Chapter 3. Amebiasis Amebiasis is a chronic protozoal disease, the distinctive feature of which is the formation of abscesses in various organs. The causative agent of the disease is Entamoeba histolytica. There are two forms of dysenteric amoebae - vegetative and in the form of cysts, which

WHO statistics report that about 10% of people on the planet suffer from amoebiasis. Pathogenic amoeba is a medical and social problem in Africa, South America, and Asia. The disease is quite dangerous and can cause death. For example, in 2010, the mortality rate from amebiasis decreased to 55,000 deaths, compared to 1990, when 68,000 people from all over the world died from this pathology. Most deaths occurred due to the development of liver abscess and other complications.

The most dramatic incident occurred in Chicago (USA) in 1933. As a result of the contamination of one of the city's main water supplies by dysenteric amoeba, more than 1,000 cases of infection and about 98 deaths were noted. In 1998, the population of Georgia suffered from amoebiasis. From May to September, 177 cases of infection were registered, of which 71 cases were due to intestinal amebiasis, and 106 to liver abscess. Over the past couple of years, the incidence of amoebiasis has increased due to the development of tourism, free movement of migrants and travelers from hot countries.

Despite the fact that the dysentery amoeba loves a humid and hot climate, it was first discovered and described by the scientist F. Lesch in St. Petersburg in 1875. After 8 years, R. Koch was able to isolate amoeba from the lumen and intestinal walls of people who died from amoebiasis. The German scientist F. Schaudin discovered morphological differences between the dysenteric amoeba and other harmless species of amoeba, and gave it the name Entamoeba histolytica.

Cause of illness

Small vegetative form (luminal form)

A unicellular small organism of irregular shape with pseudopodia, up to 12-20 microns in size. It is located in the upper part of the large intestine, where it feeds mainly on its contents and bacteria. This form is unstable in the environment and therefore dies quickly. With increased intestinal peristalsis, it is excreted from the body in feces. If the peristaltic waves are weak, then the small form further enters the lower part of the large intestine and turns into the pre-cystic form. A small form of amoeba can be detected in individuals with acute amoebiasis, in carriers and in chronic amoebiasis.

Precystic form

It is an intermediate form between the luminal form and the cyst. It is inactive, round in shape, with a diameter of up to 10-15 microns. Covered with a single-layer shell, contains 1-2 cores. Under unfavorable conditions, the precystic form quickly turns into a mature cyst.

Cyst

The cyst of the dysentery amoeba is quadruple, 10-12 microns in size, immobile. The outside is covered with a two-layer shell. Chromatin grains and chromatoid bodies are located in the cytoplasm. The cyst is resistant to environmental conditions. It can be stored in feces for more than 1 week at an air temperature of +26-+30 degrees. Survives even longer in moist soil and water. The double-circuit shell of the cyst allows it to withstand dry weather well. The cyst dies quickly when boiled or using disinfectants (except for solutions containing chlorine). This form of amoeba is found in the stool of convalescents and cyst carriers.

Large vegetative form

Under favorable conditions it turns from small. Its dimensions vary from 40 to 60-80 microns. This form is active and mobile due to pseudopods. Cytoplasm is represented by ectoplasm and endoplasm, which contains 1 nucleus. The larger form is capable of producing the enzyme hyaluronidase, which damages the intestinal mucosa and capillary walls. This form of amoeba is also called erythrophage, because it feeds on red blood cells. The capture of red blood cells is carried out by pseudopodia, then the red blood cells end up in the cytoplasm, where they are digested. Under poor living conditions, the large form is not able to transform back into the small form or form a cyst. Therefore, she quickly dies. This form of amoeba can only be isolated from the feces of patients with acute amoebiasis.

Fabric form

It is a type of large vegetative form, only smaller in size (up to 20-25 microns). It also has ecto- and endoplasm, is motile, produces hyaluronidase, and contains a specific protein lectin-N-acetylgalactosamine. The tissue form can only be detected during an acute process in the affected organ, because it is embedded in the intestinal wall and does not exit into its lumen. Very rarely, when ulcers in the wall of the large intestine disintegrate, the tissue form can be released into the feces.

Sources of infection

The source of infection is a person with asymptomatic amoebiasis, who releases cysts into the environment with feces. Patients with acute amebiasis do not pose an epidemiological danger to other people, since they secrete a large vegetative form that is unstable outside the human body. The transmission mechanism is fecal-oral. A person can become infected with amoeba cysts by eating unwashed vegetables and fruits, unboiled water, or by swimming in closed reservoirs or ingesting water. Some insects (flies, cockroaches) can carry amoebas. Sometimes you can get amebiasis by shaking dirty hands infected with cysts, or by getting cysts on household items.

Having become infected with an amoeba, a person can suffer either one of its clinical forms, or all of them sequentially. There are intestinal amebiasis (amebic dysentery), extraintestinal amebiasis (damage to the liver, brain, lungs), asymptomatic amoebic carriage.

The incubation period can be from 1 week to 2-3 months. Cysts or vegetative forms enter the stomach, where they are exposed to hydrochloric acid. In this case, the vegetative forms die, and the cysts further move into the upper part of the large intestine. With a sufficiently good immune response of the human body, either cysts remain or a luminal (small) form is formed from them. This is how asymptomatic carriage of amoebas develops with the release of cysts.

If a person has a reduced immune system or unfavorable factors (malnutrition, dysbiosis), then from a small form a large vegetative form is first formed, which then penetrates the intestinal wall and becomes a tissue form. In this case, amoebic dysentery develops with all its clinical manifestations. Pathogenic forms secrete enzymes that destroy the mucous and submucosal layers of the intestine with the formation of ulcers. The damage can be so deep that it can lead to perforation and the development of peritonitis. As a result of scarring of ulcers, stenosis of the intestinal lumen may occur.

