and food sanitation and hygiene - personal and mass.

In the first place is clinical diagnosis, taking into account the overall picture of the disease, which in typical acute cases is almost impossible to mix with any other disease. With more erased forms, the epidemiological situation, the multiplicity of diseases in limited foci, as well as anamnestic data on a previous similar illness and contact with dysentery patients are taken into account. In addition, the clinic has the last, decisive word in very frequent cases when bacteriological testing gives a negative result.

Clinical diagnosis is fairly firmly based on the typical picture of the disease: acute onset, headaches, fever, abdominal pain, tenesmus and the type of intestinal discharge. Milder forms occur under the guise of banal enterocolitis, gastroenteritis or food intoxication. There is a well-known parallelism between the clinical picture and the type of pathogen. Thus, Sonne sticks give a more violent onset with high but short-term fever, mild tenesmus and a predominance of symptoms of gastroenteritis. Flexner's dysentery occurs as ulcerative colitis with a more protracted febrile period. The Grigoriev-Shiga forms are more rare in our country; they are characterized by a severe course with pronounced intoxication. This clinical-bacteriological connection, however, is far from constant. The nature and severity of the clinical picture, as well as mortality, are also associated with the characteristics of each epidemic.

An important method is the bacteriological examination of stool or intestinal mucus taken through a proctoscope. We have already discussed the limitations of this method, which rarely gives more than 70% positive results even in the acute stage of the disease. One hundred percent positive answers are possible only in the fourth or fifth analysis, and then subject to the complete exclusion of medications. The first analysis at best gives 70%, the second - up to 84% of positive answers. There is even a proposal to increase the number of tests to nine. It is clear that such requirements in the context of the fight against dysentery are generally impossible to fulfill.

The following factors play a role in increasing the frequency of positive findings: the technique of taking the substrate, repeated, fairly frequent tests, proximity to the laboratory and the quality of the culture media. A single negative answer does not exclude bacterial infection. The early period of the study is also important, while the bacteria are still in the intestinal lumen and have not been eliminated or encysted in deep intestinal foci.

The accuracy of the bacteriological response is especially important not so much in the midst of an epidemic, when all cases of acute colitis can practically be considered as dysenteric, but in sporadic diseases, as well as in the general dynamics of observations of those who have recovered from acute dysentery. An accurate assessment of the moment of bacteriological recovery is very important. As a rule, this moment is determined by three consecutive negative tests over 5-7 days. Here, the research technique is especially important to avoid unnecessary delays in hospitalization due to the alternation of negative tests with positive ones. Even five negative consecutive tests were established for workers in food shops and childcare facilities.

Thus, bacteriological examination data are especially important for confirming the diagnosis of dysentery, establishing the timing of discharge from the hospital, and avoiding bacilli carriage as a source of new infections.

Serodiagnosis. A relative help for bacteriological research is the agglutination reaction (“dysenteric Vidal”). According to the literature, with Sonne type infection, this reaction is positive on the 6-10th day of illness in 50% of patients, on the 10-15th day - in 96 % (E.M. Novgorodskaya). According to other data (E.D. Ravich-Birger), agglutinins appear in the blood serum of 62% of dysentery patients on the 2nd day, in 73% - on the 3rd. The reaction is considered positive for Flexner cultures 1: 200, for Shiga cultures 1: 100. The precipitation reaction with hapten gives, according to E. D. Ravich-Birger, up to 60% positive results.

Scatological diagnosis is unreliable. The presence of a large number of leukocytes in the stool is by no means characteristic of a dysentery coprogram. The appearance of the discharge is typical only in the initial period of tenesmus. Later, during the period of enterocolitis with liquid or mushy feces, the coprogram no longer has anything characteristic.

Sigmoidoscopy for acute dysentery reveals catarrhal changes (swelling, intense hyperemia, slight soreness, bleeding of the mucous membrane), deposits of mucus and pus, and minor erosions. In later stages, as well as in chronic dysentery, characteristic ulcers of various shapes and sizes are noted. Ulcers form in areas of angiospastic and trophic defects and wall necrosis. The mechanism of their formation is predominantly neurotrophic, as in the case of damage to the gray tuberosity or peripheral sympathetic nerves (in animal experiments). In the rectum, oval-shaped ulcers with thickened edges and periulcerous hyperemia are especially common. The bottom of the ulcers is covered with purulent-fibrinous or mucous deposits. Deeper ulcers actively bleed and are covered with hemorrhagic clots. Necrotic changes around ulcers lead to infiltrative thickenings of the entire intestinal wall, but without developing into true granulomas and stenoses characteristic of amoebiasis. In a number of cases, copious discharge of pus in the form of real pyorrhea is described, which can cause purulent “cases” or “muffs” on the stool and lead to a state of septicopyemia. The factor of vitamin deficiency and dystrophy plays a role in the occurrence of ulcers, especially in chronic dysentery with a decline in general nutrition. Such ulcers in post-dysenteric stages have nothing characteristic and do not differ from other forms of trophic ulcers. Hence the great difficulty in differentiating dystrophic ulcerative colitis from dysenteric colitis. Anamnestic data on acute dysentery should speak in favor of the latter.

However, often only banal symptoms of proctosigmoiditis are observed (marbling, hyperemia, increased vascularization, swelling of the mucous membrane, mucus deposits), characteristic of acute colitis of any etiology, even non-infectious ones (for example, with hemorrhoidal or constipating proctitis). Therefore, basing the diagnosis of dysentery only on such nonspecific signs is extremely risky.

Timely diagnosis of acute bacterial dysentery allows for early isolation and effective therapy, localizing the epidemic focus and preventing the development of chronic forms, complications and bacilli carriage.

Differential diagnosis

Amoebas and aza are characterized by stool in the form of raspberry jelly or gelatinous lumps, funnel-shaped ulcers on the rectal mucosa and, of course, mobile amoebas or cysts in the feces. Regular examination of freshly obtained warm stool is necessary to exclude other forms of protozoal colitis. Colitis due to food toxic infections (hemorrhagic form) is difficult to distinguish from acute bacterial dysentery. However, even hemorrhagic forms of colibacillosis and salmonellosis usually occur with a picture of initial gastroenteritis, and not sigmoiditis, without tenesmus typical of dysentery. In children, acute hemocolitis can be caused by intussusception of the colon; in older people, tenesmus with bloody discharge is a common symptom of rectal cancer.

Chronic dysentery

The transition of an acute form of dysentery to a chronic form changes the “face” of the disease so much that it seems like a new disease, a new nosological unit. All signs and properties of the disease change: course, clinical picture, outcomes, response to treatment. Chronic forms, along with the associated carriage of healthy and recovered patients, are the main source of persistence of infection throughout the year and the reason for its difficult elimination.

The frequency of chronic forms depends on treatment tactics in relation to the acute period and, according to various sources, ranges from 25 to 75% of all acute dysentery diseases. The causes of chronicity lie mainly in the late and insufficiently vigorous treatment of the acute stage. In this case, bacteria resistant to sulfonamide drugs can develop, which take refuge in hermetic foci, in the deep folds of the intestinal mucosa.

Concomitant diseases, especially helminthiasis and protozoal infection, are aggravating factors. According to A.F. Bilibin, pure forms of chronic dysentery (without the participation of a second infection) occur only in 20% of cases. It should be noted that, thanks to vigorous anti-dysenteric therapy, the number of chronic cases has decreased significantly in recent years.

Chronic forms are especially common in early childhood. Duration of the disease up to a year occurs in 9% of cases, from 1 year to 5 years in 59%, over 5 years in 32%. Chronic dysentery is characterized by an alternation of true relapses (with activation of remaining bacteria) and exacerbations due to superinfection or eating errors. These options can be distinguished by determining the serological types of intestinal flora.

The transition to the chronic form occurs in some cases almost immediately after the acute stage, in others, more often, after an intermediate period of apparent recovery. All symptoms of colitis may disappear for several weeks or even months (the exact period is not established), after which a relapse occurs. In some cases, the relapse seems to repeat the picture of acute dysentery, in others it occurs less clearly, under the guise of banal enterocolitis.

Chronic dysentery is characterized by a sluggish, recurrent course, and exacerbations are usually associated not with a violation of the diet, but with an accidental new infection of the intestines, sometimes only with nervous irritations.

Diagnosis of chronic dysentery is much more difficult than in the acute form. The frequency of bacteriological data does not exceed 25-40% due to the difficulty of culturing bacteria from deep intestinal lesions. With erased forms, a precipitation reaction with a hapten sometimes helps.

Clinical diagnosis encounters certain difficulties due to the blurred picture of the disease. Characteristic dysentery symptoms in their original form, characteristic of the acute form, are relatively rare, and are inferior in frequency to the symptoms of banal enterocolitis. Due to diagnostic doubts, some experts consider all chronic diarrhea to be dysenteric. Progressive dystrophy allegedly speaks in favor of a specific etiology. Such statements, it seems to us, require great caution due to the abundance of similar clinical forms of other, non-dysenteric etiology (protozoa, salmonellosis, tuberculosis). The development of dystrophy is possible on any soil. The instability of the uniform (dysentery) position is obvious, if only in view of the frequent failure of antidysentery therapy. Only a detailed examination of patients, careful weighing of anamnestic and differential diagnostic data can clarify this complex problem and give a strong weapon into the hands of therapists.

The above does not at all deny the fact of the frequency of cases of chronic dysentery, which even many years after the onset of the disease is amenable to targeted treatment.

Treatment of dysentery

In the acute form of dysentery at a time when sulfonamides were not yet used, the most effective remedy was the early administration of a laxative, especially castor oil, for the vigorous evacuation of all parts of the intestines. Subsequently, bacteriophage was prescribed, and then tannalbin, bismuth, and chalk as astringents. Currently, we have at our disposal a large supply of sulfa drugs and antibiotics, which, with early and vigorous use, provide almost one hundred percent recovery from acute dysentery. It is recommended to use two sulfonamides simultaneously, combining their local action with a resorptive one and choosing the least toxic drugs. In first place are sulgin and phthalazole, and among the resorptive ones are norsulfazole and sulfodimezin. Dosage: 0.5 of each drug, in the first 2 days 6 times a day, on the 3-4th day - 4 times, on the 5-6th day - 2 times; total for the course 22.0-25.0.

Gramicidin enemas (50-100 ml of 0.4% solution every other day), a total of 6-10 enemas, as well as a decoction of eucalyptus, 15.0-300.0 tablespoons orally, are a good help. Painful tenesmus can be soothed with microenemas of chamomile or a weak solution of manganese.

For toxic forms, injections of bivalent serum against dysentery bacteria of the Flexner-Sonne species with desensitization according to Bezredka are indicated. For collapse - caffeine, camphor, infusion of saline with glucose.

After the first treatment stage, which stops the acute period of the disease, two more stages of treatment are carried out. The second stage prevents early relapses. Antibiotics are given in combination with sulfonamides. Levomycetin works best and is least toxic, starting with a loading dose of 1.0, then 0.5 five to six times a day, up to 15.0-20.0 per course.

The third stage prevents late relapses and is carried out against the background of practical recovery. The most effective combination of these two antibiotics with sulgin, as well as a course of treatment with biomycin (10.0-15.0 in single doses of 0.2).

In chronic dysentery, sulfonamides and antibiotics are less effective than in acute dysentery, having only a weak bacteriostatic effect on the secondary intestinal flora. The main goal of therapy is to influence the macroorganism to increase its resistance and reduce hypersensitivity. Phytoncides in the form of enemas from a decoction of garlic are less potent.

Treatment of complications of dysentery. The most persistent are infectious polyarthritis, second only to long-term physiotherapy (warm salt-pine, radon and sea baths, ion-galvanization, short-wave diathermy, etc.). For neuromyositis, injections of 5% thiamine chloride (vitamin B1, dibazol 0.005 each) are indicated. Local novocaine therapy in the form of subcutaneous injections of a 0.25% solution in the area of ​​muscles and joints is also very effective.

Treatment of collapse, dystrophy and dehydration is carried out using conventional methods.

For children with chronic dysentery, special sanatoriums have been organized, where long-term restorative treatment courses are conducted.

Diet for dysentery

Main objectives of the diet:

1) fight against intoxication and starvation, 2) accelerated elimination of bacteria and toxins from the body, 3) mechanical sparing of the large intestine due to its ulcerative lesions.

The course of diet therapy is divided into several cycles.

First cycle, during the period of fever and acute intestinal irritation with tenesmus: broth, pureed vegetable soup, sweet tea with lemon, rosehip infusion, fruit jelly are given (except blueberry and blackcurrant, which make it difficult to recognize blood in the stool).

Second cycle, 3-4 days after normalization of temperature, cessation of tenesmus: vegetable purees, white crackers, softly cooked porridge with milk and half and half water, raw juices (100-200 ml).

Third cycle, after the appearance of fecal stool, but in the presence of enterocolitis with diarrhea: steamed chopped meat and fish dishes, stale white bread, mashed cottage cheese, cheesecakes, and yogurt are added.

Fourth cycle transitional to the general table, in the period of residual effects of enterocolitis: complete, varied food in a mechanically gentle form (vegetable soups, boiled meat and fish in pieces, compotes, baked apples, coffee with milk).

The calorie content of the table increases from 1500 to 3000 calories. During the third and fourth cycles, with prolonged diarrhea, two apple days are carried out: 4 times a day, 250 g of freshly mashed raw apples without adding other food.

In chronic dysentery, even more than in the acute period, it is necessary to observe the principle of adequate nutrition, with minimal mechanical sparing. The most important task of diet therapy for these forms of dysentery is to increase the body's defenses in the fight against prolonged toxic infection.

