Amebiasis

What is Amebiasis?

Amebiasis is a protozoan invasion of a human, accompanied by a lesion of the colon and capable of generalization.

Amebiasis is a disease caused by pathogenic strains of Entamoeba histolytica, which are widespread in the world, mainly in countries of tropical and subtropical climates. The low level of sanitation typical of these areas causes a high incidence of amebiasis. Currently, amebiasis is one of the largest medical and social problems in developing countries and is one of the most common causes of death in parasitic bowel diseases. After malaria, this infection ranks second in the world in the frequency of deaths in parasitic diseases. About 480 million people in the world are carriers of E. histolytica, 48 million of them develop colitis and extra-intestinal abscesses, and 40 thousand – 100 thousand cases are fatal. Migration, the deterioration of the economic situation of a number of developing countries, low levels of sanitation contribute to the spread of amebiasis and, accordingly, to an increase in the incidence rate.

Causes of Amebiasis

The causative agent of amebiasis is histolytic, or dysenteric, amoeba – Entamoeba histolityca (Losch, 1875; Schaudinn, 1903). Dwells in the colon. In addition to pathogenic E. histolytica, non-pathogenic amoebas are detected in the human colon: Entamoeba dispar, Entamoeba hartmanni, Entamoeba coli, Endolimax nana, lodamoeba biletschlii, Dientamoeba fragilis. The causative agent belongs to the kingdom of Animalia, the kingdom of Protozoa, a type of Sarcomas tigophora, a subtype of Sarcodina.

In the life cycle of the histolytic amoeba there are vegetative (trophozoite) and cystic stages). Unlike other types of amoebae, dysenteric amoeba has four forms of the vegetative stage: tissue, E. histolytica forma magna, translucent – E. histolytica forma minuta, and predcystic.

Tissue form has dimensions of 20 – 25 microns. In the cytoplasm, there are two layers – ectoplasm and endoplasm. In the fresh preparation, the endoplasm is homogeneous, contains no inclusions. In the native preparation, the method of movement is well defined with the help of ectoplasmic pseudopodia, arising in the form of rapid shocks. Tissue form of amoeba is detected only in acute amebiasis directly in the affected tissue, rarely in feces.

E. histolytica forma magna (erythrophage) is able to phagocytose red blood cells, secrete enzymes, penetrate the intestinal mucosa and submucosa, and cause necrosis and the appearance of ulcers. The size of a large vegetative form is 20-40 microns; when moving, it stretches to 60-80 microns; the cytoplasm is also divided into a bright ectoplasm, free from inclusions, and a fine-grained endoplasm, in which the inconspicuous nucleus is located. In native smears, the tissue form is actively mobile. Movement is carried out by relatively quick, sudden ejection of light transparent ectoplasmic pseudopodia. Endoplasm with erythrocytes enclosed in it swirls in the vortex into the pseudopodia formed. Pseudopathy smoothes out and disappears. Then, on the same or in another place of the cell surface, a new pseudopodia is formed, the cytoplasm transfusion is repeated and the amoeba moves in a certain direction. Sometimes two pseudopods form at once. One of them gradually increases, and the second disappears. At the same time there are separate sedentary individuals. When the drug is cooled, the mobility of the amoebas at first slows down, then their body is rounded and they all become motionless. Nested red blood cells in native smears are located in the endoplasm and have a yellowish tint. On preparations stained with iron hematoxylin, the ectoplasm is light, transparent, and the endoplasm is monotonous, fine-grained, darker in color. The nucleus has a delicate shell with fine grains of peripheral chromatin and a centrally located point cariotomy. In the endoplasm are red-colored red blood cells, the size of which and the intensity of color depend on the stage of their digestion. A large vegetative form is found in the feces in acute amebiasis.

Luminous form – commensal, lives in the lumen of the colon, feeds on detritus and bacteria. It is detected in persons who have undergone an acute form of intestinal amebiasis, with chronic recurrent amebiasis, as well as asymptomatic amoebae. The luminous form is different from the fabric sluggish movement. Its size is from 15 to 25 microns. In native smears in the luminal form, the division into ecto-and endoplasm is not observed. The structure of the core is the same as that of the tissue form.

The predtsistnaya stage (predtsista) is a transitional form of the histolytic amoeba from the luminal to the cyst. Its size is 10 – 18 microns. The division into ecto-and endoplasm is hardly noticeable. Does not contain swallowed bacteria, erythrocytes and other cellular elements. All forms of the vegetative stage of E. histolytica die quickly in the external environment.