When the mucous membrane is damaged, the absorption of nutrients and vitamins is impaired, which negatively affects the general condition of the body. Mostly the cecum, ascending colon, sigmoid and rectum are involved in the process. Long-term destruction of red blood cells by protozoa can lead to the development of hypochromic anemia. With significant damage to the intestinal mucosa and capillaries, the amoeba can enter the bloodstream with subsequent spread to other organs (liver, lungs). Then extraintestinal amebiasis will appear. In the internal organs, the vital activity of the amoeba leads to the development of abscesses or ulcers.

Symptoms of amoebiasis

The most common form of the disease is amoebic dysentery. In most infected people, the disease begins to manifest itself in the form of diarrhea syndrome: loose stools are released up to 3-5 times a day, with an unpleasant odor. Later, mucus and blood may appear in the stool, giving the stool a “raspberry jelly” appearance. When a secondary bacterial infection occurs, pus will appear in the feces. In parallel with diarrhea, a person will be bothered by bloating, constant or paroxysmal pain, especially in the iliac region on the right. With such a clinical picture, the person’s general condition usually does not suffer.

Separately, the fulminant form of amoebiasis is distinguished. It can occur in people with reduced immunity, children and pregnant women. The disease begins acutely, intoxication increases, and all of the above symptoms manifest themselves to the maximum. This condition often leads to death.

The chronic form of intestinal amebiasis can have a continuously progressive and recurrent course. In the first case, clinical symptoms constantly increase, and there are no periods of remission. In addition to the main manifestations of intestinal damage, a general intoxication syndrome appears, anemia develops, and body weight decreases. This option is considered as an unfavorable course. With a relapsing course, intervals of several weeks or months appear between clinical symptoms when these manifestations are absent.

Extraintestinal amebiasis is one of the forms of the disease, which, in fact, is a complication of amoebic dysentery. With massive invasion and severe course, pathogenic forms (large vegetative and tissue) are able to penetrate the blood and spread to other organs.

Most often, a liver abscess develops. The abscess is predominantly localized in the right lobe of the liver, under the dome of the diaphragm. When it develops, a deterioration in the condition is observed: an increase in temperature to febrile levels, increased sweating at night, pain in the right hypochondrium. If the abscess affects the diaphragm, the pain may intensify with breathing and radiate to the right shoulder. Jaundice is not typical for amoebic liver abscess.

Lung abscess is less common, since its formation requires destruction of the liver abscess and the entry of amoebae through the diaphragm into the pleura and lungs, or hematogenous spread of amoebae from the intestine. A lung abscess is characterized by chest pain, cough with the release of viscous dark brown sputum, and shortness of breath.

If a liver abscess has formed in its left lobe, then when it ruptures, the pericardium and heart may suffer. This usually leads to the development of acute myocarditis or cardiac tamponade.

Brain abscess is a very rare pathology associated with amoebiasis. Depending on the location of the abscess, general (dizziness, headache, nausea, vomiting) or focal (paresis, paralysis, gait disturbances) neurological symptoms may appear.

In people with immunodeficiency conditions, amoebas can also cause skin lesions. As a result, erosions and ulcers are formed, which are most often found on the buttocks and in the genital area.

Complications of amoebiasis

Possible complications depend on the type of disease:

1. Intestinal amoebiasis:

• perforation of the intestinal wall with the development of peritonitis;
• intestinal bleeding;
• stenosis of the intestinal lumen;
• ameboma (tumor-like formation resulting from granulation of ulcerative defects) and obstruction of the intestinal lumen;
• dysbiosis;
• anemia.

2. Extraintestinal amoebiasis:

• breakthrough of a liver abscess into the abdominal cavity with subsequent development of peritonitis;
• breakthrough of a liver abscess into the pleural cavity with the development of pleurisy;
• secondary infection of amebic abscesses;
• decreased immunity.

Diagnostics

To make a diagnosis, not only epidemiological analysis data and clinical symptoms are important, but also the results of laboratory and additional research methods.

The picture of a general blood test depends on the severity of the course, the form of the disease, and the presence of associated complications. If with a mild and moderate course there are no changes in the blood, then with a severe progressive course there may be an increase in the number of leukocytes, acceleration of ESR, and a decrease in the level of red blood cells. Despite the fact that dysenteric amoeba often affects the liver, changes in liver tests are almost always absent.

A highly effective and informative method for detecting amoebas is PCR, which detects the DNA of the pathogen in the material.

Additional research methods include:

• Ultrasound of the hepatobiliary system;
• X-ray examination of the chest and abdominal organs;
• puncture of the abscess under ultrasound control (obtaining viscous chocolate-colored contents);
• sigmoidoscopy;
• histological examination of a biopsy taken between the abscess and healthy tissue from intestinal ulcers.

Treatment

Treatment of amebiasis is recommended in a hospital, because there is a high probability of complications. In case of manifestations of intestinal dysfunction, it is necessary to prescribe a mechanically and thermally gentle diet (warm food, without coarse fiber, fats and carbohydrates, rich in vitamins). You need to take food in fractions, i.e. in small portions 5-6 times a day.

They are prescribed mainly for the destruction of amoebas in carriers, since they act only on luminal forms (cysts and small vegetative form):

• Quiniophone - the drug contains 25% iodine, which has a detrimental effect on the pathogen. Given to adults, 2 tablets three times a day for 10 days;
• Iodoquinol is an iodine-containing drug, which is prescribed 1 tablet (0.65 g) every 8 hours with meals. The course of treatment is up to 20 days;
• Diloxanide furoate - take 1 tablet (0.5 g) every 8 hours for 10 days.