Due to the weariness and cyclical nature of the diet, the diet cannot be uniform; it must correspond to the stage of the disease. In the phase of sharp exacerbations, a diet is prescribed for the second or third cycle, with a rapid expansion to the fourth cycle. In the calm phase, it is necessary to provide all whole foods in various forms of preparation, an abundance of complete proteins (meat, fish, cottage cheese, kefir) and vitamins in the form of raw juices, yeast dishes, bran infusions and concentrates. It is necessary to limit only fresh milk, spicy seasonings, particularly coarse bulky dishes and foods such as fresh black bread, chops, and sauerkraut. It is advisable to prescribe fasting days (raw mashed apples). Any delay in mechanical sparing is not only not indicated, but is even harmful.

Along with measures for timely isolation of patients, home hospitalization is permitted.

Discharge from the hospital should be made after the disappearance of clinical manifestations, but not earlier than the 7th day from the onset of the disease. Employees of food enterprises, public catering networks, water supply systems, children's institutions, hospitals, sanatoriums, as well as children attending child care institutions, persons who have suffered acute intestinal infections, can be discharged after clinical recovery and after at least three negative bacteriological tests at intervals of 1-2 days.

Food poisoning

Intestinal diseases caused by the introduction of certain harmful substances with food are united into one general group: bacteria from the group of salmonella and cocci, toxic substances formed in infected, contaminated (contaminated) and spoiled products, and chemical poisons. The variety of etiological factors in these cases is associated with a single mechanism of infection directly through food and drink.

The main importance of this group of diseases is sanitary and hygienic. But clinically they are also of some interest, especially in their rarer, atypical forms, sometimes mistaken for acute appendicitis, dysentery, typhoid or septic condition.

The etiology of food poisoning is very diverse.

1. In terms of frequency, infection with bacteria from the Salmonella group ranks first. Of the 160 types in this group, 15 are pathogenic for humans. Typing is carried out by tests for the absorption of agglutinins and reactions to somatic, flagellar and viral antigens. The most common are Salmonella paratyphoid A, B and C, murine typhus (Breslau), swine cholera, Derby, Thompson, Newport, enteritis (Gertner). Infection occurs through meat (80% of cases of poisoning), especially cattle meat (50%), fish, milk, eggs, egg powder (mainly from duck eggs), potatoes, peas, and beans. 2. Coccal infections. 3. Botulism. 4. Intoxication, bacterial (endotoxins), nutritional (alkaloids, toxamines, ptomains) - from spoiled or poisonous foods (mushrooms, beans, potatoes). 5. Chemical poisons (heavy metals, arsenic, etc.). 6. Allergic diseases. 7. Psychogenic dyspepsia, mistaken for food poisoning.

Cases of epidemic food poisoning have been described, when up to 7 strains of staphylococci were isolated from the nasopharynx and feces of patients, as well as from food (salad, ham), which served as a source of poisoning.

The danger of foodborne diseases lies not only in the severity of the disease, but mainly in the possibility of mass outbreaks from certain local foci. The number of sick people sometimes reaches several hundred, and the severity of the disease may depend not only on the virulence of the pathogen, but also on the characteristics of the macroorganism. Food poisoning is most severe in children, the elderly and people weakened by previous diseases, such as gastritis, hepatitis, colitis, and psychoneurosis.

One should also take into account the element of seasonality, the influence of summer heat, an abundance of flies, slight contamination of food with dirty hands, increased thirst, drinking from contaminated sources, and increased sweating. A temporary decrease in gastric acidity in hot weather also plays a role, causing a weakening of resistance to foodborne infections. The undoubted fact of the sharp increase in these diseases in the hot months requires particularly strict sanitary and food control and increased personal and public hygiene during the hot season.

Symptoms

The most common diseases from the salmonellosis group deserve special attention. They include the following forms.

1. Gastroenterocolitis is trivial with the usual gastrointestinal symptoms (vomiting, diarrhea, intestinal colic). If these symptoms develop soon after poisoning, the disease progresses rapidly, but quickly ends, partly due to the regulatory mechanisms of self-cleaning of the body (vomiting and diarrhea). With a longer incubation period, toxic symptoms (headache, fever, cardiac weakness) have time to develop within 12-24 hours and the disease drags on, although it usually still retains a completely benign character.

2. Pseudodysenteric colitis is especially difficult to distinguish from bacterial dysentery against the background of an epidemic outbreak, when every case of enterocolitis, even without bloody diarrhea, should be epidemiologically regarded as true dysentery. The absence of a band shift is too unreliable a sign. The diagnosis of food poisoning becomes probable in case of mass infections from the same source. In sporadic cases, the diagnosis of dysentery is excluded in the presence of rapid disappearance of bloody discharge and repeated negative stool tests.

3. The septic form with prolonged intermittent fever and severe intoxication is most often caused by infection with Salmonella suipestifer or Cholerae suis.

4. The pseudotyphoid form is caused by infection with paratyphoid C and occurs under the guise of a “miniature” form of typhus, with an 8-10-day temperature curve, bloating, colic, mild diarrhea, and an enlarged spleen.

Similar enterocolitis can be caused by a number of other bacteria, especially Proteus bacillus, Escherichia coli, etc.

Treatment. Apart from such exceptional cases when recovery is impossible due to irreversible morphological changes in the parenchymal organs and nervous system, most food poisoning responds well to therapy aimed at quickly removing the infection from the body from food. The most urgent measures are lavage of the stomach and intestines, taking a laxative and a starvation diet. Symptomatically prescribed: stimulants, belladonna, glucose with insulin (for liver irritation), from the 2nd day sulfonamides in an antidysenteric dosage, but usually in a shortened course (3-4 days). A gradual expansion of the diet is carried out under the control of residual effects of enterocolitis and taking into account the need to prevent constipation - a common consequence of such a disease.

For some time, fresh milk, fatty meat dishes, canned food, spicy seasonings and snacks should be excluded from the diet. In the presence of gastric achylia, fried and stringy meat, fatty dishes and sauces are excluded. For residual dyspeptic symptoms, often associated with gastritis, warmed mineral waters (Essentuki, Slavyanovskaya) are prescribed, 1/2 cup half an hour before meals.

Prevention. Massive. prevention involves measures of sanitary and hygienic control over food enterprises and catering departments, including systematic medical and bacteriological control of service personnel. Personal prevention consists of following the rules of food hygiene (washing hands before eating, washing raw foods, cleanliness in food preparation, removing food waste, fighting flies). These precautions are especially important during the hot months of the year, when food poisoning tends to become more frequent.

Botulism

Botulism is caused by poisoning from Clostridium botufinum toxins. The first cases were described in connection with poisoning from sausages, and then from canned meat, fish, vegetables and fruits, mainly homemade, without the addition of acidic preservatives that destroy bacilli and their heat-stable spores. Botulism is considered the most dangerous form of food poisoning, causing up to 70% of deaths. Fortunately, this disease has become very rare in our country thanks to high sanitary and food technology and control. The severity of the disease depends not only on the high virulence of the infection, but also on the duration of the incubation period (6-36, on average 24 hours), during which toxins have time to have a depressing effect on the central nervous system. Early symptoms of gastroenteritis (vomiting, diarrhea) are not specific to botulism. They are only a consequence of a secondary food infection. Specific symptoms appear suddenly and are observed in the nervous and vascular systems in the form of severe adynamia, diplopia, nystagmus, mydriasis with a sluggish reaction to light, paralysis of the external and internal eye muscles. Bulbar symptoms include difficulty speaking, swallowing and breathing. Inhibition of the salivary glands causes dry mouth, along with increased secretion of sticky, thick mucus. Paralysis of the smooth muscles of the digestive tube leads to delayed gastric emptying, constipation and flatulence. Paralysis of the stomach with retention of eaten food in it can serve as a diagnostic sign based on the presence of botulism toxins in food debris.

The pulse is initially slow; subsequently, tachycardia develops, which, in combination with subnormal temperature, is one of the characteristic symptoms of botulism. Common symptoms include apathy and drowsiness, followed by periods of anxiety, agitation and insomnia. Consciousness is maintained until death, which occurs from paralysis of the vasomotor centers, often with symptoms of motor aphasia. Pneumonia is also a terminal symptom. Patients die within the first 3-6 days, sometimes as early as 48 hours after the onset of the disease.

Recovery is slow, and residual paresis of the skeletal and ocular muscles can last for several months.

In differential diagnosis, encephalitis and diphtheria paralysis must be excluded. Other severe food poisoning infections are characterized by high fever and a predominance of gastrointestinal symptoms, in contrast to botulism with its typical triad: a long latent period, hypothermia, and nervous symptoms. Wood alcohol poisoning is characterized by loss of consciousness, convulsions, and blindness.

Among the poisonous foods that cause intestinal damage, one should point out mushrooms (pale toadstool, alkaloid, muscarine), some types of fish (marinka), sprouted potatoes containing poisonous solanine, and powdered eggs contaminated with duck salmonellosis. All these products cause gastroenterocolitis. White bean poisoning (favism) causes hemoglobinuria, hemolytic jaundice, anuria, azotemia and hemorrhagic colitis. In Italy, fatal cases of poisoning of children with bean flour added to sausage liver have been described.

Regular cow's milk can cause mild gastroenteritis not only due to individual intolerance, but also in completely healthy individuals after drinking milk during late milking, when milk becomes “conditionally harmful.”

Poisoning by overwintered grain causes severe illnesses such as septic tonsillitis (alimentary-toxic aleukia).

Chemical poisons

Among the large number of chemical poisonings that make up the special subject of toxicology, we will point out only a few food-related sources.

Copper. The cause of poisoning is the use of poorly tinned kitchen utensils, in which toxic compounds of soluble copper and fatty acids are formed from contact with sour and fatty foods. In addition to the usual symptoms of gastroenteritis, thirst, blue-greenish vomiting, burning in the esophagus are characteristic, and late resorptive symptoms include tremors, anuria, and collapse.

Zinc. It is dangerous to eat liquid warm food cooked in galvanized pots or tanks (violation of the rules of culinary sanitation). The symptoms are the same as for copper poisoning.

Lead. One should keep in mind mainly chronic intoxication due to prolonged use of poorly tinned dishes. Symptoms: loss of appetite, weakness, anemia, gum fringes, stomatitis, lead colic, constipation, muscle paresis. Acute poisoning causes vomiting with white films and bloody diarrhea.

Arsenic. Rare cases of poisoning have been caused by eating confectionery and beer containing molasses contaminated with arsenic.

Cases of poisoning due to ingestion of sodium fluoride and anabasine sulfate, used as insecticides in the fight against kitchen pests, have been described.

Prevention of these poisonings falls within the scope of sanitary and food inspection. Individual acute diseases should be treated like any acute gastroenteritis.

Food allergies

Food allergies include sporadic cases caused by individual increased susceptibility to certain foods,

completely benign, but causing general and local pathological reactions. Allergic reactions occur partly in the digestive organs (gastroenteritis, hepatocholecystitis), partly in other body systems (chills, fever, rashes, swelling). Allergies can also explain isolated cases of poisoning by products that are well tolerated by most people, but cause reactions in particularly sensitive subjects.

Most food allergens belong to proteins, often animals (dairy, fish, meat), the rest belong to plant products (certain varieties of berries and vegetables).

Here is a list (by no means complete) of products that can cause allergic reactions (by frequency per 500 cases of food allergies), based on skin tests (according to Alvarez).

Onions (mostly raw).......
		Pork. . .
Milk, cream, ice cream........
		Tangerines. .
Apples (raw)....		Bananas. . .
Boiled cabbage. . . ,
Chocolate.......		Oranges. .
Radish........		Sweets
Tomatoes.......		Spices. .
Cucumbers........
Eggs.........
Fats, fatty seasonings
Melon (cantaloupe). . .		Fruits. . .
Beef.......
Strawberry... ...
Coffee.........		Polka dots. . .
Lettuce... . .		Potato. .
Dried beans.....
Cauliflower. . . .		Chickens. . .

In addition to those listed, there are 104 more types of food, the consumption of which causes diseases to occur less frequently.

Tuberculous diseases of the intestines

We will consider three main clinical forms of tuberculous intestinal diseases: the so-called tuberculotoxic dyspepsia, mesenteric lymphadenitis and ulcerative-infiltrative tuberculosis. They all have the same infectious etiology, but give a completely different clinical picture. Their pathogenesis is also different: in some cases, the primary focus is in the lungs, from where it spreads through the lymphatic tract into the intestinal wall, in others - in the lymph nodes of the mesentery in the absence of lung damage.

1. Tuberculous dyspepsia

The so-called tuberculous intestinal dyspepsia is very often observed in persons suffering from pulmonary tuberculosis. Dyspeptic syndrome consists of anorexia, gastric “discomfort” in the form of unpleasant sensations of heaviness, bloating, belching and general malaise after meals, bloating, and a tendency to diarrhea. Often these symptoms develop against the background of intensive fattening of patients in sanatoriums (excess fatty and sweet foods or excessive consumption of koumiss). On the part of gastric secretion there is a subacid or anacid state, in the feces there is an abundance of undigested muscle fibers, plant fiber, partly fat fractions, without admixture of inflammatory elements.

Dyspeptic symptoms are relatively mild, but pose a danger to the main process in the lungs, contribute to the deterioration of appetite and food absorption, and thereby reduce the body's defenses in the fight against infection.

Timely treatment quickly relieves dyspepsia. The first condition is to regulate your diet. Instead of excess nutrition, a regime sufficient to maintain normal body weight is established with physiological norms of proteins and carbohydrates, some restriction of fats (40-50 g per day), with fractional meals of mechanically chopped food. In addition to a light diet, pancreatin, adsorbents (infusion of chamomile, dill and mint), and mineral waters are prescribed.

In the absence of timely treatment, diarrhea becomes protracted, causing a deterioration in overall nutrition, which aggravates the process in the lungs and, in turn, aggravates the course of colitis. The main condition for success is the rapid restoration of appetite, which is impossible without a temporary reduction in total calorie content and the removal of excessively bulky and fatty foods.

