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Year of approval 2016
Professional associations

• Public organization “Association of Infectious Disease Doctors of St. Petersburg and the Leningrad Region” (AVISPO);
• Public organization “Eurasian Society for Infectious Diseases”.

Table of contents

1. Brief information 2. Diagnosis 3. Treatment 4. Rehabilitation 5. Prevention 6. Additional information

brief information

1.1 Definition

“Amebiasis” is a human protozoal disease:

• with fecal-oral transmission,
• ulcerative lesions of the intestines,
• moderately severe intoxication,
• recurrent and chronic course,
• possible extraintestinal complications in the form of abscesses of the liver, brain, lungs and other organs.

1.2 Etiology and pathogenesis of amebiasis

Etiology

Pathogen Entamoeba histolytica, order Amoebidae, protozoa Sacromastigophora.

Development cycle:

vegetative (trophozoite) with 3 forms of development:

• large vegetative (Entamoeba histolytica forma magna) - 20-60 µm, typical erythrophage, in fresh feces with acute amoebiasis;
• luminal (Entamoeba histolytica forma minuta) - 15-20 µm, in the lower part of the colon it becomes cystic, in the feces of convalescents, in chronic relapsing course and in carriers in the feces after laxatives;
• tissue - 20-25 microns, in the submucosal layer of the intestine and in organ abscesses, rarely in liquid feces with intestinal ulcers.

resting stage - 10-15 microns, cyst of varying degrees of maturity, mature with 4 nuclei, in the feces of convalescents, in remission in chronic cases and in amoeba carriers.

Pathogenesis

Stages of pathogenesis:

• Infection - entry of mature cysts into the gastrointestinal tract; in the small intestine, a 4-nuclear amoeba emerges from each cyst, from which 4 mononuclear amoebas are formed, each divided into luminal ones, living in the upper part of the large intestine without clinical manifestations.
• Transformation of luminal forms into erythrophages under favorable conditions in the body (immunodeficiency, inflammation), release cytolysins that destroy the epithelial layer.
• Intestinal damage from the cecum to the sigmoid with mucosal necrosis and ulcers after opening microabscesses.
• Introduction of Entamoeba histolytica forma magna into the submucosal layer of the colon - mainly at the edges of the ulcer, some penetrate into the submucosal layer.
• Complications of local manifestations of amebiasis are perforation of ulcers with peritonitis or peritoneal adhesions, strictures during healing of ulcers with the threat of intestinal obstruction, ameboma.
• Hematogenous spread and formation of abscesses in organs.
• The immune response in amebiasis is secretory IgA against Eh-lectin, IgM and IgG during hematogenous spread, activation of macrophages and natural killer cells for protection during reinfection after the first episode of the disease.

1.3 Epidemiology

Anthroponotic protozoal infection.

Sources of infection:

• amoeba carriers
• less often in patients with chronic amoebiasis.

In the world:

• 3rd place - after malaria and schistosomiasis among all parasitic diseases in terms of deaths - 100 thousand;
• affects about 50 million annually;
• 50% of cases in developing countries (Nigeria, Ghana, Benin, Ivory Coast),
• infection of countries in Africa, Korea, China, South and Central America;
• mortality 0.2% of all detected cases;
• extraintestinal amebiasis - about 10% of all cases.

In Russia:

• in the southern regions;
• mostly sporadic incidence;
• endemic region – Dagestan;
• extraintestinal forms are possible;
• in the border areas of Armenia, Georgia, Turkmenistan, Kyrgyzstan.

1.4 Coding according to ICD-10

Amoebiasis (A06): infection caused by Entamoeba histolytica

A06.0 – Acute amoebic dysentery;

Acute amoebiasis Intestinal amoebiasis NOS;

A06.1 - Chronic intestinal amebiasis;

A06.2 - Amoebic non-dysenteric colitis;

A06.3 - Intestinal ameboma; Ameboma NOS;

A06.4 - Amoebic liver abscess;

• Hepatic amoebiasis;

A06.5 - Amoebic lung abscess;

• Amoebic abscess of the lung (and liver);

A06.6 - Amoebic brain abscess;

• Amoebic abscess of the brain (and liver) (and lung);

A06.7 - Cutaneous amoebiasis;

A06.8 - Amebic infection of another location;

• Amoebic appendicitis;
• Amoebic balanitis;

A06.9 - Amoebiasis, unspecified.