Tissue amoebocides

These are drugs that destroy the tissue and large vegetative form, do not act on cysts and the small form, are able to penetrate the bloodstream and treat extraintestinal forms of amebiasis:

• Emetine is a drug that destroys the nuclei of amoebas and disrupts protein synthesis, which leads to death. Prescribe 1.5 ml of 1% solution IM or SC 2 times a day. The course of therapy lasts 5-6 days. It is advisable to repeat the therapy after 10 days after completing the first course;
• Delagil is a 4-aminoquinoline derivative that inhibits the formation of DNA and disrupts the function of enzymes. Take 1 tablet (0.15 g) 3 times a day for about 2 weeks. It must be taken under the supervision of liver tests, since the drug itself is hepatotoxic.

Universal amoebocides

Such drugs have an effect on all forms of amoebas:

The effectiveness of antiamoebic therapy increases if these drugs are prescribed in combination with each other or with antibiotics.

In case of chronic relapsing amoebiasis, iron supplements (ferrumlek, ferkoven) are prescribed to correct anemia. To restore the function of damaged intestines, it is recommended to take bifidum and lactobacilli. To normalize food digestion, enzymes are given (Creon, Pancreatin, Festal).

• abscess with a diameter of more than 6 cm;
• the abscess is localized in the left lobe of the liver;
• severe pain in the right hypochondrium and muscle tension.

If the abscess ruptures and it is impossible to drain it, surgical intervention is used.

ethnoscience

Chronic forms of amebiasis and amoebiasis can be cured with medications made from natural herbal ingredients that cause less side effects. Recommended:

1. Garlic tincture - take 100 g of garlic and pour 400 ml of vodka into it. It is advisable to place all this in a bottle with a tight lid so that this mixture can infuse for 7 days. Then, you need to take 10-20 drops 3 times a day before meals.

2. Decoction of bird cherry - 10 g of bird cherry leaves are poured into a glass of hot water. Drink half a glass a day before eating.

3. Tincture of caraway fruits - 20 g of caraway fruits are poured with boiled hot water and heated for the next 20 minutes in a water bath. Next, the infusion is cooled for 45 minutes. Afterwards, filter and take 200 ml 2-3 times a day after meals.

4. Infusion of hawthorn and sea buckthorn berries - 5 tablespoons of plant berries are placed in 400 ml of boiled water and brought to a boil. Then, the infusion cools at room temperature. Drink 1 glass for 5-7 days.

5. Eucalyptus leaves - 5% alcohol solution of eucalyptus leaves is added to a glass of boiled water. It is recommended to take 1 tablespoon 3 times a day half an hour before meals.

6. Horse sorrel - 5 g of sorrel leaves are poured into a glass of hot boiled water and heated for about 30 minutes in a water bath. Then, cool and filter the broth. Drink a third of a glass 3 times a day half an hour before meals.

7. A decoction of a complex of herbs - take 25 g of burnet and cinquefoil rhizomes, 50 g of shepherd's purse. The ingredients are poured into 200 ml of hot water. Take 1/2 cup 4 times a day before meals.

Prevention

Prevention of amebiasis involves compliance with sanitary standards and rules of personal hygiene, identification of patients with chronic forms and amebia carriers. The risk group for amoeba infection includes people with digestive tract problems and people living in areas without sewers and treatment facilities.

Persons who are going to travel to countries that are epidemically dangerous for amoebiasis are recommended to undergo seven days of prophylaxis by taking quiniophone 0.5 g twice a day.

Amoebiasis of the lungs- a complication of amoebic dysentery.

Etiology and pathogenesis. The cause of amoebiasis is Entamoeba histolytica. Amoebas are vegetative, small and cystic. A person is infected with the last two forms. The source of infection is a sick person. The route of infection is nutritional. The amoeba cyst enters the intestine and releases vegetative, host amoebas, which can, during the process of growth, penetrate the wall of the intestinal veins and be carried into the liver.

In the liver, amoebas multiply and cause foci of necrosis or abscess, which can break into the pleural cavity, lung, pericardium, peritoneum, and intestines. But it is also possible that amoebae can enter the lung via a lymphogenous route (through the fusion of the liver bursa with the diaphragm and pleura) or lympho-hematogenously (through the thoracic lymphatic duct and the superior vena cava into the pulmonary artery system). An exudative reaction develops in the lung at the site of penetration, followed by a patch of necrosis, which turns into an abscess.

Clinic. With pulmonary amebiasis, the bronchi, parenchyma, and pleura can be affected. Symptoms are usually the same as for bronchitis, pneumonia, pleurisy (empyema): cough, expectoration of brownish-red sputum (anchovy sauce symptom) in the presence of bronchial fistula, chest pain, fever, hemoptysis, leukocytosis, increased ESR , left-sided neutrophil shift, intoxication phenomena. Amoebas can be found in sputum.

Diagnostics: X-ray examination of the lung reveals pneumonic darkening (inflammatory infiltration), an abscess cavity with unclear contours and fluid level, localized bulging of the dome of the diaphragm on the right (liver abscess), pleural effusion (reactive pleurisy) or a symptom of hydrothorax (broncho-pleural fistula). The diagnosis of amebiasis is confirmed by a positive complement fixation reaction with an extract from an amoeba culture.

Treatment: emetine is prescribed (40-60 mg intravenously, intramuscularly for 8-12 days), and for amoebic pleural empyema it is administered intrapleurally with preliminary evacuation of pus, for bronchitis - intrabronchially. An overdose of emetine is accompanied by tachycardia, extra asystole, hypotension, nausea, diarrhea, proteinuria, and nerve inflammation.

