What diseases are not caused by non-pathogenic amoebas. Intestinal amebiasis in adults: symptoms, treatment and prevention. Pathogenesis and pathomorphology

Back in 1875, the causative agents of amoebiasis were first discovered, and in 1891, this disease was identified as an independent nosological form called “Amoebic dysentery.” The term "amoebiasis" has been used from 1906 to the present day.

Dysenteric amoeba

Tissue form (found only in acute amoebiasis in affected organs and rarely in feces);
large vegetative form (this form already lives in the intestines and is found in the coprogram, it absorbs red blood cells);
luminal form (found in chronic amoebiasis or in the stage of reconvolution after taking a laxative);
precystic form (detected under the same conditions as the luminal form).

Cysts are found in patients with chronic recurrent amebiasis in remission and in carriers of amoebae.

The resistance of the trophozoite and all its varieties is very low; in the external environment it dies within 30 minutes. Cysts are the most resistant, for example:

• at 17-20ºС they are stored for a month, in darkened and moist soil - up to 8 days;
• in chilled food products, fruits, vegetables and household items – up to 5 days on average;
• At sub-zero temperatures they can be stored for several months.

Drying and high temperature destroy the amoeba almost instantly. Of the disinfectants, only cresol and emitin have a detrimental effect on them, and even chloramine does not have a negative effect on them.

Causes of amebiasis infection

Age groups of both sexes suffer from amoebiasis, but mainly pregnant women due to physiological suppression of the immune system, namely cellular immunity. Persons who received immunosuppressant therapy (GCS, cytostatics, etc.) can also be included in the category of high risk of infection. The incidence is recorded year-round, with a maximum increase in the hot months. This disease is especially common in countries with hot climates, including the countries of Central Asia and the Transcaucasus. Carriage is quite common when there are no symptoms, but there is amoeba in the body.

The source is the person releasing the cysts, may or may not have symptoms. The release of the pathogen continues for many years; 300 million cysts or more are released per day. With severe symptoms, patients are not dangerous, because they produce vegetative forms that are not stable in the external environment.

The routes of transmission are fecal-oral (through contaminated water and food) and contact-household (through “dirty hands”, household items are contaminated with the patient’s feces).

Factors that reduce the body's resistance to the pathogen: dysbiosis, protein deficiency, concomitant helminthic infestations, pregnancy and other conditions accompanied by decreased immunity.

Symptoms will be determined by pathogenesis, that is, the technique of damaging factors. As soon as the cysts enter the intestines, the incubation period begins and lasts 1-2 weeks, that is, from the beginning of implantation until the first signs of the disease. During this time, the cysts move through the sections of the intestine and, under provoking factors, they begin to move further and penetrate the walls of the large intestine. The transverse colon and descending sections of the large intestine are most often affected.

Symptoms of “acute” intestinal amebiasis (the onset is subacute – that is, the symptoms are noticeable not on the first day, but with an increase over 2-3 days):

Loose stools 4-6 times a day, with clear mucus and a pungent odor;
the frequency of bowel movements gradually increases to 10-20 times a day and the stool is no longer fecal in nature, but in the form of glassy mucus;
after a few days or immediately, an admixture of blood appears in the stool in the form of “raspberry jelly”;
constant or cramping pain of varying intensity, aggravated by defecation;
the appearance of tenesmus - a false urge to defecate, they are painful, long-lasting and do not lead to results;
low-grade fever 37-38ºС, lasts for several days;
bloating and abdominal pain.

Chronic course (as a result of delayed treatment):

Unpleasant taste in the mouth, difficult to characterize;
the tongue is covered with a white coating;
the abdomen at this stage is retracted, despite possible flatulence, upon palpation there is pain;
asthenic syndrome (weight loss), with a deficiency of proteins and vitamins (pallor of the skin, brittle nails, dull hair, etc., there are a lot of options and they will depend on the specific vitamin deficiency);
decreased/absent appetite;
on the part of other organs and systems, decompensation is observed (but these symptoms are not constant and may be absent altogether), especially with regard to the cardiovascular system and hepatic function: on the part of the heart - tachycardia and muffled heart sounds, and on the part of the liver - it may slightly increase and soreness.

In case of immunodeficiency, as well as in young children, a fulminant course of amebiasis is possible: the disease develops during the first two days, manifests itself with high fever, severe intoxication, severe pain, frequent bowel movements, and dehydration. Extensive damage to the intestinal wall quickly occurs, which leads first to the formation of ulcers, then to paresis, and there is a high risk of perforation of the intestinal wall and the development of peritonitis. These forms have a very high mortality rate.

There are also other clinical forms of amebiasis, but they are better classified as complications, since they occur more often due to untimely treatment.

Diagnosis of amoebiasis

It is possible to use the method from simple to complex:

1. Pay attention to the dynamics of the development of the disease + the nature of the stool + epidemiological data.
2. Microscopic examination of the patient’s stool, and in the presence of complications - from abscesses of internal organs, sputum, scrapings from the mucous membranes of the nasopharynx, biopsy samples of the affected areas. Smears are stained to identify cysts and trophozoites. To obtain excrement, you can use a provocative method - laxatives, but this is applicable only in case of remission; in acute cases, it is absolutely contraindicated.
3. Endoscopy is performed when it is impossible to obtain bowel movements for one reason or another. Using this method, biopsies are taken from the walls of the intestine, and the condition of the walls, namely ulcers formed by the amoeba, is assessed. Tissue cultures of biopsies reveal a vegetative form with red blood cells inside, which is why it is called hemophage and this partly explains the development of anemia.
4. Serological methods: RIF (immunofluorescence reaction), ELISA (enzyme-linked immunosorbent assay) - methods are aimed at detecting antibodies.
5. additional methods: ultrasound of the abdominal cavity and kidneys, biochemical tests, OAC and OAM - these indicators can be informative if the presence of abscesses, decompensation of organs and systems, etc. is suspected.