1.5 Classification of amoebiasis

Clinical:

Type:

1. Typical (amoebic diarrhea, amoebic dysentery, acute amoebic colitis); 2. Atypical (latent); 3. Lightning (fulminant).

According to the presence of complications:

• No complications;
• With intestinal complications (bleeding, perforation of ulcers; strictures, polyposis, ameboma, prolapse of the rectal mucosa);
• With extraintestinal complications (abscesses of the liver, lungs, hepatitis, skin, etc.).

According to the nature of the flow:

Acute - up to 3 months; Chronic - more than 3 months:

• recurrent,
• continuously relapsing.

According to severity:

• Lung
• Medium-heavy
• Heavy

WHO classification:

1. Asymptomatic infection; 2. Manifest infection:

• intestinal amebiasis:
• amoebic dysentery;
• amoebic colitis.

3. Extraintestinal amoebiasis

• hepatic: acute hepatic; liver abscess.
• pulmonary;
• other extraintestinal lesions.

Mechanism of infection and methods of transmission

Amoebic dysentery, like other infectious intestinal diseases, is a disease of dirty hands.

The routes of infection with amoebiasis come down to two main ones. This is a nutritional route in which the cyst enters the human body through contaminated food and water. Also important is the contact and household route of infection, in which a healthy person becomes infected with amoebiasis through contact with infected objects and people.

In any case, the main method of infection is the entry of cysts into the body through the fecal-oral route in violation of basic hygiene standards.

People without obvious signs of illness pose a danger to others:

• carriers;
• patients recovering from acute amoebiasis;
• chronic patients without exacerbation.

With feces, they excrete cysts in huge quantities over many years (one gram of feces contains several tens of millions of cysts).

Acute patients and chronic patients during the period of exacerbation of the disease secrete vegetative forms of the parasite, which quickly die outside the human body and are therefore not dangerous to others. Thus, the tissue form of amebiasis can be found in the patient’s feces no later than 20 minutes after defecation, then it dies.

The routes of transmission of amebiasis are associated with direct contact with the source of the disease, for example, by shaking hands or anal sex. But you can also become infected through indirect contact through intermediate objects.

Diagnosis of amoebiasis

2.1 Complaints and anamnesis

Investigate complaints about:

• temperature increase
• intoxication (weakness, loss of appetite, drowsiness, headaches)
• dyspeptic (vomiting, diarrhea, bloating, increased passage of intestinal gases)
• stomach ache
• pathological impurities in the stool (blood, mucus, pus)
• decreased diuresis
• cough.

Epidemiological history:

• contact with patients or carriers of dysenteric amoeba,
• drinking unboiled water from natural open reservoirs, wells, springs, etc.

The most common syndromes and complications of amebiasis

The incubation period is from 7 days to 3 months, more often 3-6 weeks.

Amoebic diarrhea:

• the first phase of intestinal amebiasis,
• increased bowel movements up to 2-6 times a day,
• stool without visible signs of mucus and blood,
• Blood is detected microscopically in the stool,
• general condition is satisfactory.

Amoebic dysentery or amoebic colitis:

• mild fever,
• mild signs of intoxication,
• headache,
• pain in the hypogastrium, right (more often) and left iliac regions,
• diarrhea up to 8-12 times a day, sometimes with tenesmus,
• there are streaks of blood and copious mucus in the stool - “raspberry jelly”,
• in children, decreased turgor, rapid loss of body weight,
• low-grade fever,
• discrepancy between diarrhea syndrome and the patient’s well-being,
• with rapid progression on the 6-8th day, pronounced inflammatory changes in the colon mucosa,
• symptoms subside after 4-6 weeks,
• remission from 1-2 weeks to several months,
• chronic form up to 10 years.

Extraintestinal amoebiasis:

• often amoebic liver abscess with fever of the wrong type, pain in the right hypochondrium with radiation to the right shoulder, jaundice with large abscesses;
• amoebic hepatitis with microabscesses,
• amoebic lung abscess with fever, chest pain, cough, copious brown sputum during defecation, leukocytosis with a shift to the left, accelerated ESR, eosinophilia.