Connessin (for resistance to emetine), chlorquine, resokhin, aralen, tsirulin, vioform (for intestinal sanitation), yatrene (for colitis and dysentery) are also used. In order to prevent the activation of banal flora, antibiotics and sulfonamides are indicated; for chronic amoebic empyema, drainage of the pleural cavity; for localized chronic abscesses, lobe resection.

The disease is widespread in countries with subtropical and tropical climates. The spread of intestinal amoebiasis is facilitated by a low level of sanitary and communal amenities. Amebiasis is considered one of the “dirty hands” diseases.

According to WHO, up to 10% of people on earth suffer from amoebiasis. Up to 60% of cases of the disease are registered among residents of India, up to 20% among residents of South Asia, Africa, Central and South America. Cases of amoebiasis are recorded in the Lower Volga region and Transcaucasia. In Ukraine, cases of the disease are registered in the southern regions. An increase in tourist flows from countries with hot climates has led to an increase in amoebiasis among Russian citizens, including residents of Moscow.

Rice. 1. The photo shows a dysenteric amoeba.

Dysenteric amoeba - the causative agent of amoebiasis

Dysenteric amoeba was first discovered in the feces of a patient in 1875 by F. A. Lesh. In 1925, E. Brumpt divided Entamoeba histolityca into two types - pathogenic ( Entamoeba dysenteria) and non-pathogenic ( Entamoeba dispar ).

Dysenteric amoeba goes through two stages in its development: vegetative and cystic.

• In the vegetative stage, amoebas exist in large vegetative (tissue), cleared and precystic forms.
• During the resting stage, the amoeba exists in the form of a cyst.

Rice. 2. Forms of existence of dysentery amoeba: a - cleared, b - quadruple cyst, c - tissue form with absorbed (phagocytosed) erythrocytes.

Large vegetative form (tissue), forma magna of dysenteric amoeba

Amebiasis begins with the introduction of the trophozoite into the mucous membrane and submucosal layer of the large intestine. Under the influence of a special enzyme, tissue destruction (necrosis) occurs and ulcers appear. Dysenteric amoebas in tissue form have the ability to absorb red blood cells. The size reaches 40 microns or more. When moving, the amoeba stretches and forms pseudopodia, and its length can reach 80 microns. In tissue form, pathogens are found in the acute phase of the disease in the affected tissues, rarely in feces.

Rice. 3. The photo shows a large vegetative (tissue) form of dysentery amoeba with absorbed red blood cells.

Translucent form (translucent), forma minuta of dysenteric amoeba

This small vegetative and non-tissue form of the pathogen is found in people who have previously had intestinal amebiasis, in chronic forms of the disease, during remission and in carriers. They are distinguished by their small size (up to 25 microns) and sluggish movement, rounded shape, do not phagocytose red blood cells, feed on tissue breakdown products (detritus), and absorb bacteria that can be seen in its vacuoles.

Rice. 4. When moving, the dysentery amoeba stretches and forms pseudopodia.

Precystic form of dysenteric amoeba

The precystic form is transitional from the cleared form to the cyst. The precyst is small in size (up to 18 microns) and does not absorb bacteria.

Vegetative forms of dysentery amoeba quickly die in the external environment

Dysenteric amoeba cyst stage

Dysenteric amoeba in the cyst stage has a powerful protective shell, which ensures the survival of the species in adverse external conditions. Cysts can be found in the feces of convalescents and cyst carriers. In the lower parts of the small intestine and the upper parts of the large intestine, the cysts lose their outer shell and turn into active, rapidly multiplying forms.

The cyst has a round shape, its diameter is on average about 12 microns (7 - 20 microns), contains 4 nuclei (immature cysts contain 1 - 3 nuclei).

Rice. 5. Schematic representation of a trophozoite and cyst.

Epidemiology of the disease

The low level of sanitary and communal amenities contributes to the spread of infection. The main places where the infection spreads are countries with subtropical and tropical climates.

Vegetative forms of dysentery amoeba die outside the body within 20 - 30 minutes. Cysts have a high survival rate in the external environment. One gram of feces contains several million cysts. They pollute soil, wastewater, open water bodies, household and industrial items, food, fruits and vegetables.

• Dysenteric amoeba cysts persist on food for several days.
• They remain viable in feces from 3 to 30 days at positive temperatures (10 - 20 ° C), and up to 110 days at negative temperatures (from -1 to -21 ° C).
• Cysts remain viable for up to 60 days in natural reservoirs, up to 30 days in tap water, and up to 130 days in wastewater.
• Cysts live on the skin of the hands for up to five minutes, and in the subungual space for up to 1 hour.
• In dairy products, cysts remain viable for up to 15 days at room temperature.
• Cysts survive on glass, metal surfaces and polymers for up to 25 days.
• Cysts of dysentery amoebas die when boiled.

Rice. 6. Dysenteric amoeba.

How does infection occur (pathogenesis)

When they enter the human body, cysts of dysenteric amoebas penetrate into the distal part of the small intestine and the initial part of the large intestine, where their shell dissolves and each nucleus divides in two. From the eight-core amoeba, eight small luminal (translucent) forms are formed, each of which has one nucleus (trophozoites). The luminal forms, feeding on bacteria, multiply rapidly (division occurs every two hours). Moving along with the intestinal contents and reaching the lower parts of the large intestine, the luminal forms turn into cysts and are excreted with feces.

• In the case of an asymptomatic course, dysentery amoebas live in the lumen of the large intestine in collaboration with other microbes, feeding on detritus, bacteria and fungi.
• Under the influence of a number of factors (massiveness of invasion, inflammation and microtrauma of the intestine, helminthiasis, hormonal changes, stress and hunger), the amoeba turns into a large vegetative (tissue) form, penetrates the intestinal wall and infects it.