Treatment of amoebiasis

There are several groups of drugs that act at different stages of the disease:

1. Preparations of direct contact action (direct amoebocides), which have a detrimental effect on the luminal forms of the pathogen. Used for the rehabilitation of amoeba carriers and the treatment of chronic amoebiasis in remission. This is Hiniophone, Diyodokhin. Quiniophone can be used as enemas.
2. Drugs acting on tissue amoebocytes, i.e. against tissue and luminal forms in the stage of acute intestinal (possibly extraintestinal) amebiasis: Emetine, Dihydroemitin, Ambilgar, Quinamine (for amoebic liver abscesses).
3. Preparations of universal/combined action, applicable for all forms of amebiasis: Metronidazole (Trichopol), Furamide.
4. Antibiotics are used to change the microbial biocenosis in the intestine.
5. Drugs that restore normal intestinal microflora: prebiotics, probiotics, symbiotics, a complex immunoglobulin preparation (CIP) is possible.
6. Enzyme preparations (digestal, panzinorm) for relief of colitis syndrome.

The dosages of the drugs are not given on purpose, because a number of drugs are toxic, are often used in combination with each other or other groups of drugs (with antibiotics), and are prescribed under the supervision of laboratory diagnostics.

In parallel with drug treatment, a mechanically and chemically gentle protein diet is used. Vitamin therapy with oral access, bypassing the intestines, because absorption is impaired there. If there are abscesses in certain organs, surgical tactics are used against the background of complex treatment.

Complications of amoebiasis

The occurrence of extraintestinal amebiasis (liver abscess, pleuropulmonary amebiasis, brain abscess, skin lesions);
Intestinal perforation leading to peritonitis and high mortality;
Strictures (narrowing of areas) of the intestine;
Intestinal bleeding;
Breakthrough of abscesses.

Prevention of amebiasis

Identification and division of cyst excretors and carriers. Compliance with sanitary and hygienic measures. No specific prevention has been developed at this time.

General practitioner Shabanova I.E.

Amebiasis is common in southeastern Africa, Southeast Asia, China, and Latin America. In these countries, amebiasis is one of the most common causes of severe diarrhea, often resulting in death, and the number of people infected with dysenteric amoeba reaches 70%. In the CIS countries, the most unfavorable are the countries of Central Asia and Transcaucasia, where carriage was detected in 15–35% of the population.

This disease is of particular importance nowadays with the development of tourism and the increase in the number of trips to regions with hot climates.

Both men and women of different age groups are susceptible to infection with dysenteric amoeba.

With timely treatment, complete recovery is possible. The addition of a bacterial infection significantly worsens the prognosis. With untreated amoebiasis, the mortality rate is 5–10%.

Causes of Amebiasis

The causative agent of amebiasis is dysenteric amoeba (entamoeba hystolitica).

The source of infection with amoebiasis is a sick person or an asymptomatic carrier who releases mature cysts of dysenteric amoeba into the environment. The transmission mechanism is fecal-oral. Transmission factors include vegetables and water contaminated with cysts.

In the human body, amoeba is found in the form of vegetative forms and cysts.

Cysts form in small forms, are released into the environment and do not break down for quite a long time; when they enter the body with contaminated vegetables and water, they begin to multiply intensively.

Classification of Amebiasis

Clinical forms:

• asymptomatic amoebiasis (luminal amoebiasis, asymptomatic amoebiasis);
• amoebic dysentery (intestinal amebiasis);
• extraintestinal amebiasis (amoebic abscess (cavity filled with pus) of the liver, lungs, brain);

According to the severity of clinical manifestations:

• manifest form;
• subclinical form.

According to the duration of amoebiasis:

• acute (up to 3 months);
• subacute (up to 6 months);
• chronic (more than 6 months).

According to the nature of the flow, they are distinguished:

• amoebiasis continuously progressing;
• recurrent.

According to severity they are distinguished:

• mild course;
• moderate severity;
• severe course of amebiasis.

Symptoms of Amebiasis

Amoebic dysentery (intestinal amoebiasis)

The incubation period ranges from several days to 2 – 3 months. The onset of the disease is gradual. Loose stools with an unpleasant putrid odor appear 1 to 5 times a day, bloating, pain, localized mainly in the right iliac region. Blood-stained mucus is found in the stool, which is why the clinical sign characteristic of amoebiasis is stool in the form of “raspberry jelly.” Body temperature rises to 37.5 - 38.5.

With a continuously progressive course, clinical manifestations steadily increase; there are no periods of remission. Intestinal manifestations are accompanied by a general toxic syndrome (weakness, headaches and muscle pain, nausea, vomiting), patients lose weight, anemia appears, the liver and spleen become enlarged.

In a recurrent course, acute manifestations of the disease last 4–5 weeks, after which the process begins to subside for 1–2 months. This course of amoebiasis lasts for years.

Extraintestinal amoebiasis

• amoebic liver abscess - forms mainly in the right lobe of the liver, when amoebae penetrate through the portal vein from the colon. The first signs are weakness, pain in the stomach or right hypochondrium, loss of appetite, increase in body temperature to 37.5. As the disease progresses, clinical symptoms increase. When the abscess is punctured, a dark brown mass is obtained; when bacteria join, the contents become yellow-green. Amoebas are found on the walls of the abscess.
• amoebic lung abscess, occurs as a result of liver abscesses breaking into the pleural cavity. Cough and shortness of breath occur. When the abscess is opened, a dark brown mass is coughed up into the bronchus, the general condition then improves.
• amoebic brain abscess - this is quite rare, amoebas enter the brain through blood vessels, the size and location of the abscess subsequently determine neurological symptoms.

Diagnosis of Amebiasis

1. General blood analysis.
2. General urine analysis.
3. Coprogram - stool analysis.
4. Biochemical study: direct and total bilirubin, thymol test, transaminases (ALT, AST), total protein and its fractions.

5. Specific diagnostics:

   Serological methods:

   • RIF (immunofluorescence reaction),
   • EMA (enzyme-labeled antibody reaction),
   • RNHA (indirect hemagglutination reaction).

6. Additional diagnostic methods:

   • sigmoidoscopy;
   • Ultrasound of the abdominal organs;
   • computed tomography of the chest and abdominal organs;
   • radiography.