Cysts are the resting stage of development of the histolytic amoeba, ensuring the preservation of the species in the external environment. On unpainted cysts preparations are rounded, colorless formations with a double-circuit shell, with a diameter of 10 to 15 microns (average 12 microns). Mature cysts contain 4 nuclei. On preparations stained with iron hematoxylin, the cytoplasm is gray. It defines from 1 to 4 kernels with sickle-shaped chromatin grains on the inner shell and centrally located point cariotomy. In the cytoplasm of immature cysts, the glycogen vacuole is clearly contoured as a bright spot and rod-shaped, with rounded ends, black chromatoid bodies, the size and number of which may be different for individual cysts. Chromatoid inclusions are found in 10 – 50% of cysts of the histolytic amoeba. Cysts are found in feces of convalescents and cyst carriers.

Using the method of isoenzyme analysis inside the E. histolytica species, pathogenic and non-pathogenic strains of dysenteric amoeba were detected. The rate of movement of pathogenic histolytic amoeba strains is higher than non-pathogenic. Trophozoites and cysts of non-pathogenic amoebas differ from similar stages of the histolytic amoeba in size, shape, number, structure of nuclei, movement patterns and inclusions, etc. Trophozoites of non-pathogenic amoebas feed on bacteria, fungi, cell debris, erythrocytes do not phagocytose. Knowledge of the morphological features of non-pathogenic amoebas is necessary for the differential diagnostic diagnosis of the type of these protozoa. The sizes of non-pathogenic amoeba trophozoites are as follows: E. coli – 30–45 µm, Jod. btitschlii – 5 – 20 microns, End. nana -5-12 microns; cysts, respectively – 14-20 microns, 6-16 microns, 5-9 microns. Data from molecular biological studies have established that non-pathogenic E. dispar is morphologically the twin of E. histolytica, they can only be distinguished by DNA analysis (C. D. Huston et all., 1999).

Epidemiology.
Amebiasis – anthroponosis of protozoal etiology. The source of infection in amebiasis is a person who secretes E. histolytica cysts with feces. Fecal-oral transmission mechanism. The intensity of the allocation of cysts per day varies from 3 thousand to 3888 thousand in 1 g of feces and averages 580 thousand. One chronic clinically healthy carrier can excrete tens of millions of cysts with feces daily.
Vegetative forms of the histolytic amoeba retain viability in feces for no more than 15–30 minutes. Cyst forms have significant resistance in the environment, their survival depends on temperature and relative humidity. In feces at a temperature of +10 … + 20 ° C, they stay alive from 3 to 30 days, and at -1 … -21 ° C – from 17 to 111 days. In the water of natural reservoirs, they survive 9-60 days at a temperature of 10 – 30 ° С, in tap water – up to 30 days, in wastewater – up to 130 days; on the soil surface at a temperature of +10 … + 50 ° С – 2 – 11 days, in deep layers – up to 1 month. On the skin of the hands of the cysts remain viable up to 5 minutes. In subungual spaces – 46–60 min., In the intestines of house flies – up to 48 hours, in milk and dairy products at room temperature – up to 15 days. At a temperature of +2 … + 6 ° С and a relative humidity of 80 – 100%, E. histolytica cysts survive on objects made of glass, metals, polymers and other materials for 11-25 days, and at a temperature of +18 … + 27 ° С and relative air humidity 40 – 65% – not more than 7 hours.

Considering the significant intensity of cysts excretion in amebiasis, long periods of their survival at environmental facilities and food products, soil, waste water, water of open reservoirs, household items and production conditions, fruits, vegetables, foodstuffs, hands contaminated can be factors of amoebiasis transmission. cysts of dysenteric amoeba.

Prevalence.
The natural susceptibility of people to amebiasis is high, including reinfection. About 480 million people in the world are carriers of E. histolytica, of which 48 million (10%) develop intestinal amebiasis and its extraintestinal forms, and 40,000-100,000 cases of death occur (J. A. Walsh). The disease is widespread with prevalence of morbidity in the developing countries of the subtropical and tropical zones, mainly in settlements with a low level of communal and sanitary amenities. In temperate countries, amoebiasis is characterized by sporadic morbidity, although water outbreaks of amebiasis are described, as well as outbreaks in closed institutions (among the prisoners of high-security colonies). The deterioration of the epidemiological situation on amebiasis in countries with a temperate climate is facilitated by the introduction of invasions from endemic zones (migrants, tourists, refugees, businessmen and other groups of the population).