Phthisiatricians are well aware that such a temporary decrease in caloric intake also serves as the best means of restoring and even increasing weight in case of deficiency.

2. Mesenteric lymphadenitis

Mesenteric lymphadenitis occurs with a unique clinical picture, knowledge of which helps to recognize the true nature and cause of disorders often mistaken for other diseases: chronic appendicitis, colitis, “gastroptosis,” “solar plexus neuralgia,” etc. Patients’ complaints are focused on the abdominal cavity. Women aged 15-35 years are most often affected, but among the patients we observed there were also men aged 20 to 50 years.

The main symptom is pain in the navel or in the sides of the abdomen, aggravated by walking, physical stress and after a heavy meal. The pain is not accompanied by tenesmus or the urge to defecate, but is relieved by lying down and after the passage of gas. The pain is not particularly intense, but is persistent and exhausts the patient. Bowel movement. delayed: stool of dense consistency, defecation occurs once every 2-3 days. Occasionally, constipation is replaced by one-day diarrhea. The body temperature remains at low-grade levels, and chills and night sweats are sometimes noted. The history often indicates tuberculosis diseases in the patient himself or his family members. The Pirquet reaction is sharply positive, sometimes with axillary lymphadenitis. The disease proceeds for a long time and is sluggish, with symptoms of general intoxication. in the form of mild anemia, headaches, nervous disorders (increased excitability, followed by lethargy and apathy, loss of ability to work, drowsiness, alternating with insomnia). Overall nutrition and weight may decrease significantly.

Diagnosis is based on a careful study of the clinical picture and medical history, but especially on careful palpation of the abdomen. In the absence of muscular protection and irritation of the peritoneum, palpation reveals well-localized painful areas in the right lower and left upper quadrants of the abdomen, i.e., along the mesentery of the small intestines (Sternberg's symptom). Unlike typhlitis and appendicitis, maximum pain is localized inward from the edge of the cecum, closer to the navel, as well as up and to the left of the navel. In some cases, dense calcified lymph nodes are palpated here, sometimes of considerable size, usually the size of a pea or a roasted nut. Pain increases when sliding palpation is applied perpendicular to the root of the mesentery, due to the displacement of the latter. But even without the presence of dense lymph nodes, strictly localized painful areas of the abdomen have diagnostic value.

Final confirmation of the correctness of diagnosis is provided by a successful course of treatment with streptomycin, PAS or ftivazid with irradiation of the abdomen with ultraviolet rays and enhanced nutrition.

Among the complications of the disease, stenosis of the digestive tract due to compression by dense packs of lymph nodes is of particular importance. Compression of the pyloric area easily gives rise to the diagnosis of cicatricial ulcerative stenosis, and the presence of a similar package of nodes in the ureter area suggests kidney stone disease, especially if there is a dense shadow on the radiograph. These diseases can be especially easily mixed in cases where both processes alternate with each other.

It should be emphasized that in approximately 30% of cases the disease is caused by mesadenitis of non-tuberculous etiology. The differences relate to a number of points. The history always includes one or another intestinal infection, and often current chronic enterocolitis as the cause of regional mesenteric lymphadenitis, without indicating tuberculosis of the lungs and with a negative Pirquet reaction. The clinical picture is dominated by symptoms of colitis in the form of alternating diarrhea and constipation. When palpating the abdomen, not only the mesentery area is painful, but also the intestinal tract.

However, despite these significant differences, the main role in the pathogenesis of the disease is not played by colitis, but by damage to the mesenteric lymph nodes. This is reflected in the low effectiveness of treatment for colitis. Pain, intestinal dysfunction and general toxic symptoms are inferior only to vigorous treatment of mesadenitis, that is, mainly to ultraviolet irradiation - artificial or, even better, natural at the climate stations of the Crimea. In recent years, we have successfully used the latest anti-tuberculosis drugs in a number of cases, although we were not sure of the specific etiology of the disease. The antibiotic effect of streptomycin in non-tuberculosis infections, as is known, cannot be excluded.

Treatment of non-tuberculous mesadenitis allows the therapist to influence the primary enterocolitis, and indirectly, the complicating mesadenitis. The main elements of treatment are sulfonamide drugs and a diet limited in carbohydrates and plant fiber.

3. Ulcerative-infiltrative intestinal tuberculosis

Before the advent of new specific drugs, this severe form of tuberculosis of the intestine was considered practically incurable. Now this situation has changed radically. The development of the intestinal process occurs 1-3 years after the onset of the process in the lungs.

Common data. Tuberculous lesions of the intestines are found in 67-72°/o people who died from pulmonary tuberculosis. According to other sources, these figures reach 90% or more, and according to histological studies - 84%. The fibrous-productive form of tuberculosis accounts for 40%, and the fibrous-caseous form accounts for 72% of intestinal lesions. According to Rubin, dissemination from the lungs to the larynx is observed in 50%, to the intestines - in 2/3 of cases. With simultaneous damage to the lungs and larynx in 75°/o patients, the intestines are also involved in the pathological process.

The intestinal process often aggravates the course of pulmonary tuberculosis due to infection of the lungs from intestinal ulcers and caseous lymph nodes of the mesentery, due to a decline in nutrition, hematogenous and lymphogenous dissemination of tuberculosis bacilli located in the portal vein and thoracic duct. However, D. A. Manucharyan also observed cases where extensive intestinal ulcers did not complicate the pulmonary process. In addition, cases of primary tuberculous ileotiphlitis without lung damage have been described. These observations are confirmed by our data. Particularly indicative of the pathogenesis of the tuberculosis process is its connection with the general trophism of the body. The infectious and trophic factors are closely intertwined here, as can be seen from various cases.

In both cases, the connection between colitis and dystrophy with the activation of pulmonary tuberculosis is clearly shown.

The clinical picture is initially a little characteristic: alternating diarrhea and constipation, pain in the ileocecal region and around the navel, low-grade fever. In the presence of pulmonary tuberculosis, these symptoms are suspicious of a possible specific process in the intestine; in the absence of pulmonary tuberculosis (one can think of toxicosis due to mesadenitis. For the diagnosis of intestinal tuberculosis, anamnesis (indication of tuberculosis), the presence of tuberculosis bacilli in sputum or feces, as well as the exclusion of other etiologies of colitis are crucial.

Intestinal tuberculosis develops progressively, starting with minor clinical symptoms, dyspepsia, and mucous diarrhea. Subsequently, an ulcerative process develops with progressive intoxication and miliarization. In a number of patients in previous years, before the use of antibiotics, such dynamics of the process brought the inevitable fatal outcome closer. Currently, the mortality rate of such cases is steadily falling.

Establishing etiology poses some difficulties; in particular, it is necessary to prove the presence of a specific process in the lungs.

Diagnostics. For intestinal tuberculosis, the presence of tuberculosis bacilli in the stool is not necessary, variable, and even inconclusive, since the bacilli can be ingested with sputum. Some authors, for example D. A. Manucharyan, attach importance to the Triboulet test for soluble protein in formalized feces (it is necessary to exclude accelerated evacuation). According to our data, this test is not specific. Equally unconvincing is Guafon’s data on the supposedly specific program containing an abundance of undigested starch and fiber.

Ulcerative tuberculosis is diagnosed only on the basis of the persistent presence of blood in the stool, high temperature and pulmonary process. Even the presence of ulcers on the rectal mucosa, visible during proctoscopy, is not necessary due to the frequent localization of the process in the proximal parts of the colon, inaccessible to proctoscopy.

In X-ray diagnostics the following are important:

1) Stirlin’s symptom - a filling defect in the ileocecal region (according to P. D. Tarnopolskaya “crescent defect”); 2) absence of haustradia in a certain segment of the large intestine; 3) shortening the size of the cecum and ascending colon; 4) rigid narrowing of the lumen of the same segment; 5) paradoxical retention of barium in the cecum while the remaining segment is released.

All of the listed signs relate to the localization of the process in the cecum, the most common, but not the only one. According to D. A. Manucharyan (summary data), the ileocecal region is affected in 92% of cases, the small intestines - in 70%, the colon - in 61%, the appendix - in 30%. The process usually begins from the ileocecal region.

X-ray signs of the small intestine are less characteristic and constant; they come down to a delay in the entry of barium into the cecum from 3-4 to 7-8 hours. Functional radiological symptoms are equally uncharacteristic: spasms, increased peristalsis, acceleration of passage, spastic defects. Indications of ulcerative colitis are pathognomonic for tuberculosis only in combination with other signs of this infection. More specific is the presence of ulcers of the small intestine, especially if an X-ray examination reveals a combination of spasms with expansion of the proximal loops, disconnection of individual loops, and clearness of their contours. The most constant sign is deformation of the ileocecal contours. Changes in the ileocecal region in the form of stasis, hyperperistalsis, unevenness of the lumen of the terminal loop of the ileum serve as radiological precursors of the ulcerative period of the disease.

(Clinical forms of intestinal tuberculosis are difficult to fit into a specific classification. Bonafe’s scheme is not very convincing, distinguishing latent forms without gastrointestinal symptoms, latent forms under the guise of “atonic dyspepsia”, pain syndrome (intestinal colic), (rare cases of early intestinal bleeding and diarrheal form All these forms are characterized by emaciation.

The anatomical classification of Glan-Albrecht-Aschof is equally unconvincing. It is based on the assumption that the intestinal process reflects the form of the pulmonary process (fibrous, ulcerative, infiltrative, exudative). On the contrary, morphological dissociation of pulmonary and intestinal processes is more often observed.

D. A. Manucharyan proposed a clinical and radiological “classification” close to Boyaafe’s scheme:

1) premorbid forms,

2) inperceptual forms (early and developed),

3) ulcerative forms (early and developed).

Symptoms of intestinal tuberculosis

1. General symptoms- emaciation, fever with temperature increases in the first 2 hours after eating up to 38°, depression and irritability of the nervous system. This overexcitability is especially great in cases of fermentative dyspepsia, a frequent companion to intestinal tuberculosis.

Anemia, sometimes masked by thickening of the blood from heavy sweats and diarrhea, is usually a late symptom of intestinal tuberculosis.

2. Local symptoms. Dyspeptic complaints, anorexia, nausea, heaviness after eating are especially characteristic of intestinal tuberculosis against the background of a calm pulmonary process; during periods of exacerbation of such, dyspepsia develops due to general intoxication. Appetite changes in waves, often in parallel with fluctuations in body temperature. Nausea is associated with spasm of the bauhinium valve or with toxic hepatopathy.

Pain syndrome is at the center of the clinical picture. The pain is of a different nature. They are localized in the transverse colon or are bilateral (in the sigmoid and cecum), often depending on irritation of the transverse colon by fermentation products from the cecum. In some cases, post-dinner pain predominates due to irritation of the transverse intestine, in others - late pain, 6-7 hours after eating. True intestinal colic is also observed from tension in the mesentery (with mesadenitis) or from muscle spasms with stenotic peristalsis. Diagnostic difficulties are presented by false appendiceal syndrome, which in the presence of pulmonary tuberculosis is very suspicious of tuberculous etiology. In such cases, the section reveals ileocecal tuberculosis with a healthy process or local fibrinous peritonitis. Particularly characteristic of intestinal tuberculosis is persistent persistence or a progressive increase in pain - in contrast to flying pain in patients with pulmonary tuberculosis and simple toxic dyspepsia.

3. Objective symptoms. The tongue usually remains clean. There is flatulence, often localized in the navel area. The nature of the stool is varied: from normal to dysenteric diarrhea. However, blood in the stool is observed less frequently than with nonspecific ulcerative colitis.

As a rule, diarrhea in severe pulmonary tuberculosis is associated with a specific process, but another etiology is also possible (chronic enterocolitis, intestinal amyloidosis in 12-13% of cases). According to some data, in sanatoriums for patients with pulmonary tuberculosis, nonspecific dyspepsia is observed 4-5 times more often than specific ones.

Nevertheless, in a patient with pulmonary tuberculosis, any diarrhea - constant or alternating with constipation - is always suspicious of a specific intestinal lesion. In some cases, there are characteristic constipation associated with the presence of a gas plug in the splenic angle due to dysfunction of the diaphragm. It is noteworthy that the severity of diarrhea is not directly related to the extent of intestinal ulceration: a single ulcer can cause severe diarrhea, and multiple ulcers can occur with normal stool.

As a result, the diagnosis of intestinal tuberculosis is often made on the basis of a number of data: anamnesis, active pulmonary process, degree of exhaustion, clinical and radiological signs.

Treatment. Despite the success of treatment with antibiotics and chemotherapy drugs, intestinal tuberculosis remains a very serious disease that requires vigorous, comprehensive treatment. The difficulties of therapy are associated not only with the variety of clinical symptoms. It is especially necessary to take into account the degree of lung damage and the danger of nutritional toxic dystrophy. When prescribing a diet, one should take into account the deficiency of proteins, vitamins and mineral salts associated with tuberculosis toxicoinfection and aggravated by the dystrophic condition. The principle of sparing should not be reduced to prescribing a low-calorie, deficit regimen. It is necessary to limit only carbohydrates, coarse plant fiber, and fats, especially if hepatopathy is often present. The protein diet should be at least 100 g, if possible 120-150 g per day, with an equal amount of animal (meat, eggs, cottage cheese) and plant proteins (legumes, oatmeal, stale white bread). The preferred fats are butter, sour cream and cream. Vitamins in the form of raw juices (100-150 ml per day), citrus fruits, apples, grapes, yeast. It is necessary to ensure high palatability of food with the help of various seasonings (green onions, lemon, sour cream, raw juices) and to combat anorexia, which is dangerous for the patient, by maximizing the variety of dishes.