Treatment of Amebiasis

Etiotropic therapy

There are 3 groups of such drugs:

Amoebocides(anti-amoebic drugs) of direct action. They act on luminal forms of amoebas, so they are mainly used for the sanitation of carriers.

The most common drug from this group is Yatren (quiniophone), containing 25 - 26% iodine. It is prescribed 0.5 g 3 times a day. The course of treatment is 10 days. If necessary, the course is repeated after 10 - 12 days.

Another effective drug is diiodoquine, prescribed 0.25 g 3 to 4 times a day for 10 days.

Tissue amoebocides, capable of penetrating the intestinal wall and liver. They do not have any effect on luminal forms.

Emetine hydrochloride is prescribed intramuscularly in the form of 1% - 1.5 ml 2 times a day, the course of treatment is 7 - 10 days.

Dihydroemetine, more effective, is also prescribed intramuscularly 1% - 1.5 ml 2 times a day, duration of therapy is 10 days.

Chloroquine (delagil, rezoquin) – 0.15 g 2 – 3 times a day, daily dose – 0.3 – 0.45 g. The course of treatment is 2 – 3 weeks.

Amebocides of universal action. They act on all forms of amoebas at any location.

Metronidazole (Flagyl, Trichopolum) is prescribed 0.5 - 0.75 g 3 times a day for 5 - 10 days.

Tinidazole (Fasigin), prescribed in a daily dose of 1.2 g, course of treatment is 5 – 10 days.

Symptomatic treatment

Antispasmodics (no-spa, duspatalin), enzymes, iron supplements, vitamins, albumin transfusion, enemas with chamomile, tannin.

Traditional methods of treating amoebiasis

1. Pour cumin fruits with a glass of hot water. Take 1/3 cup 3 times a day after meals.
2. Pour 200 ml of boiled water over the bird cherry berries. Take ½ glass half an hour before meals.
3. 40g garlic, 100g vodka. Take the tincture 10-15 drops 3 times a day half an hour before meals.

But it should be understood that treatment with folk remedies is only possible together with traditional medicine, as an additional treatment, and not as the main therapy.

During treatment, a gentle, easily digestible diet is prescribed, with limited coarse fiber and carbohydrates, rich in vitamins and animal proteins. Food is taken in small portions 5 – 6 times a day.

Complication of Amebiasis

Complications of amoebic dysentery:

• intestinal bleeding that occurs when large blood vessels are damaged or when ulcers form;
• inflammation of the intestines, which is accompanied by the appearance of deep ulcers, as a result of which adhesive disease can form with the development of intestinal obstruction;
• the presence of a large number of amoebas also contributes to the occurrence of intestinal obstruction;
• peritonitis (inflammation of the peritoneum) due to perforation of the intestinal wall at the site of deep ulcers;
• formation of chronic ulcerative colitis (inflammation of the large intestine) after amoebiasis;
• formation of intestinal-genitourinary fistulas;
• dysbacteriosis;
• anemia due to impaired absorption of nutrients in the intestines.

Complications of extraintestinal amoebiasis:

• breakthrough of liver abscesses into the pleural cavity with the development of atelectasis (collapse of lung tissue or part of it);
• breakthrough of a liver abscess into the abdominal cavity with the development of peritonitis;
• if the abscess is localized in the left lobe of the liver, it may break into the pericardial cavity with the development of cardiac tamponade - due to the presence of fluid in the pericardium, the heart cannot adequately perform its work, and if timely assistance is not provided, the patient dies due to circulatory failure.

Prevention of Amebiasis

There is no specific prevention. The main preventive measures are to prevent contamination of water and food products with cysts of dysenteric amoeba. Early detection of asymptomatic amoebone carriers among the population.

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General information

Causes of amoebiasis

The causative agent of amebiasis, the histolytic amoeba (Entamoeba histolytica), belongs to the pathogenic protozoa and has two stages of the life cycle: a resting stage (cyst) and a vegetative stage (trophozoite), replacing each other depending on living conditions. Vegetative forms of amoeba (precystic, luminal, large vegetative and tissue) are very sensitive to changes in temperature, humidity, pH, and therefore quickly die in the external environment. Cysts exhibit significant stability outside the human body (they persist in soil for up to 1 month, in water for up to 8 months).

The main source of amoeba infection is patients with a chronic form of amoebiasis in remission, as well as convalescents and carriers of cysts. Flies can be carriers of amoeba cysts. Patients with an acute form or with a relapse of chronic amoebiasis do not pose an epidemic danger, since they secrete vegetative forms of amoebas that are unstable in the external environment. Infection occurs through the fecal-oral route when food and water infected with mature cysts enter the gastrointestinal tract of a healthy person, as well as through household contact through contaminated hands. In addition, transmission of amebiasis is possible during anal intercourse, mainly among homosexuals.

Risk factors for contracting amebiasis include poor personal hygiene, low socioeconomic status, and living in areas with a hot climate. The development of amebiasis can be triggered by an immunodeficiency state, dysbiosis, unbalanced diet, and stress.

Symptoms of amoebiasis

The incubation period of amoebiasis lasts from 1 week to 3 months (usually 3-6 weeks). According to the severity of symptoms, amebiasis can be asymptomatic (up to 90% of cases) or manifest; according to the duration of the disease - acute and chronic (continuous or recurrent); according to the severity of the course - mild, moderate, severe. Depending on the clinical picture, there are 2 forms of amebiasis: intestinal and extraintestinal (amoebic abscesses of the liver, lungs, brain; genitourinary and cutaneous amebiasis). Amebiasis can manifest itself as a mixed infection with other protozoal or bacterial intestinal infections (for example, dysentery), helminthiasis.

Intestinal amebiasis is the main, most common form of the disease. The leading symptom of intestinal amebiasis is diarrhea. The stool is copious, liquid, initially fecal in nature with an admixture of mucus up to 5-6 times a day; then the bowel movements take on the appearance of a jelly-like mass mixed with blood, and the frequency of bowel movements increases to 10-20 times a day. Characterized by constant increasing pain in the abdomen, in the iliac region, more on the right. When the rectum is damaged, painful tenesmus is a concern; when the appendix is ​​damaged, symptoms of appendicitis occur. There may be a moderate increase in temperature and asthenovegetative syndrome. The severity of the process in intestinal amoebiasis subsides after 4-6 weeks, after which a long remission occurs (several weeks or months).