The number of asymptomatic discharge of the histological amoeba is many times higher than the number of patients and in some countries reaches 40%. Persons older than 5 years get predominantly.

Pathogenesis during Amebiasis

The pathogenesis of amebiasis is due to the biological properties of the parasite and the susceptibility of the human body to the pathogen. Swallowed cysts under the influence of intestinal enzymes are extsisted in the lower parts of the small intestine, from the released amoeba after its division 8 mononuclear amoebae-trophozoites are formed, which descend to the place of their parasitism – in the upper parts of the large intestine. From here, as the intestine progresses, the trophozoites turn into single quad cysts, which are excreted in the feces.

Development of an invasion can proceed as an asymptomatic carriage. Then the histolytic amoebas live in the lumen of the colon, behave like commensals, feeding on bacteria, fungi, detritus (forma minuta). As a result of the action of certain factors (intensity of invasion, physico-chemical environment of the intestine, microtraumas and inflammatory changes of the mucous membrane, impaired intestinal motility, the nature of the microflora, the presence of helminths, immunodeficiency, hormonal changes, starvation, stress, etc.) amoebas can turn into tissue parasites (forma magna). In this case, they are attached to the intestinal mucosa with the help of superficial shell lectins. Parasites begin to secrete enzymes: proteases, hemolysins, which melt the tissue. Some strains revealed hyaluronidase – an enzyme that promotes the penetration of amoebas into tissues. When amoebas come into contact with neutrophils, the latter lysis occurs with the release of monoxidants, enhancing tissue melting. This leads to the destruction of the intestinal wall, the oppression of the protective role of intestinal mucus, leads to the formation of pores on the mucosa, the appearance of ulcers. The products of vital activity and the decay of the parasite are absorbed from the places of ulcerations, and the conditionally pathogenic and pathogenic microflora are inoculated. The causative agent goes deep into the submucosa, its intensive reproduction takes place, the primary focus is formed in the form of a microabscess, which is opened into the intestinal cavity with the formation of an ulcer. The diameter of the ulcers is 2 – 10 or more millimeters. In the initial period, they are most often located on the ridges of the folds of the mucous membrane. Ulcers have uneven, saped edges, the bottom is covered with necrotic masses of brown color. At the same time in the intestinal wall is a regenerative process, leading to the restoration of the defect. Gradually, the ulcers are filled with granulation tissue and scarring. The formation of granulation tissue and fibrosis can lead to the formation of amoebic structures and stenosis of the blind or sigmoid intestines.

For amebiasis is characterized by a lack of synchrony in the development of ulcers. On the mucous membrane can be small erosion, small ulcers, extensive lesions up to several centimeters in diameter (“flowering ulcers”), healing ulcers and scars after their healing. In an uncomplicated course of amoebiasis, the mucosa between ulcers retains its normal appearance.

In chronic intestinal amebiasis with multiple deep ulcers with fibrinous plaque pseudopolyps are detected. Most often, ulcers are localized in the cecum, the ascending part of the colon, the sigmoid and rectum. In severe cases of the disease, the entire large intestine, including the appendix, can be affected.

The consequence of a long inflammatory process in the large intestine is the development of pseudo-polyposis, megacolon and a specific inflammatory granuloma, amoeboma, which can reach considerable sizes. Direct amoebae from the intestine to the skin of the perianal area leads to ulceration of the skin in this area.

Intestinal ulcers can penetrate to the serosa and cause pericolitis or colon perforation. The defeat of large vessels leads to the appearance of profuse intestinal bleeding. The penetration of trophozoites into eroded areas of the vessels of the large intestine is accompanied by the generalization of the invasive process and the introduction of amoebae into the liver, lungs, less often into the brain, other organs with the formation of amoebic abscesses. More often, abscesses are localized in the right lobe of the liver. They can be opened in the biliary tract, abdominal and pleural cavities.

The development of amebiasis is controlled by the human immune system. Parasitizing of histolytic amoebas is accompanied by the production of specific antibodies. Secretory protivoamebny IgA is found in invasive amebiasis in the saliva of patients with breast milk in women. In patients with liver abscess, high titers of serum antibodies are detected already on the 17th day of the disease. Inhibition of cellular immunity (for example, in the appointment of corticosteroids) leads to the weighting of the amoebic process and its generalization.

Acquired immunity in amebiasis is unstable and non-sterile. It does not protect against relapses and re-invasions.