For mesenteric lymphadenitis, the diet is based on the degree and form of intestinal disorders. So, in the presence of pain, flatulence and constipation, only foods that cause bloating (soft bread, fresh milk, cabbage and legumes) are excluded. It is necessary to eat greens, fruits, kaffir, curdled milk, raw juices along with normal quantities of meat and oil. In the presence of enterocolitis with diarrhea, carbohydrates, coarse fiber and fats, as well as stringy fried meat, are sharply limited, especially with gastric achylia.

Irradiation of the abdomen with ultraviolet rays, both artificial and especially in the form of climatic and heliotherapy courses in the Crimea, has a good analgesic effect on mesenteric pain.

Neuralgic pain from irritation of the mesentery is often relieved by injections of a 5% solution of vitamin B1, 1-2 ml intramuscularly.

The drugs of choice for various forms of intestinal tuberculosis are streptomycin (200,000 units 2-3 times a day) and ftivazid (0.3-0.5 three times a day). In milder outpatient cases, you can combine the use of one of the above drugs with PAS (2.0 four times a day). The latter drug requires careful use due to the possibility of side effects on the liver and intestines.

Indications for use. 1) Chronic inflammatory bowel diseases (not exacerbation), accompanied by constipation. Special purpose.

Indications for use. 1) Constipation of non-inflammatory origin (absence of inflammatory bowel diseases), including neurogenic,

Intestinal infection is a group of diseases in which the main symptoms are increased body temperature, signs of intoxication and disorders of the gastrointestinal tract.

The microorganisms that cause these diseases are transmitted mainly through dirty hands.

The disease is most severe in children and the elderly, but can cause serious complications in young people.

Drug treatment and diet are required for these types of infections.

Causative agents of intestinal infections

There are many causative agents of intestinal infections.

Both bacteria and viruses can play their role, and it is impossible to say unequivocally which of them is worse: each microbe has its own toxins, with the help of which it poisons the human body. The main causative agents of intestinal infection in children and adults are:

• cholera;
• halophilesis;
• campylobacteriosis;
• Escherichiosis caused by pathogenic bacteria;
• adenovirus;
• enterovirus.

Poisoning with staphylococcal toxin and botulism are not classified as intestinal infections, occupying a niche called “foodborne toxic infections.” Fungal and gastrointestinal lesions caused by protozoa (giardia, amoebas) are also somewhat separate, so we will not consider them.

The source of infection is people - patients with severe, erased forms of the disease or carriers of this (usually this only applies to bacterial) infection.

The period of contagion for each infection is different, but for a bacterial infection it usually takes a period of time from the appearance of the first symptoms to complete recovery. With viral diseases, a person continues to be a source of infection until 2-3 weeks after all signs of the disease have subsided.

Microbes are excreted mainly in feces, but can also be found in urine, saliva, and vomit. There is no immunity to all of these microorganisms, that is, even if a person has had some kind of intestinal disease, then after a short time there is a chance of contracting the same type of infection.

They become infected from a patient when the microbe enters the mouth. This usually happens when consumed:

• raw water or milk;
• those products that cannot be thermally processed (cakes with cream, fermented milk products);
• unprocessed meat;
• bird eggs drunk raw or partially boiled/fried;
• using shared towels, dishes, contact with toilet seats, door handles, toys in the house where the patient lives or works, after which a previously healthy person did not wash his hands;
• Swimming with ingestion of water in open bodies of water.

Viral intestinal infections can also be transmitted by airborne droplets. Susceptibility to all of the listed microorganisms is universal.

More chances to get infected in the following categories of the population:

• aged people;
• premature babies;
• children who are fed formula;
• people with immunodeficiencies;
• children born with pathologies of the nervous system;
• people suffering from alcoholism.

Symptoms of intestinal infection in adults

The incubation period is 6-48 hours. The sooner adults experience any symptoms after eating contaminated food, the more severe the intestinal infection will be.

Then the following syndromes develop:

1) Intoxication, which is manifested by the following symptoms:

• weakness;
• headache;
• body aches;
• nausea.

2) Body temperature rises to different numbers.

3) Gastritis syndrome:

• stomach ache;
• nausea;
• after eating or drinking water - vomiting, after which it becomes easier.

4) Enteritis syndrome: there is almost no nausea and vomiting, only at the very beginning, but frequent loose stools appear.

5) Colitic syndrome: pain in the lower abdomen, painful urge to defecate, while the “big” walk itself is also painful. The stool is scanty, with mucus and blood. After defecation, the stomach does not become easier.

6) A combination of the three above symptoms in various combinations.

Each infection has its own combination of these symptoms, but it is not necessarily observed every time.

Sometimes you can tell what kind of infection it is by looking at the patient’s stool:

• with salmonellosis, the stool is frequent, liquid, and green (they call it “swamp mud”);
• with escherichiosis, the stool is liquid and may be yellow-orange in color;
• cholera and halophiles cause loose, watery stools in which whitish flakes of mucus are found;
• with dysentery, stool - with mucus and blood;
• Characterized by foamy brown liquid stools with a very unpleasant odor.

It is irrational to make such a diagnosis based on the nature of the stool, therefore, before starting antibacterial therapy, a diagnosis of this disease is carried out, aimed at identifying the causative agent. Therapy will be aimed at destroying a wide range of bacteria that could presumably cause the disease.

Diagnosis of intestinal infection

A preliminary diagnosis is made based on the clinical picture of the disease, the nature of the food consumed and the appearance of the stool.

The next step in children is to conduct a rapid test for the presence of rotavirus infection: so within 10 minutes, after receiving stool, you can find out whether this intestinal infection is caused by rotavirus or not.

If the test is negative, the following diagnostic methods are carried out:

1. 1) Sowing of feces, washing water and vomit on various nutrient media in order to determine the bacteria that caused the disease. The result comes only after 5 days.
2. 2) Serological methods: determination of specific antibodies in the blood to various viruses and bacteria using ELISA, RA, RPGA and RNGA methods. Blood for these studies is not drawn from a vein on the first day of illness; the results come in a few more days.
3. 3) PCR study of the genome of some bacteria in the biomaterial.
4. 4) Instrumental studies (sigmoidoscopy, colonoscopy and others) can only note changes in the intestines characteristic of a particular disease. They also help to assess damage to the gastrointestinal tract.

How to treat an intestinal infection?

1) First of all, treatment of an intestinal infection begins with the person being prescribed a diet.

Excluded from the diet

• dairy products;
• raw vegetables, berries and fruits;
• fried foods;
• fat;
• salty;
• spicy;
• smoked;
• salads.

2) A person should take the sorbent: Atoxil, Enterosgel, Smecta four to five times a day.

3) An important factor is to replenish fluid losses that occur through feces, vomiting and fever. That is, in addition to his physiological norm, a person must receive at least another 1.5 liters of fluid per day (calculation for adults). You can try to restore this fluid by drinking. You need to drink still water, dried fruit compote, and a very weak rosehip decoction. It is also necessary to use ready-made salt preparations that are diluted with boiled water: Regidron, Humana, Oralit and others.

If it is impossible to drink this amount, it is necessary to go to a hospital, where this liquid will be administered intravenously. You should also seek medical help if diarrhea and vomiting (even several times) are observed in a small child. Before the local police officer or ambulance arrives, you should try to give him water or tea, giving 5 ml every 10 minutes.

4) Antibacterial therapy – taken if a bacterial infection is suspected. In some cases, taking Norfloxacin in tablets is enough, in others, intramuscular or intravenous administration of “stronger” drugs may be required. The choice of drug is made by an infectious disease specialist.

5) Symptomatic treatment: Omez, Ranitidine are prescribed; for nausea - Cerucal.

6) Preparations of bifidobacteria and lactobacilli: Enterozermina, Yogurt, Bio-Gaya, Enterol.

Forecast

Usually the prognosis is favorable - both for recovery and for life - provided that a full and adequate course of antibacterial and rehydration therapy is carried out.

In rare cases, severe septic forms of the above bacterial infections may develop. Sometimes long-term and even lifelong carriage of these bacteria occurs.

Prevention of intestinal infections

There is no specific prophylaxis (i.e., vaccines or toxoids) for any of these infections.

Only nonspecific preventive measures are used:

• compliance with individual hygiene measures;
• boiling water and milk before drinking;
• washing hands after using the toilet;
• refusal to eat raw eggs (even those collected from your own birds);
• sufficient heat treatment of meat;
• carefully reviewing the expiration dates of the products you are going to buy;
• washing vegetables, berries, herbs, fruits before eating;
• storing finished products in the refrigerator;
• refusal to feed infants undiluted cow's or goat's milk;
• maintaining adequate sanitary conditions in the house/apartment;
• if someone in the family gets sick, boil all of their dishes, refuse to eat food from the same container, disinfect feces with chlorine-containing preparations.

Which doctor should I contact for treatment?

If, after reading this article, you think that you have symptoms characteristic of this disease, then you should

Contents of the article: classList.toggle()">toggle

ACI (acute intestinal infections) is a group of infectious diseases (about 30 types) that are caused by various pathogenic microorganisms (viruses, protozoa, bacteria); affect the gastrointestinal tract.

Causes

The following reasons lead to the appearance of acute intestinal infections:

• Contact-household infection - contact with an infected person, with a carrier of the pathogen (animal, human);
• Food contamination - ingestion of contaminated food: meat, raw water, milk, cream confectionery, unwashed vegetables, fruits and berries;
• Through contaminated household items, dirty hands;
• Swimming in polluted waters.

Classification

Types of intestinal infection:

By type of diarrhea:

• Invasive type (exudative diarrhea, liquid) - caused by bacteria: clostridia, shigella, Pseudomonas aeruginosa, salmonella, etc.;
• Secretory type (watery diarrhea without flatulence) - caused by bacterial flora: Vibrio cholerae, Campylobacter, enterotoxigenic Escherichia;
• Osmotic type (watery stools with flatulence) - formed by viruses: adenoviruses, rotaviruses, coronaviruses and others;
• Mixed type: invasive-secretory, invasive-osmotic.

Symptoms of diseases

Clinical manifestations depend on the type of intestinal infection:

OKI in children

Acute intestinal infections in children develop for the same reasons as in adults. Children under 3 years of age are most susceptible, as their immune system is not strong enough.

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OCI in children manifests itself with a pronounced clinical picture and occurs in a more severe form than in adults. The peak incidence occurs in the summer. Intestinal infections in children manifest themselves in the form of intoxication of the body (general weakness, fever, loss of appetite).

Symptoms of damage to the digestive system:

Treatment methods

When symptoms of OCI appear, it is necessary to provide first aid and then be sure to consult a doctor who will prescribe an individual course of treatment.

First aid

An infected person should be given first aid:

• Isolate the infected person from others;
• The patient should be given drinks in small quantities, but often; moisten your lips with a napkin soaked in water;
• Lay on one side; if there is vomiting, place a container;
• Unbutton, remove tight clothing;
• Ventilate the room;
• Apply ice wrapped in a cloth or a wet, cold bandage to the head;
• You cannot give food or do cleansing enemas;
• It is forbidden to apply a heating pad or give medications(painkillers, astringents, antipyretics).

All children, regardless of age, are subject to hospitalization; adults - with moderate and severe forms of infection.

For any intestinal infection, gastric lavage is mandatory. It is prescribed regardless of how much time has passed since the onset of the disease, since the pathogen can remain viable for a long time on the walls of the gastrointestinal tract.

Drug treatment

Smecta, 1 sachet diluted in ½ cup of water (50 ml of liquid), taken 3 times a day;

• Intestinal antiseptics - destroy pathogenic microflora: enterosediv, intetrix, intestopan

Intetrix, 2 capsules 2 times a day;

• Antidiarrheal drugs: chloramphenicol, enterosgel, imodium

Imodium, initial dose 2 tablets, then one tablet after each bowel movement, maximum daily dose 16 mg (8 tablets);

• Probiotics – to restore normal intestinal microflora: acipol, linex

Acipol, 1 capsule three times a day;

• Prebiotics are carbohydrates that feed “good” microorganisms: hilak-forte

Hilak-forte, 40–60 drops three times a day;

• Enzymatic preparations - to improve the functioning of the digestive system: Creon, Mezim, Pancreatin

Creon, 1 capsule per day;

• Antibacterial agents: tetracycline, ceftibuten, penicillin.

Ceftibuten, 1 capsule per day.

ethnoscience

For AEI, the following traditional medicine recipes are used:

Diet

Meals for acute intestinal infections should be divided, at least 5 times a day, enriched with vitamins, microelements, proteins and fats. It is important to drink pure liquid, at least 1.5 liters per day.

Authorized products:

• Dairy products;
• Lean meat;
• Inconvenient pastries, dried out bread;
• Cereals, cereals;
• Vegetarian soups;
• Pasta;
• Dried fruits;
• Vegetables, berries, fruits;
• Butter;
• Rosehip infusion, fruit drinks, tea and coffee with milk.

Prohibited products:

• Baking;
• Semi-finished products;
• Canned food;
• Fatty meat, fish;
• Smoked, salted, marinated dishes;
• Legumes;
• Mushrooms, cabbage, onions, garlic;
• Spices, herbs;
• Chocolate, products with cream (cake, cake);
• Carbonated and alcoholic drinks.

Complications

Acute intestinal infections can cause the following complications:

If left untreated, serious consequences can occur!

• Dehydration (dehydration);
• Infectious-toxic shock;
• Pneumonia;
• Acute renal failure;
• Death.

Prevention

Preventive measures include:

• Drinking boiled water;
• Washing vegetables and fruits;
• Compliance with personal hygiene rules;
• Short-term storage of perishable products;
• Heat treatment of food before consumption;
• Home cleaning;
• Do not swim in polluted waters.

Acute intestinal infections (AI) are a large group of infectious diseases caused by various bacteria and viruses. They are united by a similar nature of manifestations in the form of disruption of the normal functioning of the gastrointestinal tract and the presence of signs of intoxication.