Spontaneous recovery is extremely rare. Without treatment, an exacerbation develops again, and intestinal amebiasis acquires a chronic recurrent or continuous course (lasting up to 10 years or more). Chronic intestinal amebiasis is accompanied by disorders of all types of metabolism: hypovitaminosis, exhaustion, even cachexia, edema, hypochromic anemia, endocrinopathies. In weakened patients, young children and pregnant women, a fulminant form of intestinal amebiasis may develop with extensive ulcerations of the colon, toxic syndrome and death.

Of the extraintestinal manifestations of amebiasis, the most common is amoebic liver abscess. It is characterized by single or multiple abscesses without a pyogenic membrane, most often localized in the right lobe of the liver. The disease begins acutely - with chills, hectic fever, profuse sweating, pain in the right hypochondrium, aggravated by coughing and changes in body position. The condition of the patients is serious, the liver is sharply enlarged and painful, the skin is sallow in color, and sometimes jaundice develops. Pulmonary amebiasis occurs in the form of pleuropneumonia or lung abscess with fever, chest pain, cough, and hemoptysis. With amoebic brain abscess (amebic meningoencephalitis), focal and cerebral neurological symptoms and severe intoxication are observed. Cutaneous amebiasis occurs secondarily in weakened patients, manifested by the formation of mildly painful erosions and ulcers with an unpleasant odor in the perianal area, on the buttocks, in the perineal area, on the abdomen, around fistulous openings and postoperative wounds.

Intestinal amebiasis can occur with various complications: perforation of an intestinal ulcer, bleeding, necrotizing colitis, amoebic appendicitis, purulent peritonitis, intestinal stricture. In case of extraintestinal localization, a breakthrough of the abscess into the surrounding tissues with the development of purulent peritonitis, pleural empyema, pericarditis or the formation of fistulas cannot be ruled out. In chronic amebiasis, a specific tumor-like formation from granulation tissue is formed in the intestinal wall around the ulcer - an amoeba, leading to obstructive intestinal obstruction.

Diagnosis of amoebiasis

When diagnosing intestinal amebiasis, clinical signs, epidemiological data, results of serological studies (RNGA, RIF, ELISA), sigmoidoscopy and colonoscopy are taken into account. Endoscopically, with amebiasis, characteristic ulcers of the intestinal mucosa are detected at different stages of development, in chronic forms - cicatricial strictures of the colon. Laboratory confirmation of intestinal amoebiasis is the identification of tissue and large vegetative forms of amoeba in the patient’s feces and discharge from the bottom of ulcers. The presence of cysts, luminal and precystic forms of the pathogen indicates amoebic carriage. Serological reactions show the presence of specific antibodies in the blood serum of patients with amebiasis.

Extraintestinal amoebic abscesses help to visualize a comprehensive instrumental examination, including ultrasound of the abdominal organs, radioisotope scanning, survey, leishmaniasis, tuberculosis).

Treatment of amoebiasis

Treatment of amebiasis is carried out on an outpatient basis; hospitalization is necessary for severe cases and extraintestinal manifestations. To treat asymptomatic carriage and prevent relapses, direct-acting luminal amoebicides (etofamide, diloxanide furoate, iodine preparations, monomycin) are used. Systemic tissue amoebicides (metronidazole, tinidazole, ornidazole) are effective in the treatment of intestinal amebiasis and abscesses of various locations. To relieve colitis syndrome, accelerate reparative processes and eliminate pathogenic forms of amoebas, iodochlorooxyquinoline is prescribed. If metronidazole is intolerant, the use of antibiotics (doxycycline, erythromycin) is indicated. The combination of drugs, their doses and duration of therapy are determined by the form and severity of the disease.

In the absence of effect from conservative tactics and the threat of abscess breakthrough, surgical intervention may be required. For small amoebic abscesses, it is possible to perform a puncture under ultrasound control with aspiration of the contents or an opening with drainage of the abscess and subsequent introduction of antibacterial and amoebicidal drugs into its cavity. In case of pronounced necrotic changes around an amoebic ulcer or intestinal obstruction, intestinal resection with colostomy is performed.

Forecast and prevention of amebiasis

With timely specific treatment, in most cases the prognosis for intestinal amebiasis is favorable. In case of late diagnosis of amebic abscesses of other organs, there is a risk of death. Prevention of amebiasis includes early detection and full treatment of patients and amebia carriers, compliance with a sanitary and hygienic regime at home, ensuring high-quality water supply and wastewater treatment, food safety control, and health education.

Amebiasis is an intestinal infectious disease that has a long course and is characterized by the occurrence of ulcerative defects of the large intestine and damage to other organs. Amoeba was discovered by St. Petersburg scientist F.A. Lesh in 1875 while examining the stool of a patient with bloody diarrhea. In Egypt, R. Koch (1883) isolated the pathogen from intestinal ulcers and purulent cavities in the liver. Amoebiasis, called “amebic dysentery,” was classified as an independent disease in 1891.

About the causative agent of the disease

The amoeba that causes pathology (Entamoeba histolitica) belongs to the phylum Protozoa.
The life cycle goes through 2 stages:

• vetetative;
• dormancy (cysts).

The vegetative stage can take the form of:

Encysted forms:

• precystic– the amoeba is also inactive and is found in the stool of a recovering patient.
• cyst itself- a form that lives in favorable conditions outside the host for several months. Lifespan in soil is about a week. They can withstand freezing down to –20 °C, but cannot be dried out.

note: vegetative forms are unstable in the external environment. In the acute phase of the disease, tissue and luminal forms of the pathogen are found in the patient’s stool. In healthy carriers and when the disease enters the attenuation stage, both luminal and pre-cystic forms, as well as the cysts themselves, enter the feces. Cysts are stable life forms of the pathogen outside its host. The formed cyst is surrounded by a colorless shell and resembles a sphere in appearance. Its interior contains a glycogen-filled vacuole and 4 nuclei. If the cysts enter the small intestine, then a mature amoeba appears from them, which, when divided, produces 8 amoebas with one nucleus. They are capable of reproduction, transforming into vegetative forms that enter the large intestine.