Complications of amoebiasis:

• perforation of intestinal ulcers with the development of peritonitis,
• formation of an abdominal abscess,
• intestinal bleeding,
• rarely amoebic intestinal stricture, polyposis, amoebomas,
• amoebic pericarditis,
• pleural empyema,
• abscess of the retroperitoneal space due to rupture of organ abscesses,
• ulcerative-necrotic lesions of the skin of the buttocks, perineum and perianal area,
• "fulminate" amebiasis in young children with immunodeficiency.

2.2 Physical examination

Estimate:

• general state;
• signs of dehydration (turgor, elasticity of the skin and mucous membranes, large fontanel in infants and young children);
• nutrition level;
• CVS status (pulse, blood pressure, heart sounds);
• signs of respiratory failure due to dehydration;
• palpation of the abdomen (painful areas);
• size of the liver and spleen;
• bowel movements (visual).

Character of abdominal pain syndrome :

• cramping pain,
• tenesmus,
• localization in the hypogastrium,
• pain on palpation of the left and right iliac and ileocecal regions.

Hepatosplenomegaly in moderate to severe cases.

Character of the chair :

• frequent,
• liquid or mushy
• with mucus,
• soaked in blood - “raspberry jelly.”

Clinical signs of dehydration and severity are determined by percentage of body weight loss (ESPGHAN):

• 4-5% – mild degree;
• 6-9% – moderate;
• 10% or more – severe.

Clinical Dehydration Score CDS:

• 0 points – absent;
• 1-4 points – easy;
• 5–8 points – moderate and severe.

For criteria for assessing the severity of amebiasis in children, see Appendix D2.

2.3 Laboratory diagnostics

At the stage of diagnosis

Complete blood count with leukocyte formula:

• eosinophilia;
• leukocytosis;
• neutrophilia,
• increase in ESR.

Scatological research:

• vegetative forms and cysts of various types of amoebas;
• leukocytes;
• red blood cells;
• mucus (hemocolitis);
• signs of impaired digestion and absorption.

Microscopic examination of feces for vegetative forms and cysts:

• informative for the manifest form of the disease - hematophages;
• in case of carriage - luminal forms and cysts;
• The information content increases when examining fresh feces - up to 20 minutes.

Microscopic examination of the contents of intestinal ulcers for vegetative forms:

• informative in the manifest form - hematophages;
• information content increases when examining material during endoscopy.

Specific antibodies to dysenteric amoeba in blood serum during RNIF :

• titer 1:80 or more;
• for intestinal amebiasis, low effectiveness;
• with extraintestinal (abscess formation) high efficiency;
• in paired serums with an interval of 14-20 days.

Specific antibodies to dysenteric amoeba in blood serum by ELISA:

• detection confirms the diagnosis;
• low effectiveness for intestinal amebiasis;
• high efficiency in extraintestinal (abscess formation);
• study in paired sera with an interval of 14-20 days.

Detection of genetic material of dysenteric amoeba in feces using PCR :

• informative for manifest and latent forms;
• false positive and false negative results are possible;
• if the result is positive, parasitological confirmation is required;
• differentiates the luminal form from non-pathogenic Entamoeba dispar, coli, hartmanni, etc.

Detection of genetic material of dysenteric amoeba in the contents of abscesses using PCR :

• informative for extraintestinal amoebiasis.

Antigens of dysenteric amoeba using monoclonal antibodies in feces and blood serum:

• informative for manifest and latent forms.

TANK:

• glucose;
• CRP – increase during inflammatory changes;
• urea, creatinine, electrolytes - reflects the severity of dehydration;
• ALT and AST – increased in cytolysis syndrome in amoebic hepatitis;
• alkaline phosphatase - increased in cholestatic syndrome;
• amylase – increased with damage to the pancreas;
• direct bilirubin - increased in cholestatic syndrome.

2.4 Instrumental diagnostics

X-ray examination of the lungs in the clinic of lung damage: volatile pulmonary infiltrates, pneumonia, abscesses.

Ultrasound of the abdominal organs.

Fibercolonoscopy.

Survey radiograph of the abdominal organs at the clinic of “acute abdomen”.

CT or MRI for complications of amebiasis.