The source of infection with intestinal infections is a sick person, a bacteria carrier and animals. Infection occurs through the fecal-oral route.

Infection occurs by eating contaminated food; in close contact with a patient with an intestinal infection or a bacteria carrier. Infection is facilitated by non-compliance with personal hygiene rules - dirty hands, consumption of unwashed or thermally untreated foods, unboiled water from open reservoirs.

General clinical manifestations of intestinal infections.

1. Damage to the gastrointestinal tract can manifest itself in the form of:

1) gastritis, when the gastric mucosa becomes inflamed. It is manifested by pain and discomfort in the epigastric region, nausea, vomiting, or heartburn;

2) enteritis, when the pathological process mainly involves the small intestine. Enteritis can manifest itself as diffuse abdominal pain, bloating and rumbling along the intestines, copious watery stools, almost free of mucus or blood;

3) colitis, when various parts of the large intestine are affected, which can manifest as cramping abdominal pain, especially often observed in the left iliac region, false urge to defecate, frequent, loose stools, in which there is a significant admixture of mucus and blood;

4) an isolated manifestation of only one syndrome is rare; usually with intestinal infections they are combined in the form of gastroesteritis, enterocolitis or gastroenterocolitis. If blood appears in the stool, it means hemocolitis or enterohemo-colitis.

2. Intoxication is observed in the vast majority of all intestinal infections. When it occurs, the body temperature rises, headache, and vomiting appear. The child becomes lethargic and refuses to eat.

3. Dehydration (exicosis) is the appearance of fluid deficiency in the vascular system, in the tissues of the body and is manifested by dry skin and mucous membranes, thirst, disturbances in the functioning of the cardiovascular system, up to the development of shock conditions in severe forms of the disease.

4. Hepatosplenomegaly (increase in the size of the liver and spleen).

5. A rash is not observed with all intestinal infections. Its appearance is characteristic of diseases such as staphylococcal infection, yersiniosis and enterovirus infection.

6. Exhaustion, anemia, hypovitaminosis develop with severe, long-term, complicated intestinal infections.

Dysentery

Dysentery is an infectious disease caused by bacteria belonging to the genus Shigella. It occurs with primary damage to the lower parts of the large intestine and signs of general toxicosis.

Dysentery is a typical representative of the group of intestinal infectious diseases. The source of infection can only be a person suffering from dysentery, who begins to pose a danger to others on the first day of illness, since the pathogen is released into the external environment most intensively at this time.

The main routes of infection are household contact, water and nutrition.

The risk of contracting dysentery increases sharply when the population is crowded in living quarters and poor sanitary and hygienic conditions exist.

Anyone can get dysentery, but more than half of the cases occur in children under 4 years of age. Immunity after suffering from dysentery is formed very short-lived, no more than 12 months. That is, there is a risk of recurrent disease.

The entry gate of infection is the gastrointestinal tract, where the pathogen invades and multiplies.

Clinic. The incubation period is no more than 2–3 days after infection; if infection occurs through food, then this period is reduced to hours, and with household contact, the disease can develop after 7 days.

Usually, the onset of the disease is acute, but sometimes a prodromal period is possible, which is manifested by malaise, chills or headache.

Depending on the severity, dysentery can be mild, moderate, severe and very severe.

In dysentery, the large intestine is most affected.

As a rule, at the beginning of the disease, quite severe abdominal pain appears, and then frequent, loose stools appear. In addition, dysentery sometimes begins with general manifestations - the patient develops weakness, lethargy, headache, and fever.

Symptoms of the disease become most pronounced on days 2–3 of illness. In mild forms of dysentery, local manifestations prevail over general ones.

The most pronounced signs of dysentery are in the moderate to severe form of the disease. An acute onset is typical - body temperature rises to 38–39 degrees, which is accompanied by chills, which last for about 2–3 days. Weakness appears, headache bothers us, appetite decreases. Intestinal dysfunction occurs within the next 2-3 hours from the onset of the disease, and manifests itself in the form of discomfort in the lower abdomen, rumbling, periodic, cramping pain in the lower abdomen, bowel movements become more frequent 10 to 20 times a day. At first, the stool retains a fecal character, then impurities of mucus and blood appear in it, the volume of feces begins to decrease, and they acquire the character of the so-called “rectal spit” in the form of mucus and blood. Characterized by frequent urge to defecate. The skin turns pale, a thick brown coating appears on the tongue. From the circulatory system, tachycardia and a drop in blood pressure are noted. One of the main signs of dysentery is considered to be spasmodic and painful palpation of the sigmoid colon in the left iliac region.

Intoxication with a moderate form of dysentery lasts about 4–5 days. The stool usually takes on a formed character by the 8-10th day of illness, with a smooth course of dysentery, but the disease can drag on for up to 3-4 weeks.

The mild form and severe form differ from the moderate form only in the degree of severity of the symptoms.

The severe form of dysentery is characterized by more pronounced and prolonged intoxication and severe intestinal damage. Bowel movements may become more frequent up to 35–40 times a day. The phenomena of hemocolitis are quite pronounced, when blood appears in the stool.

Gastroenterocolitic (damage to the entire gastrointestinal tract) and gastroenteric (damage to the stomach and small intestine) variant of dysentery is characterized by a short incubation period. The onset of the disease is sudden and violent, and toxicosis and intestinal manifestations develop in parallel. Vomiting appears, stools are very frequent, copious, watery, mixed with blood and mucus, and diffuse abdominal pain is noted. Subsequently, the volume of feces decreases, and false urges to defecate appear.

Complications include the development of infectious-toxic shock, shock from dehydration (hypovolemic), acute heart failure, toxic dilatation of the colon, peritonitis, intestinal bleeding, intestinal perforation, dysbacteriosis, myocarditis, reactive polyarthritis.

Chronic dysentery. The duration of the disease is more than 3 months, which is caused by the presence of one pathogen in the human body. General manifestations are mild. Intestinal disorders are less pronounced compared to the acute course, but significant disturbances develop in other organs and systems of the body in the form of anemia, hypovitaminosis, severe dysbacteriosis and dystrophic disorders.

Yersiniosis

Yersiniosis refers to a whole group of acute infectious diseases, which are characterized by a variety of manifestations. When they affect the gastrointestinal tract, musculoskeletal system, liver and other organs, phenomena of general intoxication and a protracted course are noted.

The causative agent of the disease belongs to the genus Yersinia.

Yersinia can exist for a long time in the environment - in soil (up to 4 months) and in water (from a month or more).

The main source of infection are animals and birds. The possibility of infection from humans remains highly doubtful.

Most of the yersinia fall on vegetables, which are stored in cellars and vegetable stores and are perishable. The pathogen accumulates on vegetables and in the environment. Vegetables pose the greatest risk of infection in late winter and spring.

Yersiniosis can affect people of any age, but most often children aged 2-3 months and elderly people with weakened immunity get sick. Also, children aged 4–9 years old get sick quite often.

The incidence of yersiniosis has a distinct autumn-spring seasonality. The peak incidence occurs every 2–3 years. In countries with cool climates, yersiniosis occurs more often.

Clinic. The incubation period is about 3-10 days. Initially, after the first signs of the disease, after a temporary improvement on the 13-15th day, about a third of patients experience deterioration again.

The forms of yersiniosis can be: eczematous (skin lesions predominate), arthritic (the leading symptom is joint damage), icteric (involvement of the liver in the process), meningeal (with inflammation of the meninges) and mixed. In rare cases, yersinia sepsis develops.

These options are characterized by common features such as an acute onset, the presence of intoxication (chills appear, body temperature rises to 38–40 ° C) and signs of damage to the gastrointestinal tract, which is manifested by nausea, vomiting, stomach pain and the appearance of loose stools. From the first days of the disease, patients are bothered by muscle and joint pain, and there is hyperemia of the sclera, conjunctiva and soft palate. Characteristic is the appearance of a “crimson” tongue and a rash on the skin.

The duration of the disease, in most cases, does not exceed 1.5 months, and in case of protracted yersineosis - 3 months.

Food poisoning

Food poisoning is a collective concept that includes a diverse group of diseases, but they are united by two common features.

1. The main route of spread is nutritional, when the pathogen enters the body with infected food. The most common foodborne infections are caused by streptococci, staphylococci, Proteus, enterococci, and Salmonella.

2. The main reason for the development of food poisoning is not the microorganisms themselves, but the toxins they secrete.

Most often, pathogens enter food products during their preparation, storage, transportation and sale. Often, contaminated products are practically no different in appearance and smell from normal products.

Most pathogens are capable of producing toxins not only in food products, but also in the human body. When pathogens are destroyed, additional portions of the toxin are released in the gastrointestinal tract.

Clinic. Toxins released by pathogens cause inflammation of the mucous membrane of the stomach and intestines. The developed inflammatory process in the mucous membrane leads to increased intestinal motility, impaired absorption and digestion of food, and the development of dysbiosis.

All these disorders are manifested by abdominal pain, nausea, frequent vomiting and diarrhea. At the beginning of the disease, stool becomes more frequent up to 10–15 times a day; at first it looks like liquid stool, and then becomes watery, copious and fetid. All these symptoms may appear within 2–4 hours after eating contaminated products.

At the next stage of the disease, toxins released by microbes from the intestine begin to be absorbed into the blood, as a result of which almost all organs and systems of the body are affected. Such as the heart, central nervous system, liver, which is the filter of the entire body, purifying the blood of any toxic substances. As a result, all manifestations of foodborne toxic infection develop: body temperature rises, the patient shudders, tachycardia is noted, arterial hypotension appears, and there is a risk of seizures. Frequent vomiting and diarrhea lead to the development of severe dehydration.

Most patients, by the beginning of the second day from the onset of the disease, begin to notice relief, and for the next 2-3 days only general weakness remains.

It is extremely rare, especially if timely treatment has not been started, that toxic or hypovolemic (due to dehydration) shock develops, quite often leading to death.

Salmonellosis

Salmonellosis is an infectious disease caused by bacteria of the Salmonella genus, which has various manifestations. Most often, the gastrointestinal tract is first affected, which is expressed in the development of gastroenteritis and enterocolitis.

The pathogens include a large group of Salmonella. Most salmonella can cause disease in humans, animals and birds. Bacteria can survive for a long time in the external environment. In meat and dairy products, salmonella not only persists, but also multiplies, while the appearance and taste of the products does not change. When salting and smoking, salmonella do not die, and when frozen, the survival time of microbes in products even increases.

Pets and birds are the main sources of infection, but humans can also be an additional source of infection. In animals, salmonellosis occurs as an acute disease. The most dangerous animals are bacteria-carrying animals without signs of disease.

Humans, as a source of infection, pose the greatest danger to infants, who have increased sensitivity to all infectious diseases.

Infection with salmonellosis occurs through the nutritional route, when foods contaminated with a large number of salmonella are consumed. The reason for the heavy contamination of products is usually impaired culinary processing, when infected products, especially meat, are in conditions suitable for the propagation of the pathogen. The highest incidence of salmonellosis is observed in the warm season.

Clinic. The incubation period after infection can range from 6 hours to 3 days (usually 12–24 hours). If the outbreak occurred in an organized group, this period is extended to 3–8 days.

Salmonellosis can occur in various forms, the most common can be noted.

1. Gastrointestinal form, which mainly affects the intestines and stomach.

2. Generalized form, in which typhus-like and septic variants are distinguished.

3. Bacterial carriage, when there are no clinical manifestations of the disease.

Most often people suffer from the gastrointestinal form of salmonellosis.

The disease is characterized by an acute onset, the temperature, especially in severe forms, rises to 39 °C and above, the patient feels chills, general weakness appears, headache, nausea, vomiting, pain in the epigastric and periumbilical region is noted. Then comes diarrhea. Symptoms of salmonellosis are most pronounced on days 2–3.

In mild forms of the disease, the body temperature does not rise above 38 °C, vomiting occurs once, stools become loose and watery, the frequency does not exceed 5 times/day, diarrhea persists for 1–3 days, fluid deficiency is no more than 3% of body weight.

The moderate form of salmonellosis is characterized by a rise in body temperature to 38–39 °C, a feverish period of up to 4 days, diarrhea of ​​up to a week, repeated vomiting, increased bowel movements up to 10 times a day, tachycardia, decreased blood pressure, and fluid deficiency of up to 6% of body weight.

In severe cases, the temperature may exceed 39 °C, and the febrile period lasts 5 or more days. Severe symptoms of intoxication, repeated vomiting continues for several days. The frequency of stool exceeds 10 times a day, the stool becomes profuse, watery, and foul-smelling. An admixture of mucus may appear in the stool, and diarrhea continues for more than a week. The liver and spleen enlarge, yellowness of the skin and sclera appears, cyanosis, tachycardia, blood pressure decreases. Kidney damage occurs, as a result of which urination decreases, urine tests determine protein, red blood cells and casts, and renal failure may develop.

Typhoid-like form of salmonellosis. In this form, the onset of the disease is acute. Intestinal disorders, fever and symptoms of general intoxication appear. Within 1–2 days, intestinal dysfunction stops, and the temperature continues to remain high, the phenomena of general intoxication progressively intensify, which is manifested by a febrile reaction lasting from 1 to 3 weeks, lethargy, and apathy. A blistering rash appears on the skin, bradycardia, decreased blood pressure, bloating, and an enlarged liver and spleen are noted.

Septic form of salmonellosis. It is one of the most severe variants of salmonellosis.

The onset of the disease is acute, in the first days it resembles a typhoid-like form. In the following days, the patient's condition worsens. The fever is constant, and septic foci form in various organs. Damage to the musculoskeletal system is manifested by osteomyelitis, arthritis, the cardiovascular system - endocarditis, aortitis, the lymphatic system - tonsillitis, cervical purulent lymphadenitis, the central nervous system - meningitis (especially in children).