How does infection occur?

The source of infection is a person who releases various vegetative types of amoebas and cysts into the external environment. Typically, the sources of the disease are carriers of the infection, patients with chronic forms of the disease or those recovering from an acute form of amoebiasis. The release can take years. During the day, sometimes up to 900 million cysts are released. note: patients with acute amoebiasis are not sources of infection, since they contain non-infectious vegetative forms. A person becomes infected when cysts enter the body with unwashed food and dirty hands. Contaminated dishes, clothes, and linen also pose a danger. Mechanical carriers are flies and cockroaches. Men aged 20 to 50 years are most often affected. There is no immunity to the disease. Amebiasis is reported throughout the world, but is especially common in countries with humid and hot climates.

In the intestine, the cystic form transforms into a vegetative form, which penetrates the intestinal wall, secretes enzymes that break down tissue and promote the formation of ulcers. Defects are formed from small erosions and abscesses (ulcers) having the structure of nodules containing vegetative forms of amoebas. An ulcer is a collapsed nodule. The diameter of ulcerative formations can reach 2.5 cm with undermined edges and a purulent bottom. Ulcers can merge, affect the muscular layer and even cause intestinal perforation. This is a very life-threatening complication that provokes peritonitis (inflammation of the peritoneum). Bleeding is also possible as a result of destruction of blood vessels. During the healing stage, narrowing of the intestinal walls and subsequent obstruction may develop. Note:the entry of amoebas into the blood often results in damage to the liver, lung tissue, and brain. Untreated, long-term amebiasis can cause tumor-like amoebiomas in the intestine - formations from granulation tissue and body cells.

Types of clinical manifestations of the disease

WHO identifies three forms of amoebiasis:

• intestinal;
• extraintestinal;
• cutaneous

Intestinal amoebiasis: symptoms, course of the disease, complications

the most common form of the disease . The period from the onset of infection to the development of complaints can last from 1-2 weeks to 3 months.

Symptoms of intestinal amoebiasis

The disease occurs in mild, moderate and severe degrees. Develops gradually. People with intestinal amoebiasis experience the following symptoms:

• low temperature,
• weakness,
• increased fatigue,
• distension in the abdominal area, minor pain.

Important: the main symptom of amebiasis is. It is profuse, frequency 4-6 times a day, and resembles mucus. As the disease progresses, the frequency of stool increases to 15-20 per day, its fecal appearance is lost, blood appears in the mucus (like raspberry jelly), and cramping pain in the abdomen increases. The patient experiences a constant painful urge to lower himself (tenesmus). The listed symptoms of amoebiasis persist for up to a week, then improvement occurs. The disease enters the stage of attenuation (remission). After a few weeks or months, complaints return and the pathology worsens. This is how it goes recurrent form. At continuous The course of the disease occurs in the form of periods of intensification and weakening of complaints. note: Without treatment, amebiasis can last 10 years or more. Chronicity of the disease is accompanied by pronounced weakening of the body (asthenia). Protein deficiency and vitamin deficiency develop. Patients note a change in taste, soreness of the oral mucous membranes. A coating forms on the tongue, and appetite decreases. The skin becomes dry, facial features become sharper. The abdomen is painful when palpated, retracted.

Complications of intestinal amoebiasis

With prolonged amebiasis, complications of the cardiovascular system develop - the heart rate increases, arrhythmia periodically occurs, manifestations of malnutrition of the heart muscle (deafness of tones). Damage to the nervous system is accompanied by cases of mood swings, apathy, insomnia, and increased irritability. Severe complications of intestinal amoebiasis:

• perforation of the intestinal wall;
• narrowing of the intestine (stricture);
• intestinal bleeding;
• inflammation of the peritoneum (peritonitis) - amoebic pericolitis is especially dangerous (in 9-10% of patients), accompanied by a clinical picture of peritonitis with fibrinous cohesion of areas of the intestinal serous membrane at the sites of ulcers, adhesions.
• purulent peritonitis - occurs with a sharp deterioration in health, abdominal pain, high fever, vomiting, flatulence;
• ameboma is a tumor-like formation of the cecum and ascending colon. It can cause intestinal obstruction;
• development of an adenomatous polyp (from glandular tissue, the size of a walnut);
• sometimes occurs;
• amoebic appendicitis (a severe form of complication with high mortality - up to 80-90%). Usually manifests itself at the height of the acute course of the disease.

Extraintestinal amebiasis can occur in various forms. The course of the disease and its symptoms depend on the damage to the organ in which the amoeba has settled.

Hepatic amebiasis: symptoms, complications

It can be expressed in the form of inflammation of the liver () or an encysted abscess (abscess). Patients complain about. Upon examination, attention is drawn to an increase in the borders of the liver, thickening of the edges, and pain. Jaundice may appear, often with fever. The pain may radiate to the right shoulder and intensify with breathing or changing position. The temperature increase is not natural and can change throughout the day. The appearance of patients is emaciated, the skin is dry and flabby, pointed facial features, sunken eyes, cheeks. Sometimes swelling of the legs occurs. The stomach is swollen. note: as the process becomes chronic, the patient’s exhaustion increases. Abscesses can be single or multiple. This form of the disease is severe, and deaths are much more common than with other forms. When an abscess ruptures into the abdominal cavity, peritonitis occurs. It is possible that the contents of the abscess may enter the pleural cavity. Then, as a complication of amebiasis, pleuropneumonia occurs or a lung abscess begins. Inflammatory processes of lung tissue often become chronic.

Symptoms of other forms of amoebiasis

Amoebas can enter the brain through the vascular bed. In this case, the corresponding clinical picture of brain abscess develops. Patients experience general cerebral and focal complaints - convulsions, headaches, sensory disturbances, paresis and paralysis. There are amoebic abscesses of the spleen, female genitalia, and kidneys, accompanied by complaints characteristic of the main diseases of these organs.