Symptoms of Amebiasis

According to the WHO classification, asymptomatic and manifest amebiasis is isolated, including intestinal (amebic dysentery and dysenteric amebic colitis) and extraintestinal (liver: acute nonpurulent and abscess of the liver; pulmonary and other extraintestinal lesions).

Amoebic dysentery (dysenteric colitis) – the main and most common clinical form of the disease – can occur acutely and chronically, in severe, moderate and mild forms. The incubation period is from 1 – 2 weeks to 3 – 4 months or more. The main clinical signs of the disease is a speeded up chair: in the initial period up to 4-6 times a day, abundant feces with mucus, then up to 10-20 times a day with blood and mucus with a loss of fecal character. The feces take the form of “raspberry jelly.” The disease, as a rule, develops gradually, without symptoms of general intoxication, the body temperature is normal or subfebrile. In case of severe invasion, there may be a high temperature and pulling or cramping pain in the lower abdomen, which increases during defecation. There are painful tenesmus.

In severe cases of colitis, signs of intoxication are increasing, which is manifested by an increase in temperature (usually of an irregular nature), decreased appetite, nausea, and sometimes vomiting. The stomach in the acute period is soft, painful along the large intestine.

With endoscopy (rectoromanoscopy, fibrocolonoscopy) inflammatory changes in the rectum and sigmoid colon are found in the initial period in 42% of patients. On the 2nd – 3rd day from the onset of the disease, on the background of the normal mucous membrane, there are areas of hyperemia (diameter 2-5 mm), somewhat elevated above the level of the unchanged sections of the intestine. From the 4th to the 5th day of the disease, small nodules and ulcers (up to 5 mm in diameter) are detected at the site of these areas of the hyperemia, from which, when pressed, yellowish cheesy mass is released. Around the ulcers a small area of ​​hyperemia. From the 6th to the 14th day of the disease, ulcers of up to 20 mm in size are found with saped edges and filled with necrotic masses. Thus, changes in the intestinal mucosa typical for amebiasis are formed during the first 2 weeks of the disease. With a rapidly progressing course, such changes are found already on the 6th – 8th day of the disease.

The acute process lasts no more than 4-6 weeks, then comes remission lasting from several weeks to 1 or more months. After remission, the disease resumes and becomes chronic, which can last for years without specific treatment.

Chronic process proceeds in the form of recurrent or continuous forms. With a recurrent form of exacerbation, they are replaced by remissions, during which patients notice only small dyspeptic symptoms (mild meteorism, rumbling in the abdomen, pain without a certain localization). When exacerbating the health of patients is not significantly disturbed, the body temperature remains normal. At this time, there are marked pains in the right abdomen, in the ileocecal region (appendicitis is often mistakenly diagnosed), and stool disorder. With a continuous course of chronic amebiasis, there are no periods of remission. The disease proceeds with the intensification of all manifestations (abdominal pain, diarrhea, alternating with constipation, stool mixed with blood, sometimes the body temperature rises), then with their weakening. With a long-term course of chronic intestinal amebiasis, patients become exhausted, their working capacity decreases, asthenic syndrome, hypochromic anemia develops, the liver often increases, eosinophilia, monocytosis are noted, and in advanced cases cachexia. In the chronic course of intestinal amebiasis, asthenic syndrome, vitamin and protein-energy deficiency develops. Patients complain of lack of appetite, unpleasant taste in the mouth, weakness. On examination, the facial features are pointed, the patient is pale, the tongue is lined with white or gray bloom, the stomach is usually drawn in, and palpation is painless or slightly painful in the iliac region. In many patients, symptoms of cardiovascular pathology are expressed: muffled heart sounds, tachycardia, pulse lability. When sigmoidoscopy revealed ulcers, polyps, cysts, amoeba.

Complications of intestinal amebiasis are: perforation of the wall of the large intestine, development of purulent peritonitis, bleeding, appendicitis, strictures of the large intestine, amoeboma, megacolon, etc. The most serious complication is perforation and gangrene of the large intestine, the mortality rate among which in non-operated patients is 100%.

In children, intestinal amebiasis often begins with symptoms of severe intoxication: an increase in temperature to 38–39 ° C, drowsiness, nausea, and vomiting. There are liquid or mushy stool mixed with a large amount of mucus, stool frequency up to 10-15 times a day, dehydration is possible.