Escherichiosis

Escherichiosis is a group of infectious diseases caused by pathogenic Escherichia coli (Escherichia), occurring with symptoms of intoxication, fever, and mainly affects the gastrointestinal tract, less often, the urinary, biliary tract, and other organs may be involved in the process. Sepsis may develop; infants are more likely to get sick.

Escherichiosis, in its course, is in many ways reminiscent of dysentery; bacteria are able to invade and multiply in intestinal cells.

The main route of spread of Escherichia is fecal-oral. Human infection occurs by consuming contaminated food and water.

Clinic. Under the influence of Escherichia, an inflammatory process develops in the small intestine, which is expressed in signs of intestinal infection, usually in children of the first year of life and newborns.

The main symptoms of the disease are severe abdominal pain, vomiting, and watery stools without blood. The course of these diseases is particularly severe and lasts 2 weeks or more.

E. coli can be of several varieties, depending on this, the disease can manifest itself in different ways.

When affected by enteroinvasive E. coli, the upper parts of the large intestine are usually affected. Clinically, this is characterized by severe abdominal pain and profuse watery diarrhea. There may be blood in the stool.

Under the influence of enterotoxigenic E. coli, cholera-like forms of intestinal infections develop in people of any age. Clinically, these forms are distinguished by the appearance of frequent, watery stools, which quickly lose their fecal character and the rapid development of dehydration.

Enterohemorrhagic Escherichia causes diarrhea mixed with blood, which is called hemorrhagic colitis. In addition, there is a complete absence of fever, the addition of symptoms of renal failure and a pronounced drop in the number of platelets in the blood.

Intestinal infections caused by enteroadhesive Escherichia are observed much less frequently and in their course resemble moderate forms of dysentery.

With all types of escherichiosis, signs of intoxication develop, which are in many ways similar to intoxication in other bacterial intestinal infections. The severity of the sick child’s condition is determined by the severity of intoxication.

Complications. The most common complication of escherichiosis that can develop during an intestinal infection, caused by enterohemorrhagic Escherichia coli, is hemolytic-uremic syndrome, which can be recorded in 5–10% of patients. This syndrome is characterized by the toxic destruction of red blood cells, resulting in anemia and the development of acute renal failure (ARF). Signs of acute renal failure usually appear at the end of the first week after the earliest signs of intestinal disease appear.

Cholera

Cholera is an acute intestinal infection, the peculiarity of which is that it primarily affects the small intestine, which is accompanied by a violation of water-salt metabolism with varying degrees of dehydration, which occurs due to massive loss of fluid with vomiting and profuse watery stools. The disease is considered a particularly dangerous infection and can quickly spread throughout the population.

Cholera is caused by Vibrio cholerae. There are two main ones - the classic one, which causes Asian cholera and El Tor.

The main route of infection with cholera is waterborne, when unboiled water from open reservoirs is consumed.

After passing through the stomach, the vibrio enters the small intestine, where it colonizes and multiplies on the surface of the intestinal epithelium. However, in sick people, vibrio can be found in any part of the gastrointestinal tract.

Having reached a certain concentration during reproduction, vibrio causes disease.

As the disease develops, a huge amount of fluid and salts of sodium, potassium, chlorides and bicarbonates are lost. Vibrio cholerae affects people of all ages. The disease is most severe in people who abuse alcohol, who have undergone surgery to remove part of the stomach, and in young children.

Clinic. The incubation period for cholera can range from several hours to 5 days, but on average it is 2–3 days. If a person took antibiotics prophylactically, but still fell ill, the incubation period can extend to 9-10 days.

Cholera is characterized by a sudden onset. The most pronounced manifestation of cholera is diarrhea, which appears first. The stool characteristic of cholera looks like a watery, cloudy-white liquid with flakes floating in it. The stool is similar in appearance to rice water and has no odor. One of the first signs of cholera is muscle weakness and cramps in the calf muscles. Subsequently, loose, watery stools are accompanied by profuse, frequent vomiting.

With cholera, there are several degrees and stages of dehydration.

I degree. At this degree, body weight loss occurs in the range of 1–3%. Diarrhea and vomiting become more frequent from 2-3 to 5-6 times a day, and the duration of these disorders is 1-3 days. The patient's well-being usually suffers little. The patient may feel slight general weakness, thirst, and dry mouth. The color of the skin and mucous membranes does not change, pulse rate, blood pressure, and urine output remain within normal limits.

II degree of dehydration is characterized by a body weight deficit of 4–6%. Stools become more frequent up to 15–20 or more times a day, sometimes slight pain appears in the epigastric region, diarrhea is accompanied by frequent vomiting. General and muscle weakness, dry skin and mucous membranes become more pronounced, the tongue becomes dry and a white coating appears on it. There is constant cyanosis of the lips and mucous membranes, hoarseness and roughness of the voice. In rare cases, there may be short-term cramps of the masticatory muscles and muscles of the feet, hands and legs. In many patients, tachycardia is registered, blood pressure decreases, and the volume of urine excreted decreases.

Body weight deficiency with degree III dehydration is already 7–9%. Bowel movements may become more frequent up to 25–35 times a day or more, and vomiting may occur repeatedly. This degree is characterized by severe general weakness and indomitable thirst. Muscle cramps in the limbs and abdomen become frequent and painful. The skin and mucous membranes are constantly cyanotic. The skin is cold to the touch. The patient's voice is hoarse, almost silent. Body temperature can drop to 35.5 °C. There is a sharp decrease in blood pressure, tachycardia, shortness of breath, and patients almost completely stop urinating. Noteworthy are the sharpening of facial features, sunken cheeks and eyes.

With IV degree of dehydration, a loss of over 10% of body weight occurs. Characterized by rapid development of cholera symptoms with very frequent diarrhea and vomiting. The condition of the patients is extremely serious. Signs of dehydration reach their maximum severity. Facial features become sharpened, cyanosis of the skin and mucous membranes is widespread, the skin is cold to the touch and covered with sticky sweat. There is pronounced cyanosis around the eyes, “washerwoman’s hands”, a pained expression on the face. Cramps of all muscle groups develop, they are often repeated and very painful. Body temperature drops to less than 35 °C, voice is completely absent. The functioning of the cardiovascular system is sharply disrupted: tachycardia, muffled heart sounds, pulse and blood pressure can no longer be detected, rapid and shallow breathing.

Viral intestinal infections

Intestinal infections caused by viruses are a group of diverse acute infectious diseases that are united by signs of general intoxication and predominant damage to the stomach and small intestine (individually or in combination), i.e., they most often manifest as gastroenteritis or enteritis. Other organs and systems of the body are also affected.

Most often, the gastrointestinal tract is affected by rotavirus infection, followed by 2 types of intestinal adenoviruses.

Less commonly, gastrointestinal disorders can be caused by enteroviruses and reoviruses.

Rotaviruses multiply in the upper small intestine.

Reoviruses are in many ways similar in structure to rotaviruses.

Reoviruses multiply in the mucous membrane of the small intestine and upper respiratory tract, so these parts of the body are affected first. Reoviruses can infect animals.

Adenoviruses primarily affect the respiratory tract, and only two types of adenoviruses cause diarrhea. In addition to the upper respiratory tract, adenoviruses also infect the small intestine.

Among the enteroviruses that can cause diarrhea, Coxsackie viruses deserve attention.

All viruses that cause diarrhea are stable in the external environment. Enteroviruses can survive well in water. All viruses tolerate low temperatures, even freezing.

Children are most often affected by intestinal viruses, but adults are also affected.

The source of infection with rotavirus infection is a sick person or a virus carrier. The patient excretes most of the viruses in the stool. The main route of infection is the fecal-oral route, when infection occurs with food, through dirty hands. Another route of infection is airborne. The maximum increase in incidence occurs in the autumn-winter period.

The main difference between reovirus infection is that you can become infected not only from humans, but also from animals. This infection is usually contracted from virus carriers, since most often the disease is asymptomatic. The airborne route is the main route for the spread of infection. But the pathogen can be transmitted through water, food and personal contact.

Adenovirus infection is contracted from sick people, and sometimes from virus carriers. The main way of spreading the infection is through airborne droplets; transmission through utensils and common objects is possible. The peak incidence is the autumn-winter period.

The greatest danger when contracting an enterovirus infection is the virus carrier. The fecal-oral route of infection is the main route, although airborne transmission is also important. A combination of these infection mechanisms is possible.

Clinic. The incubation period for rotavirus infection ranges from 15 hours to 3–5 days, but does not exceed 7 days. In rare cases, it can extend up to 9 days.

The vast majority of patients become ill with rotavirus infection within the first 24 hours. In half of the patients the disease is mild. Gastroenteritis is the main manifestation of rotavirus infection. In addition to frequent loose stools, patients experience vomiting. But vomiting does not always happen.

Vomiting is not particularly frequent and lasts, on average, about a day. After vomiting stops, the stool becomes foamy, watery and yellowish-greenish in color. There are no bowel movements more than 10–15 times a day. The duration of diarrhea is from 3 to 5 days. Patients may experience abdominal pain. The intensity of the pain is moderate, it is felt in the upper abdomen or throughout the entire abdominal cavity. Pain is not always felt; abdominal discomfort is usually noted.

Signs of intoxication are moderate. Not everyone experiences an increase in temperature. If fever occurs, the temperature does not exceed 38 °C. The duration of the febrile period is 1–3 days. The most common symptom is intoxication, which manifests itself as weakness and loss of appetite. Brief fainting is possible. The symptoms of intoxication disappear earlier, before stool normalization. Every second patient has pharyngitis, in the form of hyperemia of the posterior pharyngeal wall, and a rare cough. Lesions of the upper respiratory tract are more common with reovirus infection.

Adenovirus infection is characterized by longer intoxication and fever. In many patients, the temperature rises above 38 °C and the febrile reaction lasts from 5 to 7 days. Damage to the gastrointestinal tract is manifested by signs of gastroenteritis or enteritis. The stool becomes liquid, watery, and its frequency is 5–7 times a day. In addition to diarrhea, in some cases there is vomiting during the first 1–2 days. A typical symptom of adenovirus infection is swollen lymph nodes. Sometimes the liver and spleen become enlarged (hepatosplenomegaly), and conjunctivitis often develops.

A type of enterovirus infection that primarily affects the gastrointestinal tract, in most cases it has a mild course. Intoxication, as with all viral diarrhea, is combined with damage to the gastrointestinal tract in the form of moderate enteritis, which is manifested by loose, watery stools up to 5-7 times a day. But with this infection, other organs and systems of the body are also involved in the pathological process: patients develop a rash, mainly on the extremities, the upper parts of the respiratory tract are affected, a sore throat is typical, in which transparent bubbles (vesicles) appear in the pharynx, and everyone’s liver and spleen.

Treatment of intestinal infections

Diet of patients with intestinal infections. Patients with intestinal diseases are prescribed a gentle diet. Preference is given to products that slow down intestinal motility and contain a large amount of tannin, which is found in blueberries, bird cherry, strong tea, products with a viscous consistency such as slimy soups, pureed porridges, cottage cheese, kefir and jelly. You can eat crackers and steamed dishes made from lean meat and fish. Consumption of fried and fatty foods, raw vegetables and fruits is prohibited.

Gastric lavage. This procedure is a mandatory component of the treatment of foodborne diseases. Gastric lavage is performed at any time from the onset of the disease, due to the ability of infectious agents to persist for a long time in the cells of the mucous membrane of the gastrointestinal tract.

Therapy aimed at reducing intoxication and replenishing fluid in the body.

Fluid replenishment in cases of mild or moderate dehydration due to intestinal infections is sufficient only by oral administration of appropriate solutions. Currently, solutions such as re-hydron and citroglucosolan are used.

Oral (through the mouth) fluid replacement (rehydration) for dehydration is carried out in two stages.

1. During primary rehydration, the main goal is to replenish the deficiency of water and salts that exists at the beginning of treatment. This procedure is carried out during the first 4–6 hours. Calculation of the required volume of fluid for the initial stage of rehydration depends on the degree of dehydration and weight.

Primary rehydration for mild dehydration is carried out for 4 hours, and for moderate dehydration - 6 hours.

2. The second stage of rehydration is maintenance.

At this stage, the ongoing losses of water and electrolytes that occur with vomiting and diarrhea are replaced and additional fluid requirements are provided. During maintenance rehydration, for every next 6 hours, the same volume of fluid is administered as the patient lost over the previous 6 hours. To determine this volume, losses with diarrhea, vomiting, and also with hyperthermia are calculated for each degree in excess of 37–10 ml/kg.

If there is shortness of breath - for every 20-30 breaths above the age norm - 10 ml/kg.

The solution can be drunk from a cup in sips or tablespoons at the required intervals.

In addition to special solutions for rehydration, you can partially use just drinking water, mineral water, herbal infusions and tea.

The disease can be accompanied by severe intoxication at any degree of dehydration, therefore, immediate infusion and detoxification therapy (administration of medicinal solutions intravenously) is required.

Infusion therapy is usually started with the introduction of colloidal solutions - fresh frozen plasma, Albumin, Reo-polyglucin, Hemodez, etc.

To compensate for the deficiency of water and salts, glucose-saline solutions are used, glucose is used in the form of a 5-10% solution.

Saline solutions are used in the form of polyionic solutions, “Quartasols”, “Trisols”, potassium chloride solution (the concentration of potassium chloride in the solution cannot exceed 1%), 4% sodium bicarbonate solution.

During the first 6–7 hours, the patient must be administered a volume of fluid approximately equal to the calculated fluid deficit; usually up to 50% of the fluid is administered intravenously; in severe conditions accompanied by frequent vomiting, the portion of the fluid administered intravenously reaches 70–80% of the volume.

Infusion therapy must be carried out under the control of diuresis, i.e. the amount and rate of urine excretion are taken into account.