Cutaneous amoebiasis

When amoebae enter the skin, it leads to the development of erosions and ulcers. Location: perineum, buttocks. The ulcers are deep, slightly painful with dark edges and a strong, unpleasant odor.

Disease prognosis

Timely detection and treatment leads to a cure. Neglected and untreated cases result in chronicity, complications and death.

A preliminary diagnosis is established based on:

• epidemiological data;
• examination of the patient and his complaints;
• urgent laboratory test data.

Laboratory diagnosis of amoebiasis

• feces - detection of tissue forms and large vegetative cell forms;
• sputum, contents of abscesses, materials from the bottom of ulcers.

The presence of luminal forms and cysts in feces is not the basis for a diagnosis of amoebiasis. note: stool examination must be carried out no later than 10-15 minutes after defecation. It is better to repeat the analysis several times. In the stage of attenuation of clinical manifestations, stool examination is carried out after the patient has taken a saline laxative. If it is not possible to analyze fresh material, then it is necessary to resort to preservation. The material is examined, both in unprocessed form and with fixation with hematoxylin or Lugol's solution. A more long-term method for diagnosing biomaterials for amoebiasis is the cultivation of amoebae on nutrient media.

Serological types of studies

Immunological tests are considered an auxiliary method in determining the disease. The most revealing among them was the fluorescent body test (XRF). The second most important reaction is the complement fixation reaction (CFR). A study may also involve the method of infecting laboratory animals with pathological secretions.

Instrumental types of diagnosis of amoebiasis

The complex of diagnostic measures includes:

• sigmoidoscopy– examination of the rectum and part of the sigmoid colon. The condition of the mucous membrane, the presence of ulcers, erosive changes, amoebas, polyps, cystic formations, etc. is determined with the ability to remove the contents from the bottom of these formations for examination;
• – allows you to supplement diagnostic data by examining the liver, assessing the condition of the tissue structure of this organ, size, presence of abscesses and other formations;
• , especially its modern types. With its help, you can determine the size and number of pathological formations, as well as conduct an examination of the brain, lungs, and other organs;
• radioisotope methods necessary in case of controversial cases to distinguish an amoebic abscess from a bacterial one;
• – X-ray examination of the large intestine against the background of contrast agents.
• microresonance tomography– used in difficult cases and in weakened patients.

Therapeutic measures for amebiasis consist of the use of three types of drugs that affect different groups of problems. These include:

Additionally, amoebiasis is treated with drugs that restore normal intestinal flora. These include pro(pre)biotics. Also, according to indications, cardiovascular drugs, hepatoprotectors, immunostimulants and other drugs are used, the need for which is determined by the doctor.

7 types of amoebas can be identified from human feces: Entamoeba histolytica, Entamoeba dispar, Entamoeba hartmanni, Entamoeba coli, Endolimax nana, Iodamoeba butschlii And Blastocystis hominis, but only E. histolytica can cause invasive infections in humans.

The previously noted dissonance between the high frequency of excretion E. histolytica and, at the same time, a relatively low frequency of clinical manifestations, in part, as it turned out, is associated with the presence in the population E. histolytica two types of amoebas - potentially pathogenic strains E. histolytica, and non-pathogenic E.dispar, which can only be distinguished by DNA analysis. In recent years, a sensitive and specific PCR method has been developed, which allows for relatively simple and rapid identification in feces at the same time. E. histolytica And E.dispar .

E. histolytica belongs to the genus Entamoeba belonging to the family Entamoebidae, squad Amoebida, class Lobosea, superclass Rhizopoda, subtype Sarcodina, type Protozoa.

Cysts E. histolytica enter the gastrointestinal tract with water or food products. In the small intestine, under the action of intestinal enzymes, the cyst shell dissolves and eight mononuclear amoebae are formed. As a result of subsequent divisions, they turn into vegetative luminal stages, trophozoites ranging in size from 10 to 60 microns, on average 25 microns, having a single nucleus, the habitat of which is the lumen of the upper parts of the large intestine. As they move through the intestine, trophozoites transform into one-to-four-nucleated cysts (on average 12 μm in diameter), which are excreted in the feces.

Invasive or so-called tissue stages of amoebas are larger in size than luminal ones, can phagocytose red blood cells, have proteolytic properties and surface pectins that promote their attachment to the intestinal mucosa [,].

Recently it has been established that the main virulence factor in E. histolytica are cysteine ​​proteinases that are absent in E.dispar. Further research in this direction may contribute to the development of cysteine ​​proteinase inhibitors, which can be used to create new amoebicides.

In accordance with the pathomorphological changes and clinical picture, “invasive” amebiasis is distinguished, in which pathological changes develop, and “non-invasive” amebiasis.

“Invasive” amoebiasis is characterized by:

• clinical symptoms of an infectious disease;
• the presence of hematophagous trophozoites in feces;
• characteristic changes in the intestinal mucosa during endoscopic studies;
• the presence of specific antibodies detected by serological tests.

“Non-invasive” intestinal amebiasis (this condition is also defined as “carriage” of amoebic cysts) is characterized by:

• asymptomatic;
• absence of hematophagous trophozoites;
• absence of pathological changes during endoscopic examinations;
• lack of specific antibodies.

Only a small proportion of amoeba-infected individuals will develop invasive amoebiasis. In countries where E. histolytica widespread, 90% of infected individuals have non-invasive amebiasis, who are thus “asymptomatic carriers” of luminal forms of amoebae, and only 10% of infected individuals develop invasive amebiasis [ , , ].

Pathological changes and clinical manifestations of invasive amebiasis vary widely from colitis with mild clinical manifestations to fulminant colitis and amoebic liver abscess. The most common clinical manifestations of invasive amoebiasis are amebic colitis and amebic liver abscess, with amebic colitis occurring 5 to 50 times more often than amebic liver abscess.

The main causes of death in amebiasis are liver abscess and fulminant colitis [, ,].

Clinical forms of invasive amoebiasis

Intestinal amoebiasis

Asymptomatic presence (carriage) of luminal forms E. histolytica in the large intestine may persist for many years. However, at any time, luminal forms can transform into tissue forms, causing “invasive” or clinically significant amebiasis.