Extraintestinal amebiasis occurs as a complication of the intestinal as a result of hematogenous or direct introduction of amoebae from the intestines. Most often, it manifests itself in the form of amoebic hepatitis or liver abscess, occurring acutely, subacutely or chronically. Liver damage may occur during the development of acute amoebic colitis or several months or even years after infection. Acute amebic hepatitis is more often formed on the background of intestinal amebiasis. With it, the liver is enlarged, compacted, moderately painful; subfebrile temperature. Perhaps the development of hepatomegaly.

In amebic abscesses, there is an increase in the liver, tenderness at the site of localization, high temperature (up to 39 ° C) of a remitting, hectic or permanent type with chills and excessive sweating at night. Single or multiple abscesses are more often formed in the right lobe of the liver. With large abscesses, jaundice may develop, which is a bad prognostic sign. With the involvement of the diaphragm in the pathological process, a high standing of its dome is revealed, and mobility is limited. Perhaps the development of atelectasis.

In 10–20% there is a long latent or atypical course of an abscess (for example, only fever, pseudocholecystitis, jaundice) with possible subsequent breakthrough, which can lead to the development of peritonitis and damage to the organs of the chest cavity. In the hemogram with amoebic abscess of the liver, neutrophilic leukocytosis (15-50-109 / l) is detected with a shift to the left. ESR accelerated.

In amoebic liver abscess, indications of previously transferred intestinal amebiasis are detected only in 30–40% of patients, amoebae in feces are detected less than in 20% of patients.

Pleuropulmonary amebiasis is a consequence of liver abscess breaking through the diaphragm into the lungs, less often due to the hematogenous spread of amoebas. Manifested by the development of pleural empyema, lung abscesses and hepatic bronchial fistula. Characterized by chest pain, cough, shortness of breath, pus and blood in the sputum, chills, fever, leukocytosis.

Cerebral amebiasis has hematogenous origin. Single or multiple abscesses may be located in any part of the brain, but more often in the left hemisphere. The onset is usually acute, lightning fast and fatal. It is rarely diagnosed in vivo.

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

Skin amebiasis develops as a secondary process in debilitated and debilitated patients. Erosions and ulcers are localized mainly in the perianal region, perineum, buttocks.

Cases of urogenital amebiasis, which develops due to the direct entry of pathogens through the ulcerated surface of the rectal mucosa into the genitals, are described, and in the majority of the cases described, a cervical tumor has been suggested. In homosexuals, there may be lesions in the form of wart ulcerations in the genital area and anus.

Diagnosis of Amebiasis

The diagnosis of amebiasis is established on the basis of the epidemiological history, the clinical picture of the disease and the results of laboratory research.

Decisive for the diagnosis are the results of a parasitological study. Parasitological diagnosis of amebiasis is made when a tissue and a large vegetative form, trophozoite-erythrophages, is detected in the material under study. The material for the study can be: feces, rectal swabs selected during sigmoidoscopy, biopsy material of ulcerative lesions, aspirate the contents of a liver abscess, and tissue forms are localized mainly in the outer walls of the abscess, and not in necrotic masses located in the center.

From the first day of illness, microscopy of native smears from freshly excreted feces in saline and smears stained with Lugol’s solution is performed. In the acute and subacute course of the disease, the vegetative tissue form of the amoeba is sought, and in convalescents and asymptomatic carriers, the small translucent form and cyst are found. You can also prepare permanent hematoxylin stained preparations according to Heidenhain. Identifying only the luminal forms and amoebic cysts in the feces is not enough for a definitive diagnosis.

To increase the effectiveness of parasitological studies, multiple (up to 3-6 times) research of freshly isolated feces (no later than 10-15 minutes after defecation) and other biological substrates, collection of material in preservative liquids for long-term storage of the preparation, enrichment methods are used.

In the presence of clinical signs of intestinal amebiasis and negative results of parasitological studies, serological reactions are used based on the detection of specific anti-anesthetic antibodies. Used RIF, RSK, ELISA, hemagglutination inhibition reactions and neutralization with paired sera (increase in antibody titer 4 or more times). Serological tests are positive in 75% of patients with intestinal amebiasis and 95% of patients with extra intestinal amebiasis.

For diagnosis of extraintestinal amebiasis, in addition to immunological, a comprehensive instrumental examination is carried out: ultrasound, x-ray, computed tomography and other methods that allow you to determine the location, size and number of abscesses, as well as monitor the results of treatment.