In case of potassium deficiency, a solution of potassium chloride diluted with glucose or saline is administered. In case of acidosis (increased blood acidity), a 4% solution of sodium bicarbonate is administered.

Other areas of therapy for intestinal infections.

One of the main directions in the treatment of intestinal infections is therapy that helps reduce the frequency of stools and normalize them.

For this purpose, indomethacin is prescribed for diarrhea.

During the first day, this drug is prescribed orally. In some cases, indomethacin may be prescribed the next day. In addition to reducing diarrhea, indomethacin can relieve cardiac dysfunction.

To reduce diarrhea syndrome, calcium supplements are sometimes used in combination with vitamin B2 (ergocalciferol). Calcium is prescribed in the form of intravenous injections of a 10% solution of calcium gluconate in a 3-day course.

Great importance in the treatment of diarrhea in patients with intestinal infections is attached to the use of drugs such as. These primarily include activated carbon, produced in tablets or powder form.

Similar in mechanism of action is the complex preparation of activated carbon KM, consisting of activated carbon, white clay, and sodium salt of carboxymethylcellulose. This drug is more active. It is released in the form of tablets taken orally.

A good effect is observed from the use of carbolong, which contains activated stone charcoal powder.

One of the widely used sorbents is a drug such as polyphepan. The drug is obtained by processing lignin, which is a product of hydrolysis of the constituent substances of wood. It is taken orally in the form of granules, which are mixed well in water before use.

The most effective sorbent is considered to be smecta, which has a pronounced enveloping effect. Smecta is able to protect the intestinal epithelium from damage. The release form of the drug is powder, packaged in bags. To use, the contents of 1 sachet are dissolved in 100 ml of water and drunk little by little over several hours. The drug has no contraindications; it can be prescribed to children of any age.

Another group of antidiarrheal drugs includes drugs that have an opioid effect. Representatives of this group are loperamide and trimebutine. The peculiarity of opiates is that they are able to inhibit intestinal motility. They are usually prescribed to older children and adults for diarrhea, in capsule form.

Trimebutine, used in tablets, has a positive effect on intestinal motility, normalizing the smooth muscles of the entire gastrointestinal tract.

Not so long ago, somatostatin began to be used to treat diarrhea, which has a normalizing effect on the processes of absorption and secretion in the intestine. When exposed to this hormone, the rate of absorption of water and salts in the small intestine increases, the frequency of stools and the weight of feces decreases. The drug solution is available in ampoules for subcutaneous administration.

With intestinal infections, dysbacteriosis almost always develops, or this condition is the result of the use of antibiotics. In the complex treatment of dysbacteriosis, agents that normalize the intestinal flora are used - bifidum-bacterin, coli-bacterin, bificol, linex, etc. (for more details, see rehabilitation).

Intestinal antiseptics. Previously, the following drugs from this group were used to treat intestinal infections: Intesto-pan, Intetrix and Enterosediv.

Recently, ercefuril (nifuraxazide), which is a derivative of nitrofuran, has been used in the treatment of intestinal infections. This drug acts primarily in the intestinal lumen and is used to treat diarrhea caused by bacteria.

Quite often, furazolidone is used among the drugs in this group. Among the causative agents of intestinal infections, the most sensitive to furazolidone are the bacteria of dysentery, typhoid fever, and paratyphoid fevers A and B. In addition, bacterial resistance to this drug develops slowly.

Antibiotics. Antibiotics are prescribed only for moderate to severe forms of intestinal infections.

In the treatment of intestinal infections, antibiotics can include groups of penicillins, cephalosporins, monobactams, carbapenems, aminoglycosides, tetracyclines, polymyxins, quinolone drugs, nitrofurans, sulfonamides.

Cephalosporins are one of the largest classes of antibiotics. They have a wide antibacterial spectrum of action and low toxicity. The most commonly used for the treatment of intestinal infections are: cefotaxime (can be produced under the name claforan, cephabol, etc.), routes of administration - intramuscular or intravenous; Ceftriaxone (also called longacef, rocephin, cefaxone, etc.) is also administered intravenously and intramuscularly.

There are three generations of quinolones. Registered in Russia are drugs belonging to the first and second generations. Fluoroquinolones have a broad antimicrobial spectrum of action. Widely used for intestinal infections: ciprofloxacin (also called cyprinol, cyprobay, ciprolet, etc.), ofloxacin (other names - zanocin, tarivid), norfloxacin (nolicin, normax), Lomoflox (lomefloxacin, maxaquin). All of the drugs listed are taken orally or administered intravenously.

Of the tetracyclines, the most commonly used is doxycycline (also called vibramycin, doxal and tetradox), which has a broad spectrum of action. This drug can only be prescribed to children over 8 years of age; it is contraindicated in pregnant and breastfeeding women, patients suffering from severe liver diseases and kidney failure. Available in capsule form for oral administration.

Aminoglycosides include drugs such as streptomycin, neomycin, kanamycin, netromycin, gentamicin, tobramycin, amikacin.

Antibiotics of this group can have a toxic effect on the kidneys and can lead to deafness. Mainly used in the treatment of adults. When prescribing to children, special care is taken, therefore two methods of dosing drugs are used: traditional, when the drug is administered 2 times a day, and a single administration of the entire dose. In the treatment of intestinal infections the following are usually prescribed: gentamicin (garamycin), netromycin, amikacin (selemycin, farcycline). Mostly these drugs are administered intravenously or intramuscularly.

Treatment of cholera, as a particularly dangerous infection, has its own characteristics.

All cholera patients must be hospitalized and isolated to prevent the spread of infection.

In addition to symptomatic treatment, which is aimed at eliminating fluid deficiency, both orally and intravenously, patients with cholera are prescribed antibiotics, which helps reduce the duration of diarrhea and water-salt losses. Antibacterial drugs such as doxycycline, tetracycline, chloramphenicol succinate, erythromycin, and ciprolet (ciprofloxacin) can be prescribed internally.

The average course of antibiotic treatment is 3 to 5 days.

Oral antibiotics can be used only after dehydration has been eliminated and there is no vomiting, which can be achieved 4–6 hours from the start of therapy. In case of severe dehydration, tetracycline and chloramphenicol are administered intravenously during the first hour of treatment, and then the drugs are given orally.

There are three main directions in the prevention of acute intestinal infections, which depend on the links in the epidemiological chain that determine the spread of the infection. These include:

1) impact on the source of infection;

2) interruption of distribution paths;

3) reducing the body’s susceptibility to infection. Source of infection. Activities aimed at complete

and early detection and neutralization of the causative agent of intestinal infections are the main means in combating the spread of diseases. All children who suffer from intestinal dysfunction, from the onset of the disease, are subject to bacteriological examination and isolation. Patients are usually isolated in specialized hospitals and, only sometimes, isolation at home is allowed, subject to the sanitary and epidemiological regime. It is prohibited to leave infected children in organized children's groups. Isolation is terminated after complete recovery and the presence of negative results of subsequent bacteriological control.

Children who have had dysentery are allowed to be discharged only after stool normalization, at a normal temperature for three days and if there is a negative result of a bacteriological examination, which is carried out not two days after stopping the course of antibiotics.

Patients with chronic dysentery should continue treatment in special sanatoriums (if this is not possible, they are discharged home) after the exacerbations have stopped, with normal stools and temperatures for 10 days, as well as in the presence of a negative result of a bacteriological test, which is carried out 2 days after discontinuation of the antibacterial treatment.

Patients with dysentery in the convalescent stage are under dispensary observation, which is carried out by the clinic for 1 month. Patients who have suffered protracted and chronic forms of the disease are observed for up to 3 months.

Patients who have had a coli infection are discharged from the hospital after clinical recovery and a negative bacteriological examination. Convalescents who have suffered salmonellosis are discharged after clinical recovery and in the presence of a double negative bacteriological test result.

To identify the sources of infection, it is necessary to conduct a bacteriological study of stool from people who have been in contact with the patient. In cases of dysentery and salmonellosis, everyone around them of any age is examined. If there have been cases of coli infection and staphylococcal infection, all children 1–2 years of age are examined, and mothers of newborns are also examined in maternity hospitals. If carriers are identified, they are isolated (at home or in a hospital) and subjected to preventive treatment.

In order to identify probable sources of infection, a bacteriological examination is carried out on all children who are newly admitted to children's institutions, as well as children admitted to hospitals. Adults who work in child care institutions, kitchens, and stores are also subject to preventive examinations. They are examined upon entry to work, and subsequently periodically during routine medical examinations. If carriers are identified, they are suspended from work.

Paths of distribution. At the source of infection, current and then, after hospitalization or recovery of the patient, final disinfection is carried out. Among the preventive measures, disinfection of toilets and potties in preschool and school institutions, control of flies, improvement of children's institutions, properly organized water supply and maintenance of sewage systems, strict control over the anti-epidemic regime, especially in food units, control over storage and food processing.

When preventing the spread of intestinal infections, great importance is attached to sanitary and educational work among the population, in particular among parents of children. Prevention of salmonellosis, in addition to the above, additionally includes the implementation of measures by the veterinary service in the retail chain, especially with regard to the supervision of the storage and sale of meat products. In order to prevent the possibility of the spread of staphylococcal infection, persons with pustular skin diseases are excluded from caring for infants and working in catering units. For intestinal infections of a viral nature, the main preventative measure is the isolation of sick children until they recover.

The possibility of increasing specific immunity through active immunization is very limited. For several years, attempts were made to use active immunization with the Bezredka vaccine against dysentery, but due to low efficiency it ceased to be used. Of no small importance is the use of bacteriophages for prevention, which are used in children's schools (up to 10 years of age) and preschool institutions that are disadvantaged by high incidence rates during the period when the highest seasonal increase in incidence is observed. The most effective phaging scheme is to conduct a preventive course among children and institutional staff every 3 days.

Particular attention should be paid to increasing nonspecific protective mechanisms, creating conditions that ensure the possibility of harmonious physical and neuropsychic development of children, adequate feeding of infants, etc.

Rehabilitation

Diet therapy during the period of convalescence for intestinal infections. Food should be mechanically and chemically gentle and contain sufficient amounts of proteins, fats, carbohydrates and vitamins. It is quite reasonable to exclude hot, spicy dishes and smoked foods from the diet, and limit the consumption of coarse plant fiber. If there is a malabsorption of carbohydrates, the so-called disaccharidase deficiency, then a diet is prescribed that excludes milk sugar - lactose. It is better to give preference to lactose-free mixtures, such as NAN Lactose-Free. Porridges are best prepared with vegetable broths; the use of vegetable dishes made from zucchini, cauliflower, and potatoes has a good effect. It is recommended to administer cottage cheese dishes and three-day kefir. The prescription of therapeutic nutrition, which contains fermented milk lactobacterin, bifi-lact, anacid bifilact, is widely used. You can use the addition of biologically active additives (BAA), such as BAD-1L (with lysozyme), BAD-1B (with bifidumbacterin), BAD-2 (with lysozyme and bifidum-bacterin).

Specific bacteriophages. Prescribed for 5–7 days if the pathogenic pathogen is re-isolated.

Probiotics. Prescribed from 2 weeks to 2–3 months, subject to the abolition of antibacterial drugs, specific bacteriophages, lactoglobulins. When prescribing, monitoring of intestinal microbiocenosis indicators must be carried out. In this case, it is rational to prescribe bifidumbacterin, lactobacterin, bificol, colibacterin, bifilong, travis, bactisubtil, biosporin, nutrolin B, acipol, enterol 250, biobacton, bifiform, acylact.

Enzyme therapy. Indications for prescribing enzyme therapy are severe symptoms of secondary enzymopathy. Therapy is prescribed in the form of both mono- and polyenzymes. Treatment is monitored using a coprocytogram.

The most commonly prescribed enzymes are:

Oraza - for 2-4 weeks, Pancreatin - 4-6 weeks, Mezim-Forte - for a course of up to 2 months, Creon - for 2 weeks, Festal, Digestal, Panzinorm Forte - also for a course of 2 to 4 weeks.

Phage therapy. When pathogens of intestinal infections are persistently isolated from feces in high concentrations, the administration of specific bacteriophages is rational. The following drugs are used: combined pyobacteriophage, pyo-ceaneus, purified polyvalent Klebsielosis bacteriophage, purified Klebsielosis pneumoniae bacteriophage, staphylococcal bacteriophage, coliprotean bacteriophage, intesti-bacteriophage, dysenteric bacteriophage with pectin base, dysenteric with acid-resistant coating, polyvalent Salmonella bacteriophage.

The average duration of treatment with bacteriophages is 1 month, but may be longer, depending on the results of bacteriological examination of stool.

Phytotherapy. The bactericidal purpose of decoctions and infusions of herbs such as St. John's wort, calendula, eucalyptus, yarrow, bloodroot, sage, lingonberry, plantain. To increase the secretory activity of the gastrointestinal tract, yarrow, wormwood, plantain, and cabbage juice are prescribed. In order to correct immunity, a decoction of nettle, plantain, string, and lemon balm is used. For unstable, frequent stools, you can give rice broth or a decoction of bird cherry fruits.

St. John's wort decoction.

Required: crushed St. John's wort herb - 1 tbsp. l. Preparation and use. Pour 1 cup of boiling water over the chopped herb, cook for 10 minutes, strain.

Take 50 ml 4 times a day 30 minutes before meals (daily

This decoction has a good effect on diseases of the digestive system and during the recovery period from intestinal infections.

Calendula infusion.

Required: calendula flower baskets - 1 tbsp. l.

Preparation and use. Brew flower baskets with 1 cup of boiling water, leave for 40 minutes, wrap warmly, strain.

Take 1 tbsp. l. 3 times a day 0.5 hours before meals after an intestinal infection and with vitamin C deficiency.

Decoction of eucalyptus leaves.