The primary manifestations of amebiasis are the formation of small areas of necrosis in the colon mucosa, which can progress to the formation of ulcers. The ulcer can grow not only along the periphery due to the submucosal layer, but also in depth, reaching the muscular and even serous membrane. A deep necrotic process leads to the formation of peritoneal adhesions and is the cause of perforated peritonitis. Amebic ulcers can spread throughout the entire length of the large intestine, but are more often localized in the cecum.

Typical amoebic ulcers are sharply demarcated from surrounding tissues and have uneven edges. At the bottom of the ulcer there are necrotic masses consisting of fibrin and containing amoeba trophozoites. The inflammatory reaction is mild. The necrotic process in the center, undermined and raised edges of the ulcer, reactive hyperemia and hemorrhagic changes around it constitute the most typical features of ulcerations in intestinal amebiasis.

Along with changes in the mucosa and necrosis, a regenerative process occurs in the intestinal wall, leading to restoration of the defect through the formation of fibrous tissue. Such a process in chronic amebiasis can lead to the formation of strictures and stenosis of the intestinal lumen, usually in the ascending and descending sections of the large intestine. When a secondary bacterial infection occurs, an exudate containing neutrophils, lymphocytes, histiocytes, and sometimes eosinophils is formed.

When lesions are localized in the rectosigmoid area of ​​the large intestine, the clinical picture may correspond to dysentery syndrome with tenesmus and, relatively rarely, with an admixture of mucus, blood and pus. When lesions are localized in the cecum, constipation is usually observed with pain in the right iliac region, characteristic of the clinical picture of appendicitis (in some cases appendicitis actually develops). Localization of amoebic lesions in the ileum is much less common [, ,].

Clinical variants of the course of intestinal amebiasis

Acute intestinal amebiasis (acute amoebic colitis)- usually manifests itself in the form of one diarrhea. The syndrome develops less frequently amoebic dysentery: acute onset, cramping abdominal pain, tenesmus, loose stools with blood and mucus. High fever and other systemic manifestations are usually not observed. Young children usually have fever, vomiting, and dehydration [, ,].

Fulminant amoebic colitis (fulminant colitis). A severe necrotizing form of intestinal amebiasis, characterized by toxic syndrome, total deep damage to the intestinal mucosa, bleeding, perforation, and peritonitis. More often observed in pregnant women and women in the postpartum period. May develop after administration of corticosteroids. The mortality rate reaches 70% [, ,].

Prolonged intestinal amebiasis (primarily chronic amebiasis, post-dysenteric colitis). Characterized by impaired intestinal motility, loose stools, constipation (in 50% of cases) or diarrhea alternating with constipation, pain in the lower abdomen, nausea, weakness, poor appetite. In some cases, chronic intestinal amebiasis is a consequence of amoebic dysentery.

Extraintestinal amoebiasis

Pathological changes in extraintestinal amebiasis can develop in almost all organs, but the liver is most often affected.

Liver abscess

In patients with amoebic liver abscess, indications of previous intestinal amebiasis are detected only in 30 - 40% of cases, and amoebas in feces are found in no more than 20% of patients. Amoebic liver abscess develops more often in adults than in children and in males more often than in females. Single or multiple abscesses form more often in the right lobe of the liver. The abscess consists of three zones: the central zone of necrosis, containing liquid necrotic masses mixed with blood, usually sterile (bacterial infection occurs in 2-3% of cases); middle, consisting of stroma and outer zone containing amoeba trophozoites and fibrin.

The clinical picture of amoebic liver abscess is characterized by fever with chills and profuse sweating at night; an increase in the size of the liver and pain in the area of ​​​​the liver projection, moderate leukocytosis. With large abscesses, jaundice may develop, which is a poor prognostic sign. When the diaphragm is involved in the process, a high position of its dome and limited mobility are revealed; development of atelectasis is possible.

Relatively often (in 10-20% of cases) there is a long-term hidden or atypical course of the abscess (for example, only fever, pseudocholecystitis, jaundice) with a possible subsequent breakthrough, which can lead to peritonitis and damage to the chest organs [,].

Pleuropulmonary amoebiasis

It is a consequence of a liver abscess breaking through the diaphragm into the lungs, less often due to hematogenous spread of amoebas. It manifests itself by the development of pleural empyema, abscesses in the lungs and hepatobronchial fistula. Characterized by chest pain, cough, shortness of breath, pus and blood in the sputum, chills, fever, leukocytosis [,].

Amoebic pericarditis

Usually develops due to the rupture of a liver abscess from the left lobe through the diaphragm into the pericardium, which can lead to cardiac tamponade and death.

Cerebral amoebiasis

Form of hematogenous origin. Abscesses can be single or multiple; are located in any part of the brain, but most often in the left hemisphere. Usually an acute onset and a fulminant course with a fatal outcome.

Cutaneous amoebiasis

It occurs more often in weakened and exhausted patients. Ulcers are usually localized in the perianal area, at the site of abscess rupture in the fistula area. In homosexuals, it is possible in the genital area.

Laboratory and instrumental diagnostics

The simplest and most reliable method for diagnosing intestinal amebiasis is microscopic examination of feces to identify vegetative forms (trophozoites) and cysts.

Trophozoites are usually detected in patients during the period of diarrhea, and cysts - in formed stool. For this purpose, native preparations are prepared directly from feces and/or from enriched samples.

During primary microscopy, native preparations from fresh fecal samples with saline are examined. Subsequently, to identify amoeba trophozoites, native preparations from fresh fecal samples are stained with Lugol's solution or buffered methylene blue. To identify cysts, native preparations prepared from fresh and/or preservative-treated fecal samples are stained with iodine. Detection of amoebas is more effective when feces are immediately examined after collection.

If there are doubts about the species of trophozoites and cysts and the need for long-term storage of preparations, for example, for the purpose of sending them to a reference laboratory for expert assessment, permanently colored preparations can be prepared. For these purposes, the trichrome staining method is usually used.