From modern research methods, detection of dysenteric amoebae antigens in feces and other material using monoclonal antibodies is used; determination of parasitic DNA by PCR.

Amebiasis treatment

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

For the treatment of non-invasive amebiasis (asymptomatic “carriers”) use luminal amebocides. It is also recommended that lumen amebocides be prescribed after completion of treatment with tissue amebocides to eliminate amoebas remaining in the intestine in order to prevent recurrence. In particular, there are observations on the development of amebic abscesses of the liver in persons with intestinal amebiasis who received only tissue amebocides without the subsequent administration of luminal amebocides. In particular, the recurrence of amebic liver abscess in a patient 17 years after the newly successfully diagnosed liver abscess was described.

In conditions when it is impossible to prevent re-infection, the use of luminal amebocides is impractical. In these situations, it is recommended to appoint luminal amebocides only according to epidemiological indications, for example, persons whose professional activity may contribute to the infection of other persons, in particular, employees of catering enterprises.

Luminous amebocides

Etofamid (Kithnos)
Clephamide
Diloxanide furoate
Paromomycin

For the treatment of invasive amebiasis, systemic 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.

Systemic tissue amebocides

5 – nitroimidazoles:
Metronidazole (Trihopol, Flagil)
Tinidazole (Tiniba, Fasizin)
Ornidazole (Tiberal)
Secnidazole

In addition to drugs from the group of 5-nitroimidazoles, dehydroemetin dihydrochloride and chloroquine are recommended for the treatment of invasive amebiasis and, above all, amoebic liver abscesses.

In clinically significant cases, with a corresponding epidemiological history, when a large number of non-pathogenic amoebas are found in feces, it is also recommended to treat with amoebocides, since in these cases a high likelihood of co-infection with E.histolytica is high.

The heterogeneity of the pathological process and clinical manifestations in amoebiasis in different geographic regions, the presence of strains Resistant to standard 5-nitroimidazole chemotherapy regimens require varying treatment regimens in the light of experience gained in a particular area.

After successful chemotherapy of liver abscess, the residual cavities usually disappear within 2-4 months, however, the cavities may persist for up to 1 year.

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

Aspiration (or percutaneous drainage) is recommended for large abscesses (more than 6 cm), localization of an abscess in the left lobe of the liver or high in the right lobe of the liver, severe abdominal pain and tension of the abdominal wall due to the possible threat of abscess rupture and chemotherapy within 48 hours of its onset. Aspiration is also recommended for abscesses of unclear etiology. In case of impossibility of closed drainage, abscess rupture and peritonitis development, open surgical treatment is performed.

With the appointment of corticosteroids in patients with amoebiasis severe complications can develop, up to the development of toxic megacolon. In this regard, if necessary, treatment with corticosteroids of residents of endemic areas who have a high risk of infection with E.histolytica requires a preliminary examination for amebiasis. If the results are doubtful, it is advisable to prescribe amebocides with the subsequent appointment of corticosteroids.

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

Amebiasis Prevention

Measures for the prevention of amebiasis are aimed at identifying infected with histolytic amoeba among risk groups, their rehabilitation or treatment, as well as to break the transmission mechanism.

Risk groups for amebiasis infection include patients with gastrointestinal pathology, residents of non-canalized settlements, employees of food enterprises and food trade, greenhouses, greenhouses, sewage treatment plants, people returning from amebiasis-endemic countries, homosexuals.

Persons entering work for food and similar enterprises (child care centers, sanatoriums, water supply facilities, etc.) are subject to a scatological (for helminth eggs and intestinal protozoa) examination. At revealing of a dysenteric amoeba they are subjected to sanitation. Among the risk groups, planned protozoological studies are carried out once a year by parasitological laboratories of territorial sanitary and epidemiological stations. Patients with acute and chronic intestinal diseases are protozoologically examined by the clinical and diagnostic laboratories of the relevant medical institution.

Dispensary observation of the patients is carried out for 12 months. Medical observation and laboratory tests are carried out once a quarter, as well as with the appearance of intestinal dysfunctions. Employees of food and equivalent institutions, infested with dysenteric amoeba are kept at the dispensary until complete sanation from the amebiasis pathogen.

Measures aimed at breaking the transmission mechanism include the protection of environmental objects from contamination with invasive material through sewage of populated areas, providing the population with good-quality drinking water and food, disinfecting items exposed to contamination from the patient’s discharges in treatment-and-prophylactic and other institutions means and boiling. An important place in the prevention of amebiasis belongs sanitary and educational work.