Required: eucalyptus leaves – 2 tsp.

Preparation and use. Brew the leaves with 1 cup of boiling water, bring to a boil, boil for 1-2 minutes, leave until cool, strain.

Take 1 tsp. 3 times a day after meals with unstable stools.

A decoction of yarrow herb.

Required: yarrow herb - 1 tbsp. l.

Preparation and use. Brew the herb with 1 cup of boiling water, simmer for 15 minutes over low heat, leave for 1 hour, strain.

Take 1 tbsp. l. 3-4 times a day after meals. Potentilla decoction.

Required: crushed cinquefoil leaves - 1 tbsp. l.

Preparation and use. Pour a glass of boiling water over the crushed rhizomes of the plant with roots, boil for 15 minutes, strain.

Take 1 tbsp. l. 3-4 times a day 1-1.5 hours before meals for gastrointestinal diseases, and can also be used for rheumatism and gout.

Infusion of cinquefoil rhizomes.

Required: crushed cinquefoil rhizomes - 1 tbsp. l.

Preparation and use. Brew crushed rhizomes with 1 cup of boiling water, leave, wrapped warmly, for 3 hours, strain.

Take 1 tbsp. l. as a choleretic agent after gastritis and enteritis, when there is reduced acidity of gastric juice.

Infusion of sage leaves.

Required: crushed sage leaves - 1 tbsp. l.

Preparation and use. Pour a glass of boiling water over sage leaves, leave for 20 minutes, cool, strain. The infusion is good for 2–3 days. Store in a cool place.

Take 1 tbsp. l. 3 times a day for unstable stools.

Infusion of lingonberry leaves.

Required: lingonberry leaves - 1 tbsp. l.

Preparation and use. Pour 100 ml of boiling water over lingonberry leaves for 2 hours, then strain.

Take 1-2 tbsp. l. 3-4 times a day before meals for diseases of the gastrointestinal tract. It can also be used for diseases of the kidneys, liver, bedwetting, gout, and rheumatism.

Infusion of lingonberry fruits.

Required: lingonberry fruits – 200 g.

Preparation and use. Pour boiling water over the fruits in a colander, then leave in 400 ml of chilled boiled water for 6 hours.

Take 100 ml 4 times a day before meals for constipation, due to dysbacteriosis, gastritis, colitis.

Infusion of leafy lingonberry branches.

Required: chopped leafy lingonberry branches - 1 tbsp. l.

Preparation and use. Brew the raw material with a glass of boiling water, leave for 30 minutes, strain.

Take 2 tbsp. l. 4-5 times a day to increase the body's resistance.

A decoction of lingonberry leaves.

Required: lingonberry leaves - 2-3 tbsp. l.

Preparation and use. Boil the leaves in 3 glasses of water for 10 minutes, then leave for 1 hour and strain. Drink 200 ml 3 times a day before meals for gastritis and colitis. The decoction has a good effect on colds and coughs.

Infusion of plantain leaves.

Required: dried plantain leaves - 100 g.

Preparation and use.

Brew dried leaves with 500 ml of boiling water, leave for 2 hours, strain.

Take 1 tbsp. l. 3 times a day before meals for gastritis that has developed after intestinal infections, when there is low acidity, hemorrhoids.

Infusion of plantain seeds.

Required: plantain seeds 25 g.

Preparation and use. Brew the seeds with 200 ml of boiling water, shake for a long time, strain.

Drink 1 tbsp. l. 3 times a day 15–20 minutes before meals for constipation caused by intestinal dysbiosis after intestinal infections.

Cabbage juice.

Preparation and use. Cabbage juice is obtained by squeezing fresh cabbage leaves. It has a pleasant smell and delicate taste. The patient should drink raw juice after eating a light meal, depending on age, from 200 ml to 1 liter per day. Drinking juice helps to eliminate sensations such as sour belching and pain. The course of treatment is 4–5 weeks.

A decoction of wormwood and sage leaves.

Required: wormwood leaves – 2 tbsp. l., sage leaves - 2 tbsp. l.

Preparation and use. Mix wormwood and sage leaves in equal proportions. 2 tbsp. l. Boil the mixture in 400 ml of water for 30 minutes, strain.

Take 1 tbsp. l. after 2–3 hours for lesions predominantly of the large intestine.

A decoction of nettle roots.

Required: crushed roots and rhizomes of wormwood - 1 tbsp. l.

Preparation and use. Boil the raw materials in 200 ml of sugar syrup or honey for 15 minutes.

Take 1 tbsp. l. 5–6 times a day after gastritis and colitis. Can be used for coughs, urolithiasis, furunculosis, rashes and acne.

Infusion of lemon balm herb.

Required: lemon balm herb - 1.5 tbsp. l.

Preparation and use. Brew the herb with 180 ml of boiling water, leave, wrapped warmly, for 1 hour, strain.

Drink this dose 3-4 times a day for gastrointestinal problems associated with constipation.

Melissa tincture.

Required: lemon balm herb - 1 tbsp. l.

Preparation and use. Pour 100 ml of alcohol or 1 glass of vodka over the grass, leave for 2 weeks in a dark place, strain.

Take 15 drops 3 times a day for gastrointestinal diseases and bloating.

Rice water against diarrhea.

Required: rice - 1 tea cup.

Preparation and use. Pour 6-7 cups of water over the rice, place over low heat and boil. Cool the resulting broth and strain.

Give a child 1β cup, an adult a cup every two hours for diarrhea.

Decoction of bird cherry fruits.

Required: bird cherry fruits – 1 tbsp. l.

Preparation and use. Pour a glass of boiling water over the fruits, cook over low heat for 10 minutes, leave for 1-2 hours, strain.

Drink 1/2 glass 2-3 times a day as an astringent for diarrhea.

Vitamin therapy. Multivitamins and vitamin complexes such as Lifepack Junior+, Nutrimax+, Sveltform+, Mystic, Passilate, Coopers can be used. The course of treatment is 1.5–2 months.

Immunomodulatory therapy. Prescribed after severe invasive intestinal infections.

1. Methyluracil is available in tablets for oral administration 3-4 times a day after meals. The course of treatment is up to 1 month.

2. Sodium nucleinate is prescribed in drops 3-4 times a day for 2-3 weeks.

3. Lysozyme is available in the form of a dry substance and is prescribed 20–30 minutes before meals 3–4 times a day for 7–10 days.

4. Immunal (or Echinacea tincture) is prescribed in drops 3 times a day for 1 month.

5. Cycloferon is available in tablets and in injection solutions and is prescribed once a day according to the following scheme: 1-2-4-6-8 days of treatment.

Treatment of intestinal dysbiosis, which occurs as a complication of intestinal infections or antibiotic treatment.

Therapy for intestinal dysbiosis should be comprehensive. A protective regime is organized, which includes the creation of a favorable psychological environment, the patient must spend a long time in the fresh air, sleep must be long, and the diet must be appropriate for the child’s age.

Diet. The diet of children who have developed intestinal dysbiosis should be complete in terms of calories and the content of basic food ingredients. Food should be taken at the same hours, it is advisable to adhere to the rhythm of digestion. The diet should be as varied as possible; food can be saturated with vitamin complexes: Lifepack Junior+, Mystic, Passilate, Sveltform+, Chromevital+, etc.

It is advisable to include in your diet foods that stimulate intestinal microflora. Such products include products in the preparation of which wheat, rice, corn, buckwheat, and millet are used. Vegetables include cabbage, carrots, zucchini, pumpkin, and tomatoes. In addition, it is advisable to consume fresh fruits, lean meat and fish, fermented milk products, and vegetable fats. The best food for young children is mother's milk, which contains all the necessary nutrients, as well as substances that support microflora and immunoglobulins that protect the intestinal mucosa. If the mother does not have breast milk, then it is preferable to use adapted milk formulas with probiotic supplements (Nutrilak, Prenutrilak, NAN 6-12 with bifidobacteria) for feeding. For children over one year old, it is rational to prescribe kefir, yogurt, Biolacta, Bifidok, Narine. The treatment regimen for intestinal dysbiosis consists of 3 consecutive stages.

First stage. At this stage, the main task is to change the chemical processes in the intestines and eliminate opportunistic flora. To suppress the vital activity of opportunistic microorganisms, it is advisable to prescribe bacteriophages. They are microbial viruses and, unlike chemotherapy drugs, have a selective effect on specific types of bacteria, and they do not affect normal microflora.

Staphylococcal bacteriophage is a sterile filtrate of phagolysate, which has the ability to destroy the corresponding species of staphylococci. Can be prescribed to children of any age. Available in solutions for oral administration, for therapeutic enemas and in the form of suppositories for insertion into the rectum. Prescribed 2-3 times a day.

The Coliprotean bacteriophage contains components that are active against the most common serological groups of pathogenic Escherichia and Proteus.

Klebsiella polyvalent bacteriophage and Klebsiella bacteriophage contain filtrates of phagolysates of Klebsiella pneumoniae, ozena, rhinoscleroma and antibiotic-resistant Klebsiella.

Pseudomonas aeruginosa bacteriophage (pyocyaneus) contains a phagolysate that is capable of destroying Pseudomonas aeruginosa.

Pyobacteriophage combined contains components that are capable of destroying staphylococci, streptococci, Escherichia, Proteus and Pseudomonas aeruginosa.

Coliproteus, Klebsiella, Pseudomonas bacteriophage, pyobacteriophage are prescribed to children in the same age dosage as staphylococcal bacteriophage.

Intestibacteriophage contains phagolysates that destroy both pathogenic pathogens of intestinal infections, in the form of Shigella, Salmonella, pathogenic Escherichia, and opportunistic pathogens - enterococci, staphylococci, Proteus, Pseudomonas aeruginosa. For children, the age-appropriate dosage of intestibacteriophage is prescribed 3 times a day orally and 1 time in an enema. The drug is given 1 hour before meals. The initial course of treatment is 5–7 days.

To improve the cleansing of the intestines from pathogenic flora, the prescription of specific lactoglobulins is justified. The drug is a purified fraction of globulins, which are obtained from cow colostrum. The therapeutic effect of the drug is associated with the presence of specific antibodies to pathogenic Escherichia, Proteus, Klebsiella and Staphylococcus. The drug is prescribed orally 2-3 times a day, half an hour before meals. The duration of treatment is 5 days.

A good effect is achieved by using a complex immunoglobulin preparation (CIP). The therapeutic effect is associated with the content of immunoglobulins of 3 main classes (1d O, 1d M, 1d A). This drug acts on both pathogenic and opportunistic flora. CIP can be prescribed to children, starting from the first month of life, 1-2 times a day, half an hour before meals. The course of treatment is 5 days.

Second phase. It consists of populating the intestines with normal microflora by prescribing live bacterial preparations (probiotics). This takes into account age and the state of the intestinal microflora. The duration of treatment depends on the severity of dysbiosis and ranges from 1 to 3 months.

Probiotics are preparations containing living dried bacteria that maintain or restore the normal composition of intestinal microflora.

The group of probiotics includes the following drugs:

1) bifidumbacterin dry - consists of a suspension of living bifidobacteria. One dose of the drug contains at least 10 units of live bifidobacteria;

2) bifidumbacterin forte - is a preparation that contains a dried microbial mass of living bifidobacteria and a sorbent - activated carbon. One dose of the drug contains at least 10 units of bifidobacteria;

3) Lactobacterin dry – is a monocomponent preparation that contains a microbial mass of live active lactobacilli;

4) dry colibacterin contains a dried microbial mass of living E. coli bacteria;

5) bificol dry – the preparation contains co-grown cultures of E. coli and bifidobacteria;

6) bifilong – consists of the biomass of two varieties of bifidobacteria;

7) bifiform – is a combination drug that contains bifidobacteria and enterococci. In addition, the drug has antagonistic activity against pathogenic and opportunistic microorganisms;

8) biobakton contains a culture of acidophilus bacillus, which is characterized by high antimicrobial and acid-forming properties;

9) acipol – live acidophilus lactobacilli and heated kefir grains. The drug is characterized by high acid-forming and antagonistic activity. Kefir grains act as immunomodulators that stimulate the body's defenses;

10) acylact – is a complex preparation that contains 3 varieties of acidophilic lactobacilli. When taking this drug, the growth of lactobacilli and bifidobacteria in the intestines is stimulated;

11) Linex - is a multicomponent drug that has the property of inhibiting the growth of opportunistic bacteria. In addition, it improves the absorption of monosaccharides and stabilizes intestinal epithelial cells;

12) bactisubtil - is a drug that contains spores of special bacteria. Vegetative forms of such bacteria secrete enzymes involved in the breakdown of carbohydrates, fats and proteins, promote the synthesis of vitamins P and K, and suppress the growth of Escherichia, Staphylococcus, Streptococcus, Proteus;

13) biosporin dry consists of living microbial bacilli cells, which have the ability to suppress the growth of pathogenic and opportunistic bacteria;

14) Nutrolin B is a combined preparation consisting of lactobacilli and vitamins PP;

15) Enterol 250 contains lyophilized yeast Saccharomycetes boulardii. This drug restores normal intestinal microflora and has a pronounced antidiarrheal effect. In addition, the drug inhibits the growth of pathogenic and opportunistic microorganisms;

16) Travis contains two types of lactobacilli, bifidobacteria and one of the strains of streptococcus. The drug has an antagonistic effect on some pathogenic and opportunistic bacteria.

Third stage. The task of this stage is to increase the body’s nonspecific defense reactions, resulting in the formation of normal intestinal microflora. To stimulate the growth of microorganisms of normal intestinal flora, drugs of various groups are used. This is achieved by administering calcium pathoge (stimulating the growth of bifidobacteria), pamba (promoting the growth of lactobacilli, normal bacilli and bifidobacteria), hilaka forte, which helps restore normal intestinal microflora, lactulose, which enhances the growth of bifidobacteria.