Differential diagnosis:

• with acute bacterial intestinal infections (shigellosis, campylobacteriosis, salmonellosis, etc.);
• with other parasitic diseases (balantidiasis, hookworm disease, intestinal schistosomiasis, etc.);
• with inflammatory bowel diseases (ulcerative colitis, Crohn's disease);
• with acute surgical pathology of the abdominal cavity (appendicitis, acute intestinal obstruction, etc.);
• with intestinal tuberculosis.

Causes of amoebic dysentery

The sources of the causative agent of this disease are patients and carriers of the infection. Cysts are released with feces, which are very resistant to various natural factors and disinfectant products. They remain alive in water for several months.

Infection occurs through oral and fecal routes. Infection often occurs through contaminated fruits, vegetables, water and other foods. Cysts are also carried by various insects, such as cockroaches or flies. You can often become infected from swallowing water in public bodies of water.

When an amoeba cyst enters the digestive tract, infection occurs. If vegetative forms enter the acidic environment of the stomach, they die.

If dysbacteriosis and decreased immunity are present, the cyst, after the destruction of its membranes, turns into a luminal form. At the same time, it releases active components cytolysins and enzymes that damage the intestinal wall, which leads to its inflammation. The vegetative form of the amoeba enters the intestinal tissue, transforming into a larger tissue form. When it becomes saturated with red blood cells, it forms a large number of ulcers and can also cause tissue necrosis (necrosis).

If the tissue form of the amoeba also enters other human organs through the blood vessels in the body, then an abscess begins to form in the lungs, liver and other organs.

Treatment of amoebiasis

The choice of treatment method depends on:

• clinical picture
• severity of the disease
• presence of complications.

Treatment of amebiasis includes:

• mode;
• diet No. 4 according to Pevzner with restriction of milk and dairy products;
• taking medications;
• means of etiotropic therapy
• means of symptomatic therapy;
• means of normalizing intestinal microbiocenosis;
• non-drug treatment methods;
• physical methods of reducing temperature;
• physiotherapeutic methods of treatment.

Indications for hospitalization

Outpatient treatment of cyst-bearing children with a history of acute invasive amebiasis.

Patients are subject to hospitalization in infectious diseases departments:

• with a clinically manifest form;
• with complications of the disease.

3.1 Conservative treatment

Etiotropic therapy

Goals:

• eradication of dysenteric amoeba;
• reducing the severity of the disease;
• reducing the risk of complications.

Etiotropic therapy is carried out taking into account the form of the disease.

Drugs for the treatment of amebiasis from the group of 5-nitroimidazoles:

• metronidazole
• ornidazole
• Secnidazole

Treatment regimens for intestinal amebiasis and amoebic abscess:

• Metronidazole 30 mg/kg/day in 3 doses, orally, intravenously for 8-10 days;
• Ornidazole 40 mg/kg/day up to 12 years; 2 g/day over 12 years old in 2 divided doses for 3 days;
• Secnidazole 30 mg/kg/day up to 12 years; 2 g/day over 12 years old in 1 dose for 3 days.

For the rehabilitation of parasite carriers with a history of amoebiasis:

• Metronidazole 750 mg 3 times a day orally for 8-10 days;
• Diloxanide furoate 500 mg 3 times a day; children – 20 mg/kg/day in 3 divided doses for 10 days (not used in the Russian Federation);
• Paromomycin (monomycin) 25-30 mg/kg 3 times a day orally for 7-10 days (potentially nephro- and ototoxic).

Symptomatic therapy

Goals:

• reduction of intoxication;
• elimination of fever syndrome;
• correction of water-electrolyte balance disorders;
• elimination of dyspeptic disorders;
• elimination of abdominal pain syndrome;
• Antibacterial therapy for bacterial complications.

If oral rehydration is ineffective, intravenous administration of solutions is recommended for moderate and severe forms of amebiasis, including complications.

Systemic glucocorticosteroids :

• with severe amebiasis;
• in patients with severe manifestations of allergies.

Antihistamines - piperazine derivatives (cetirizine orally) for moderate allergies:

• urticarial exanthema;
• Quincke's edema;
• atopic dermatitis.

Probiotic preparations for the correction of intestinal microbiocenosis disorders:

• loose stools;
• bloating.

Adsorbent intestinal preparations (dioctahedral smectite, hydrolytic lignin) for:

• diarrhea;
• flatulence;
• flatulence.