Rice. 7. Enzymes specially produced by dysentery amoebas (proteases and hemolysins) melt the tissue of the intestinal wall and penetrate deep into the organ.

Intestinal damage in the acute period of amoebic dysentery

In places where amoebas are localized, microabscesses form, which break into the intestinal lumen. The diameter of the formed ulcers is 2 - 20 mm. They have jagged, undermined edges and brown necrotic masses at the bottom. Over time, the ulcers clear and heal. The resulting fibrous tissue tightens the intestinal loops, which leads to stenosis of the cecum and sigmoid colon. On the intestinal mucosa, you can simultaneously see small erosions, “blooming” ulcers, healing and scar tissue.

Rice. 8. Multiple ulcers due to intestinal damage by dysenteric amoeba.

Intestinal damage in chronic amoebic dysentery

In the chronic form of intestinal amebiasis, the pathological process is localized mainly in the blind, ascending part of the colon, sigmoid and rectum. In severe cases of the disease, the entire large intestine is affected, in which pseudopolyps, ameboma (inflammatory granuloma) and megacolon (acute dilatation of the large intestine) develop.

• When amoebas spread to the skin of the perianal area, ulcerations form.
• When amoebae penetrate into the mesenteric vessels and spread with blood, internal organs are affected. Amoebic abscesses form in the liver, bile ducts, abdominal cavity, lungs, pleura, brain, kidneys and pancreas.
• Intestinal ulcers can lead to intestinal perforation, which leads to the development of peritonitis.
• Destruction of large vessels can lead to profuse intestinal bleeding.

Rice. 9. Ulcerative lesions of the wall of the large intestine with amoebiasis.

Immunity in amoebiasis

In addition to activating the cellular component of immunity, the introduction of dysenteric amoeba into the human body is accompanied by the production of specific antibodies - IgA immunoglobulins. Thus, with liver abscess, high antibody titers are recorded in the blood serum of patients on the 17th day of the disease. Secretory IgA-protivootherne are found in breast milk and saliva of patients.

With amoebiasis, immunity is acquired, unstable and non-sterile. It does not protect against relapses of the disease and repeated infections.

Forms of the disease

• Clinical forms of amebiasis: intestinal, extraintestinal and cutaneous.
• According to the clinical course, amebiasis is divided into asymptomatic (85 - 95%) and symptomatic (5 - 15%).
• The course of the disease can be fulminant, acute, chronic and latent.
• There are recurrent and continuous course of intestinal amebiasis.
• Clinical form of the continuous form of chronic intestinal amebiasis: slowly progressive and rapidly progressive.
• Clinical forms of extraintestinal amebiasis (5%): amebiasis of the liver, spleen and pericardium, bronchopulmonary, cerebral, cutaneous and genitourinary amebiasis.

Symptoms of acute intestinal amoebiasis

The incubation period of intestinal amebiasis ranges from 1 week to 4 months or more. The disease begins with frequent bowel movements up to 6 times a day. Excessive feces mixed with mucus. There are no symptoms of intoxication in the initial period.

Gradually the patient's condition worsens. After 5-7 days, the fecal character of stool disappears. They are glassy mucus, in which blood appears over time. The stool takes on a “raspberry jelly” appearance. Signs of intoxication are increasing. Body temperature rises, appetite disappears, and the patient experiences nausea and vomiting. Bloating and pain in the lower abdomen, pain along the large intestine appear. The disease can affect different parts of the intestine - the cecosigmoid, rectal, and damage to the appendix.

During endoscopic examination in the large intestine, ulcers from 2 to 20 mm in diameter are found, located on the crests of the intestinal folds and in the deep layers of the mucous membrane. They have uneven, undermined edges. Brown necrotic masses are visible at the bottom. Each ulcer is surrounded by a “belt” of hyperemia. The surrounding mucous membrane is not changed.

During irrigoscopy Uneven filling of all parts of the large intestine, areas of spasm and rapid emptying are revealed.

Amebiasis in children begins acutely. Body temperature rises to 39°C. Nausea and vomiting appear. The child becomes sleepy. Stool up to 15 times a day, liquid or pasty. Dehydration develops quickly.

The duration of the acute period is 4 - 6 weeks. Then a period of remission begins, lasting up to one month or more. Without adequate treatment, the disease recurs and becomes chronic over many years.

Rice. 10. Ulcers in amoebic dysentery on the tops of the ridges of the intestinal mucosa, 2 - foci of deep decay (photo on the right).

Symptoms of the fulminant form of intestinal amoebiasis

In 10% of cases, a fulminant form of amoebic dysentery is recorded, occurring with profuse diarrhea. Toxicosis and dehydration quickly develop, leading to exhaustion of the patient. Extensive ulcers appear in the intestines. The destruction of large vessels leads to bleeding. Intestinal perforation leads to the development of peritonitis. Liver abscess and amoebic hepatitis often develop.

The fulminant form of intestinal amebiasis develops in weakened and immunodeficient patients. Young children, elderly people, pregnant women and patients receiving hormonal therapy are susceptible to the disease.

Rice. 11. Endoscopic picture of intestinal amoebiasis.

Symptoms of chronic intestinal amoebiasis

Relapsing course of the disease characterized by periodic bloating and rumbling in the abdomen, stool upset, pain in the right lower abdomen, which is often mistaken for manifestations of appendicitis. During periods of exacerbations, the general condition remains satisfactory, body temperature does not rise.

With a continuous course of amoebiasis there is a gradual increase in symptoms such as abdominal pain, diarrhea alternating with constipation, stool frequency increases, blood appears in the stool, sometimes body temperature rises, and the liver gradually enlarges. Insufficient absorption of proteins and vitamins leads to exhaustion of the body and the development of asthenic syndrome. Hypochromic anemia develops. The patient loses weight. Appetite decreases, an unpleasant taste appears in the mouth, facial features become sharper. The tongue is thickly coated with a gray coating, the abdomen is retracted, heart sounds are muffled, and the heart rate increases.

