Amoebiasis 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 dysentery amoebas - vegetative and in the form of cysts, which can transform into one another depending on the living conditions in the host’s body.
In acute manifestations of the disease, the patient's feces contain tissue and luminal forms; in carriers and subsidence of the disease - luminal forms and cysts. The tissue form contains phagocytosed red blood cells on which it feeds.
The size of the amoeba is 23–24 microns. Tissue forms turn into luminal forms, which are capable of turning into cysts. The luminal form lives in the contents of the cecum. Due to the formation of proteolytic enzymes, the luminal form causes tissue dissolution.
When cysts enter the human small intestine, their membranes are destroyed and a quadrinuclear maternal form of amoeba emerges, which, when divided, produces 8 mononuclear amoebas. Under favorable conditions, they turn into vegetative forms that live in the proximal parts of the colon.
In wet feces at temperatures of 17–20 °C, cysts do not lose viability for about 1 month, and in soil - up to 8 days. In refrigerated foods, cysts persist for several days. Drying destroys cysts instantly. A 5% solution of formalin and a 1% solution of chloramine have no effect on them; in a solution of sublimate, the cysts die within 4 hours.
Amebiasis is an intestinal anthroponosis, the source of infection is a person releasing cysts into the environment. The most dangerous are carriers of amoebas, convalescents, and patients with chronic amoebiasis in the improvement stage; The cysts continue to appear for years. Patients with acute manifestations of the disease excrete predominantly vegetative forms in their feces, which are unstable in the external environment.
Infection with amebiasis occurs through the fecal-oral route, spread through food, water, contact and sales methods (the pathogen is transmitted through food, rarely with water, through shared underwear, door handles). Flies and cockroaches contribute to the dispersal of amoeba cysts. Mostly men aged 20–58 years are affected; pregnant women are susceptible. The disease is recorded all year round, with a peak in the hot months. The incidence of amebiasis in the form of sporadic cases is recorded in Central Asia, Transcaucasia, and the Lower Volga region.
Pathological process in intestinal amebiasis it is mainly localized in the cecum and ascending colon, sometimes the rectum is affected. Deep ulcers form in the intestinal wall, the bottom of which is covered with pus containing amoebas, the surrounding tissues are hyperemic and edematous. Deep ulcerations of the intestinal wall are accompanied by intestinal bleeding.
Extraintestinal amebiasis and the formation of abscesses in the liver, lungs, and brain are the result of hematogenous (with blood) spread.
Forms of amoebiasis
Clinically, the following forms of amebiasis are distinguished: intestinal; extraintestinal; cutaneous
The incubation period for intestinal amebiasis (amebic dysentery) ranges from 1–2 weeks to 3 months. Amebiasis occurs in severe, moderate and mild forms. In the acute form, the patient’s well-being does not suffer, there is no intoxication, the temperature does not rise above subfebrile (37.5 ° C), general weakness, fatigue, headache, loss of appetite, a feeling of heaviness in the stomach, short-term abdominal pain, flatulence are possible.
Stool disorder always develops: initially, the stool is copious, fecal, with clear mucus, 4–6 times a day, with a pungent odor. Then the frequency of stool increases to 10–20 times a day, the fecal character disappears, the feces acquire the character of mucus, later mixed with blood, in the form of raspberry jelly.
In the acute period, constant or cramping pain in the abdomen is possible, aggravated by defecation. When the rectum is involved in the process, complaints of tenema (the urge to defecate) appear. During examination, the abdomen is swollen, painful on palpation along the large intestine.
Endoscopically, ulcers of the colon are found ranging in size from 2 to 10–20 mm in diameter, with undermined edges, the bottom reaches the submucosa, covered with pus and necrotic masses. The rest of the mucosa is little changed, with slight swelling and mild hyperemia.
Irrigoscopy will reveal uneven filling of the colon, spasm and rapid emptying. The duration of the acute phase is no more than 4–6 weeks. The improvement lasts for several weeks or even several months, then the disease becomes chronic and continues for many years without specific treatment. Chronic intestinal amebiasis has a recurrent and continuous course.
In the recurrent form, periods of exacerbation alternate with periods of remission, during which the stool becomes formed. With a continuous course, there are no periods of remission, the disease proceeds with periodic weakening or intensification of clinical manifestations.
The chronic course of intestinal amebiasis is accompanied by asthenia and severe exhaustion. The pain syndrome is not expressed, complaints of an unpleasant taste in the mouth, a burning sensation in the tongue. The abdomen is swollen, painful in the iliac regions. In an uncomplicated course, the liver is slightly enlarged and painless, the spleen is not enlarged. Laboratory findings: anemia, eosinophilia, monocytosis, lymphocytosis, increased ESR. Endoscopically, in chronic cases, ulcers, cysts, and polyps are detected. X-rays reveal the same changes as in the acute stage, additionally there are no haustrations, and sometimes cicatricial changes can be detected.
Complications of amoebiasis
Intestinal complications of amebiasis: perforation (perforation) of the intestinal wall, gangrene of the mucous membrane, bleeding, pathological narrowing of the intestine, rectal prolapse. Extraintestinal amebiasis is most often represented by the liver; it is diagnosed during acute intestinal amebiasis or after a longer period of time; men are more often affected.