Papaverine and its derivatives (drotaverine) for the relief of abdominal pain syndrome.

3.2 Surgical treatment

For complications:

• liver abscess;
• lung abscess;
• brain abscess;
• peritonitis, etc.

3.3. Other treatment

Physical methods of reducing temperature:

• with febrile fever of the “red type”;
• not recommended for febrile fever of the “white type” in children with pallor, coldness of the extremities - the basis for parenteral myotropic antispasmodics with antipyretics.

Physiotherapeutic methods for abdominal pain and subsidence of acute inflammation in the colon.

Prevention of amebiasis

General approaches to prevention

Isolation of the patient until complete clinical recovery (2-3 weeks) and persistent disappearance of dysentery amoeba from feces:

• at home;
• in a separate box of the hospital;
• in a hospital ward with children suffering from amoebiasis.

After clinical recovery, the child is admitted to the educational organization without anti-epidemic restrictions.

A set of anti-epidemic measures is carried out at the source of amoebiasis.

Providing the patient with separate dishes and care items.

Contact faces:

• parasitological examination of feces,
• without quarantine and isolation measures.

Specific prevention of amebiasis has not been developed.

Dispensary observation:

• for intestinal form 6 months,
• for extraintestinal 12 months,
• for residual effects after surgery 2 – 3 years.

Observation includes:

• examination by an infectious disease specialist.
• surgeon, gastroenterologist and other specialists - according to indications.
• laboratory examination (examination of feces, serology if necessary) once every 3 months.

Additional information affecting the course and outcome of the disease

Poor prognosis factors:

• late application;
• lack of treatment with antiparasitic drugs;
• inadequate doses of antiparasitic drugs;
• incorrect antiparasitic therapy regimens;
• inadequate pathogenetic treatment.

Risk of complications:

with a high level of development (no more than 7-10%):

• prolapse of the rectal mucosa,
• intestinal bleeding;

with an average level of development (no more than 5-7%):

• intestinal stricture,
• polyposis,
• ameboma,
• protein-calorie malnutrition,
• abscess of the liver, lungs,
• amoebic hepatitis;

with a low level of development (no more than 3-5%):

• perforation of intestinal ulcers,
• peritonitis,
• abscesses of the liver, lungs,
• pericarditis,
• amoebic skin lesions of the perianal area,
• pleural empyema,
• abscess of the retroperitoneum.

Pathogenesis

Once in the stomach, the cysts are exposed to gastric juice. The gastric secretion dissolves the cell membrane, and the amoeba passes into a vegetative form. Vegetative cells enter the intestines, and the development of the disease begins. In the large intestine, amoebas lyse cells of the intestinal mucosa and invade the tissue. In this case, ulcers with a diameter of 2–2.5 mm are formed on the surface of the mucosa. The ulcers may fester and areas of necrosis may appear. In severe cases, perforation of the intestine may occur, followed by the development of purulent peritonitis.

Amoebas can enter the bloodstream, spread throughout the body and affect various organs - extraintestinal amoebiasis develops. Settling in other tissues, the protozoan lyses the cells of the human body in the same way, forming necrotic areas and ulcers. Amoebic abscesses most often develop in the liver, lungs, and brain. This protozoan can also cause amoebic pneumonia and inflammation of the pleura, damage to the kidneys and genitals, abscesses and skin ulcers.

Without proper treatment, the disease becomes chronic. The patient does not have pronounced symptoms of pathology. In chronic amebiasis, under the influence of protozoa, polyps, cysts and amoebomas (tumor-like formations) can form in the large intestine.

The chronic form of the disease can last for years or decades. In this case, periods of remission alternate with periods of exacerbation, when clinical symptoms of amebiasis appear. A continuous course of chronic amoebiasis with periods of intensification and weakening of symptoms is also possible.

Possible complications of intestinal amebiasis:

• pericolitis (inflammation and deformation of the peritoneal wall);
• purulent infection of the intestinal mucosa;
• perforation of the wall of the small intestine;
• intestinal bleeding;
• purulent peritonitis.

During the healing of these ulcers, connective tissue adhesions are formed. Connective tissue can grow, preventing the bolus from moving through the intestines. In some cases, even complete intestinal obstruction may occur due to the blocking of its lumen by overgrown connective tissue.