Sigmoidoscopy reveals ulcers, cysts, polyps and amoebomas (inflammatory granulomas), which on radiographs show a filling defect, stimulating tumors. The development of scar tissue leads to stenosis (narrowing) of the intestine.

In 70% of cases, chronic intestinal amebiasis progresses slowly with subtle symptoms. Stool about 5 times a day, sometimes there is an admixture of mucus and blood. After some time, pain in the intestines appears.

In 30% of cases the disease becomes progressive. Diarrhea and cramping abdominal pain appear simultaneously. Already on the 2nd - 3rd day of the disease, mucus and blood appear in the stool. Body temperature is subfebrile. Insufficient intake of nutrients and vitamins into the body quickly leads the patient to asthenia and exhaustion.

Rice. 12. With the progressive course of the disease, asthenia and exhaustion of the patient quickly occur.

Extraintestinal amoebiasis

Extraintestinal forms of amebiasis account for about 5%. There are amebiasis of the liver, pericardium and spleen, bronchopulmonary, cerebral, genitourinary and cutaneous amebiasis. When the disease occurs, abscesses form in the internal organs - single and multiple. The disease often lasts a long time. Periods of remission are followed by periods of exacerbation. A number of scientists consider extraintestinal forms of amebiasis as a complication of intestinal amebiasis.

Amebiasis of the liver

Liver amebiasis has an acute, subacute and chronic course, occurring in the form of liver abscess or amoebic hepatitis. The disease occurs both during the period of acute intestinal amebiasis and months and even years after it. In 30-40% of cases, it is not possible to identify signs of intestinal damage in the patient. Amoebas in the intestines are detected in every fifth patient. Men get sick 24 times more often than women. Every fourth patient dies from complications of the disease.

Rice. 13. The photo shows an amoebic liver abscess.

Amoebic hepatitis

Amoebic hepatitis develops during the period of acute intestinal amebiasis. The liver gradually enlarges over several days, sometimes significantly. There is pain in the right hypochondrium. Temperature reaction is moderate. The level of leukocytes in the blood increases. Amoebic hepatitis can be acute, but more often has a chronic course.

Amoebic liver abscess. Acute course

It is believed that amoebic hepatitis is the first stage of suppuration (abscess formation). Abscesses with amoebiasis can be single or multiple, most often located in the right lobe of the liver. The disease occurs with symptoms of severe intoxication and severe pain in the right hypochondrium.

The acute course is characterized by increased body temperature and increasing weakness. The fever is often of a hectic type with repeated chills. Pain appears in the right hypochondrium, which gradually intensifies, radiating to the right shoulder blade and shoulder with the slightest movement. On palpation, an enlarged liver is determined, hepatic dullness increases more upward; with large abscess sizes, a fluctuating area can be identified on the anterior surface of the liver. The abdomen is swollen, and on palpation it is tense in the right hypochondrium. With large abscesses, jaundice develops.

In the blood, an increase in ESR and neutrophilic leukocytosis is detected, sometimes reaching 50x10 9 / l. Gradually, the patient loses weight, the cheeks fall in, facial features become sharper, and skin turgor decreases. Heart sounds become muffled. Blood pressure decreases.

Liver abscesses are detected by ultrasound and radioisotope scanning. An X-ray examination reveals a high position of the diaphragm, reduced mobility of the right dome, and when the abscess is localized in the subphrenic region of the liver, effusion is detected in the right pleural sinus.

The duration of the disease is no more than 10 days. Complications develop very quickly.

Rice. 14. Opened amoebic liver abscess.

Amoebic liver abscess. Chronic course

The chronic course of amoebic liver abscess is calm, without pronounced symptoms of intoxication and often with normal body temperature. Over time, bursting pain appears in the right hypochondrium, the liver enlarges and becomes painful on palpation. As the abscess grows, a tumor-like formation is detected on its surface, sometimes reaching 10 cm in diameter.

On the 17th day of the disease, high titers of specific antibodies - immunoglobulins - are detected in the blood of patients.

Rice. 15. Chronic liver amebiasis.

Complications of amoebic liver abscess

• When an abscess ruptures, a subphrenic abscess, encysted peritonitis, purulent pericarditis, pleurisy and mediastinitis can form.
• When an abscess ruptures into the bronchus, a hepatobronchial fistula is formed. At the moment of breakthrough, the patient develops a cough with a large amount of sputum containing necrotic masses. Amoebas can be found in sputum.
• When an abscess breaks through the skin in the area of ​​the fistula, a specific lesion develops.

Amoebiasis of the lungs

Amoebas can enter the lungs both hematogenously and when an abscess breaks into the pleural cavity.

Amebic abscesses in lung tissue tend to be chronic. Low-grade body temperature is periodically replaced by sharp rises. Sputum is produced in large quantities; due to the presence of blood, it takes on a chocolate color or the appearance of “anchovy sauce.” Sometimes amoebas are found in sputum. The radiograph reveals a cavity with a horizontal fluid level.

Amoebic abscess is complicated by purulent pleurisy, empyema, pneumothorax, pericarditis, hepatopulmonary fistula.

Rice. 16. The photo shows an amoebic liver abscess. A horizontal liquid level is visible at the bottom of the cavity.