The simplest and most reliable method for diagnosing intestinal amebiasis is microscopic examination of fresh feces. Microscopy requires a high quality microscope and trained personnel. However, even an experienced laboratory technician may not be able to differentiate non-pathogenic protozoa, leukocytes, macrophages containing erythrocytes or partially digested plant fiber from amoeba trophozoites, as well as identify protozoan cysts. If it is impossible to provide high-quality diagnostics on site, it is possible to preserve feces and then transport them to specialized laboratories.

If clinical data indicate possible intestinal damage, recto- or colonoscopy is recommended. During recto- and colonoscopy, it is advisable to obtain a biopsy from the affected areas of the intestine in order to identify amoebae and differential diagnosis, in particular with carcinoma. These methods can detect the presence of ulcers in the intestines, amoebomas, strictures and other pathological changes. A characteristic feature of changes in amoebiasis is a focal rather than diffuse type of lesion [,].

Diagnosis of extraintestinal amebiasis, in particular liver abscess, is carried out by ultrasonography and computed tomography, which make it possible to determine the location, size and number of abscesses, as well as monitor the results of treatment. X-ray examination reveals a high position of the dome of the diaphragm, the presence of effusion in the pleural cavity, and abscesses in the lungs.

If necessary, aspiration of the abscess contents is carried out. Amoebas are rarely found in the center of necrotic masses, and are usually localized in the outer walls of the abscess. To diagnose amebiasis, serological tests can be used to detect specific antibodies. These tests are especially useful for diagnosing extraintestinal amoebiasis, since in these cases invasive stages are present in the feces E. histolytica usually absent.

Since the administration of corticosteroids for amebiasis can contribute to a sharp deterioration in the course of the disease, serological diagnosis is also recommended for all patients in whom amebiasis may be suspected and for whom corticosteroids are planned.

Treatment

In general, all drugs used to treat amebiasis can be divided into 2 groups: “contact” or “luminal” (affecting intestinal luminal forms) and systemic tissue amoebocides (Table , , , ).

For treatment non-invasive amebiasis (asymptomatic “carriers”) use luminal amoebicides (). Luminal amoebicides are also recommended to be prescribed after completion of treatment with tissue amoebicides to eliminate amoebae remaining in the intestine in order to prevent relapses. In particular, there are observations of the development of amoebic liver abscesses in individuals with intestinal amebiasis who received only tissue amoebicides without subsequent administration of luminal amoebicides [,]. In particular, a relapse of an amoebic liver abscess in a patient 17 years after a successfully treated newly diagnosed liver abscess was described.

In conditions where it is impossible to prevent re-infection, the use of luminal amoebicides is inappropriate. In these situations, it is recommended to prescribe luminal amoebicides only for epidemiological indications, for example, to persons whose professional activities may contribute to the infection of others, in particular employees of food establishments.

Table 1. Luminal amoebocides

Etofamide (Kythnos ®)
Clefamid
Diloxanide furoate
Paromomycin

1 not registered in the Russian Federation

To treat invasive amebiasis, systemic tissue amoebicides are used (). The drugs of choice from this group are 5-nitroimidazoles, which are used both for the treatment of intestinal amebiasis and abscesses of any localization.

Table 2. Systemic tissue amoebocides

5 - nitroimidazoles:

Metronidazole (Trichopol ®, Flagyl ®)
Tinidazole (Tiniba ®, Fasigyn ®)
Ornidazole (Tiberal ®)
Secnidazole

In addition to drugs from the group of 5-nitroimidazoles, it is recommended to use Dehydroemetine dihydrochloride(not registered in the Russian Federation) and Chloroquine [ , ] .

Table 3. Chemotherapy drugs used to treat amoebiasis

1 - drugs of the 5-nitroimidazole group are well absorbed and are usually prescribed per os. Parenteral (IV) administration of these drugs is used in severely ill patients who cannot take them orally.
2 - due to possible severe adverse reactions, primarily cardiotoxic effects, dehydroemetine is a reserve drug and is recommended to be prescribed by intramuscular injection to patients with extensive abscesses; patients in whom previous courses of 5-nitroimidazoles were ineffective, as well as severely ill patients in whom it is impossible to take the drugs per os.
3 - Chloroquine is prescribed in combination with dehydroemetine in the treatment of amoebic liver abscesses.

Table 4. Treatment regimens for amoebiasis

In clinically pronounced cases with an appropriate epidemiological history, when a large number of non-pathogenic species of amoebas are found in the feces, it is also recommended to treat with amoebicides, since in these cases there is a high probability of concomitant infection E. histolytica [ , ] .

The heterogeneity of the pathological process and clinical manifestations of amebiasis in different geographical regions, the presence of strains resistant to standard chemotherapy regimens with 5-nitroimidazoles, require varying treatment regimens taking into account the experience accumulated in a particular area. [ , , ] .

After successful chemotherapy for a liver abscess, residual cavities usually disappear within 2-4 months, but persistence of cavities for up to 1 year is possible.

In seriously ill patients with amoebic dysentery, due to possible intestinal perforation and the development of peritonitis, it is recommended to additionally prescribe antibacterial drugs active against intestinal microflora.

Aspiration (or percutaneous drainage) is recommended for large abscess sizes (more than 6 cm), localization of the abscess in the left lobe of the liver or high in the right lobe of the liver, severe abdominal pain and tension in the abdominal wall due to the possible threat of rupture of the abscess, as well as in the absence of effect from chemotherapy within 48 hours of its start. Aspiration is also recommended for abscesses of unknown etiology. If closed drainage is impossible, the abscess ruptures and peritonitis develops, open surgical treatment is performed [, , ,].

When corticosteroids are prescribed in patients with amebiasis, severe complications can develop, including the development of toxic megacolon. In this regard, if it is necessary to treat residents of endemic areas with a high risk of infection with corticosteroids E. histolytica preliminary examination for amoebiasis is necessary. In case of doubtful results, it is advisable to prescribe amoebicides followed by corticosteroids [,].

Currently, amebiasis is an almost completely curable disease, subject to early diagnosis and adequate therapy.

Prevention

The source of infection is a person who excretes cysts in feces E. histolytica. Infection occurs when cysts are ingested in contaminated water and food, usually through uncooked raw vegetables and fruits.