Cerebral amoebiasis

Cerebral amebiasis develops as a result of the spread of protozoa through the hematogenous route. Abscesses in the brain can be single or multiple. Most often located in the left hemisphere. Both focal and cerebral symptoms occur. Severe headaches, nausea and vomiting are the main ones. Neurological symptoms depend on the location of the pathological focus and the degree of damage to brain structures. Diagnosis of an abscess during life is difficult. In acute cases, the disease always ends in death.

Rice. 17. The photo shows an amoebic brain abscess.

Cutaneous amoebiasis

Cutaneous amebiasis most often develops in people with immunodeficiency, weakened and exhausted patients. The process is localized mainly on the skin of the perianal area, buttocks and perineum. Amoebas penetrate the skin from fecal matter, where they are found in large numbers. Sometimes amoebas spread with blood from primary lesions and affect the skin around fistulas or near surgical sutures applied after opening abscesses. The infection is transmitted among homosexuals who have warty ulcerations in the genital area and anus.

At the beginning of the lesion, single erosions form. Further, the erosions turn into deep, painless ulcers with purulent-hemorrhagic discharge, blackened edges, and an emanating foul odor. Sometimes dense tumor-like granulomas form on the skin (usually the abdomen) with amebiasis.

Vegetative forms of pathogens are often detected in scrapings from ulcers.

The disease lasts a long time. Ulcers can reach enormous sizes and often cause the death of the patient.

Rice. 18. The photo shows cutaneous amoebiasis.

Urogenital amoebiasis

Urogenital amebiasis develops through direct contact with a sick person. The source of amoebas can be ulcers located on the mucous membrane of the rectum and genitals. The infection is transmitted among homosexuals who have warty ulcerations in the genital area and anus.

With genitourinary amebiasis, the head and inner layer of the foreskin (balanoposthitis), the urethra, prostate and seminal vesicles in men, the vagina in women, the bladder and kidneys are affected.

Amoebic balanoposthitis characterized by the appearance in the area of ​​the foreskin of painful round ulcers with purulent discharge, having an unpleasant odor, resistant to therapy. Often, with the disease, regional lymph nodes become inflamed.

Amoebic urethritis Most often it proceeds sluggishly, when urinating the patient experiences unpleasant sensations and scanty mucous discharge is noted. In acute urethritis, dysuric phenomena are significantly pronounced.

Amoebic prostatitis often recorded together with urethritis. Usually the disease proceeds calmly, for a long time, with mild symptoms. Acute amoebic prostatitis occurs with elevated body temperature, pain in the perineum, groin and lower abdomen.

Amoebic vaginitis occurs with mucopurulent discharge. Ulcerations ranging in size from 0.5 to 3 cm in diameter appear on the mucous membrane, bleeding when pressed. Sometimes specific inflammation of the cervix develops - amoebic cervicitis.

Amoebic cystitis often has a chronic course. Remissions are replaced by exacerbations.

In homosexuals, warty ulcerations are observed in the anus and genitals.

Cystitis, pyelonephritis and cervical cancer are complications of amebiasis in women. Epipidymitis and prostatitis are complications of amoebiasis in men.

Rice. 19. Amoebiasis of the skin.

Amoebic pericarditis

Amoebic pericarditis develops when a liver abscess located in the left lobe ruptures through the diaphragm into the pericardium, which leads to cardiac tamponade and often death.

Complications of the disease

Intestinal amebiasis is complicated by bleeding, perforation of the intestinal wall with subsequent development of peritonitis, cicatricial narrowing of the colon, development of inflammatory granuloma (amoeba), megacolon (enlargement of the colon), prolapse of the rectum, gangrene and detachment of the mucous membrane, specific appendicitis.

Ameboma (inflammatory granuloma) most often develops in the ascending and cecum. Upon palpation, a tumor-like formation is determined. During endoscopy, an amoeba can be regarded as a sarcoma.

The development of complications with intestinal amebiasis is the main feature of the disease.

Diagnosis of amoebiasis using microscopy

Diagnosis of amebiasis is based on data from an epidemiological investigation, clinical and laboratory research methods.

For microscopic examination, feces, rectal aspirates, and biopsy material from affected areas, including from the walls of an abscess, where tissue forms of amoebas are predominantly localized, are used. Repeated examination (3 - 6 times) of fresh feces increases the effectiveness of the study.

Rice. 20. Microscopy in native smears reveals the characteristic mobility of vegetative forms of Entamoeba histolityca.

Microscopy of smears stained with hematoxylin

In smears stained with hematoxylin, the ectoplasm is transparent, the endoplasm is dark-colored and fine-grained. The color and color of red blood cells depend on the stage of their digestion.

Rice. 21. The photo shows an amoeba in a large vegetative form (trophozoite). Trapped red blood cells (dark in color) are visible in the cytoplasm.

Microscopy of smears stained with Lugol's solution

Rice. 22. The photo shows an amoeba in the form of a cyst under a microscope.

Sigmoidoscopy followed by microscopy of a rectal smear

Sigmoidoscopy followed by microscopy of a rectal smear is a reliable diagnostic method. Due to the rapid destruction of tissue forms of amoebas in the external environment, feces are examined within the first 15 to 20 minutes. First of all, unformed feces mixed with blood and mucus are examined.

Colonoscopy with biopsy

Colonoscopy with biopsy of lesions is the most accurate method for diagnosing intestinal amebiasis. Microscopy allows you to identify protozoa in the area of ​​ulcerative lesions.

The detection of trophozoites - large vegetative (tissue) forms with phagocytosed red blood cells in smears confirms amebiasis of the intestine and other organs.

Rice. 23. The photo shows amoebas.

Diagnosis of amebiasis using serological tests

Due to the fact that with amoebiasis it is not always possible to identify amoebas in feces and aspirates, a serological study is carried out. Positive serological reactions are recorded in 75% of cases in patients with intestinal amebiasis, in 95% in patients with extraintestinal forms of amebiasis.

Indirect immunofluorescence reaction (RNIF) allows you to detect specific antibodies in the patient’s blood serum. A titer of 1:80 or more is diagnostic. In patients with amebiasis RNIF, the reaction is positive in 90 - 100% of cases. The reaction is negative in carriers of translucent (illuminated) forms. In patients with amoebic liver abscesses, RNIF is always positive and in high titers.

Indirect hemagglutination reaction (IRHA) is less informative, since it gives positive results not only in patients with amebiasis, but also in those previously infected.

Enzyme-linked immunosorbent assay (ELISA) used to detect specific antibodies.

Diagnosis of extraintestinal amoebiasis

• When diagnosing extraintestinal forms of the disease, in addition to the clinical picture of the disease and cases of long-term intestinal disease with mild and moderate symptoms of intoxication, it is important to indicate to the patient that he is in an area where amoebiasis is endemic.
• If the disease is suspected, sigmoidoscopy is performed. In the absence of specific damage to the mucous membrane, fibrocolonoscopy is performed. Detection of ulcers on the mucous membrane of the large intestine, round in shape with undermined edges, surrounded by a zone of hyperemia and normal mucosa between them is an important diagnostic sign. During an endoscopic examination, a biopsy and fecal matter are collected.
• When identifying amoebic abscesses, the X-ray method, ultrasound and radioisotope studies, magnetic resonance and computed tomography are used.
• In some cases, laparoscopy is used.

Rice. 24. Dysenteric amoebas under a microscope.

Differential diagnosis

Intestinal amebiasis is similar not only to infectious diseases, but also to a number of other diseases. Among infectious diseases, amoebic dysentery should be differentiated from dysentery (shigellosis), salmonellosis, campylobacteriosis, schistosomiasis and balantidiasis. Of non-infectious diseases, differential diagnosis is carried out with nonspecific ulcerative colitis, diverticulosis, pellagra, colon neoplasms, Henoch-Schönlein disease.

Treatment of amoebiasis

Intestinal forms of the disease are mainly treated on an outpatient basis. Patients with severe disease and extraintestinal manifestations are subject to hospitalization. In the treatment of intestinal amebiasis, luminal and systemic amoebicides are used.

Luminal amoebocides

Luminal amoebicides are used to treat asymptomatic forms of the disease (carriers). They are also prescribed to prevent relapses of amebiasis after completion of a course of treatment with tissue amoebicides. Luminal amoebicides are represented by drugs such as Etofamide (Kythnos), Diloxanide furoate, Clefamide, Paromomycin. Well tolerated Paromomycin And Diloxanide furoate. Diloxanide furoate used for 10 days, 4 times a day, 50 mg.

• Paromomycin used for 10 days, 3 times a day, 30 mg.

Rice. 25. Paromomycin and Diloxanide furoate are used in the treatment of asymptomatic forms of the disease.

Systemic tissue amoebocides

Systemic tissue amoebicides are used to treat symptomatic (invasive) amebiasis and abscesses of any location. Representatives of this group are 5-nitroimidazoles. Metronidazole And Tinidazole are the drugs of choice.

For intestinal amebiasis, one of the following drugs is used:

• Metronidazole (Flagyl, Trichopolum) used for 10 days, 750 mg three times a day.
• Tinidazole (Fasigin, Tiniba) used for 2 - 3 days in one dose of 50 mg/kg for children under 12 years of age and 2 g. - over 12 years old.
• Ornidazole (Tiberal) used for 3 days in two doses of 40 mg/kg for children under 12 years of age and 2 g. per day - over 12 years.
• Secnidazole used for 3 days in one dose of 30 mg/kg for children under 12 years of age and 2 g. per day - over 12 years.

If it is impossible to prevent re-infections, it is not advisable to use luminal amoebicides. They are prescribed only for epidemic indications.

Rice. 26. Metronidazole and Tinidazole are the drugs of choice for the treatment of amoebiasis.

Alternative treatment regimens for amoebiasis

• Dehydroemetine dihydrochloride administered intramuscularly for 4 - 6 days.
• Chloroquine 600 mg per day for two days and then 300 mg for 2 - 3 weeks.

The final stage of treatment for amoebiasis

After a course of treatment with systemic tissue amoebicides, luminal amoebicides are prescribed for the final destruction of amoebicides Etofamide or Paromomycin.

• Paromomycin applied for 5 - 10 days, 0.5 g in 2 doses.
• Etofamide applied for 5 - 7 days, 0.6 g in 2 doses.

Antibiotics for the treatment of amoebiasis

Antibiotics for the treatment of amebiasis are prescribed in case of intolerance to metronidazole and in the development of such complications of the disease as intestinal perforation with subsequent development of peritonitis. Antibacterial drugs are used Tetracycline And Erythromycin.

• Tetracycline used for 10 days, 4 times a day, 250 mg.
• Erythromycin used for 10 days, 4 times a day, 500 mg.

To accelerate the elimination of pathogenic amoebas, it is used Enteroseptol(iodochloroxyquinoline).

The prognosis for amebiasis is usually favorable

Prevention

The basis for the prevention of amebiasis is measures to improve the material and living conditions of the population and food safety, high-quality water supply, prevention of fecal pollution of the environment, timely identification and adequate treatment of patients and carriers, full implementation of anti-epidemic measures in the outbreak, and health education.

Catering and water supply workers are subject to periodic medical examinations.

Food processing plants should constantly control flies, ants and cockroaches.

Disinfection is carried out at the outbreaks of the disease.

Thorough and frequent hand washing, eating thermally processed foods and vegetables and fruits washed under running water.

Rice. 27. Amebiasis is considered one of the “dirty hands” diseases.