Intestinal amoebiasis It is not always possible to identify. Amebiasis occurs acutely, subacutely or chronically in the form of amoebic hepatitis or liver abscess. With amoebic hepatitis, the liver is enlarged, sharply painful, dense, and jaundice is rare. The temperature is low-grade (37.5 °C), with periodic rises to high numbers, but there may not be an increase in temperature. Moderate leukocytosis.
With an abscess, the liver is enlarged, there is pain in the right hypochondrium, fever, and the increase in temperature can be with sharp fluctuations or constant, accompanied by chills and severe intoxication. The patient has sharpened facial features, the skin has an earthy tint, and is swollen. Heart sounds are muffled, hypotension, tachycardia.
Sometimes jaundice develops. The abdomen is moderately swollen, participates little in the act of breathing, and muscle tension is detected in the right hypochondrium. X-ray - high position of the dome of the diaphragm, decreased mobility, effusion in the right pleural sinus with subphrenic localization of the abscess. In the chronic course of the abscess, weakness, exhaustion, constant pain in the right hypochondrium. The liver is enlarged and painful.
Abscesses form as single or multiple, and are most often localized in the right lobe of the liver.
Laboratory tests reveal neutrophilic leukocytosis, ESR is elevated, and hypochromic anemia gradually develops. Complications of liver abscess: perihepatitis (inflammation of the tissue surrounding the liver), subphrenic abscess, purulent inflammation of the peritoneum, inflammation of the pleura, pericardium. The mortality rate for amoebic abscesses exceeds 25% if no treatment is carried out.
Amoebiasis of the lungs has a clinical picture of specific pleuropneumonia or lung abscess: chest pain, cough with sputum, possibly mixed with blood; temperature is normal or subfebrile (low); X-ray - infiltrative changes; in the blood - neutrophilic leukocytosis, ESR is increased.
Amebic lung abscesses have a chronic course with low-grade fever, bloody sputum, in which amoebas can be found; X-ray - a cavity in the lung. Complications: purulent pleurisy, empyema (accumulation of pus in a closed cavity), accumulation of pus and air in the pleural cavity, hepatopulmonary fistulas.
Brain amebiasis is characterized by the occurrence of amoebic abscesses with the development of focal and cerebral symptoms.
When diagnosing, epidemic data and the clinical picture, data from sigmoidoscopy, ultrasound, radioisotope scanning of the liver, and laparoscopy are taken into account. The diagnosis is confirmed by the detection under a microscope of tissue forms in sputum, the contents of abscesses, as well as a large vegetative form of amoeba in feces. Detection of luminal forms and cysts of amoebae in stool is not enough for a final diagnosis.
Freshly excreted feces are examined (no later than 10–15 minutes after defecation, the examination should be repeated multiple times). To recognize all forms of amoebiasis, serological reactions are used.
Differential diagnosis is carried out with other protozoal infections, bacterial dysentery, ulcerative colitis, and intestinal cancer. Amoebic liver abscess must be differentiated from purulent cholangitis, bile duct cancer, and sometimes malaria.
Bacterial dysentery, unlike intestinal amebiasis, has a short incubation period, acute onset, high fever, frequent bloody stools, and severe intoxication. During sigmoidoscopy, superficial ulcerations are visible.
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If the carrier of the cysts does not adhere to the rules of personal hygiene, the cysts with his feces can end up in wastewater, in the soil, in the water of open reservoirs, and from there - on vegetables and fruits grown on private farms. If, after visiting the toilet, the cyst carrier does not wash his hands thoroughly, he can transfer the cysts to household objects or food; finally, it can infect another person simply by shaking hands. Without washing your hands before eating or eating unwashed vegetables and fruits, a healthy person brings cysts into his mouth, from where they spread further along the gastrointestinal tract.
This method of transmission of infection is called fecal-oral.
Mechanism of disease development
Having reached the large intestine, the cysts turn into the active form of dysenteric amoeba. But amoebiasis does not always develop. Amoebas can simply live in the large intestine, feeding on its contents, and without causing harm to the health of a person, who, however, begins to release amoeba cysts into the external environment with their feces. This is called asymptomatic carriage.Ulcers are located, most often, in such parts of the large intestine as the rectum, sigmoid and cecum. In severe cases, the entire large intestine and even the appendix (appendix) can be affected.
The depth of the ulcers can be significant; they can even eat right through the colon, causing it to perforate (perforate). As a result, the contents of the intestine enter the abdominal cavity; a serious complication develops - peritonitis, i.e. inflammation of the peritoneum.
If a large blood vessel passes through the site of the ulcer, another danger to the health and life of the patient arises - massive intestinal bleeding. In addition, amoebas in their active form, once in the blood, are spread throughout the body. Their penetration into the liver, brain, and lungs causes the development of amoebic abscesses - large ulcers - in these organs. Most often, amoebic abscesses form in the right lobe of the liver. Late detection of such ulcers is fatal for the patient.
Classification. Forms of amoebiasis
According to the international classification, all forms of amoebiasis are divided into 2 large groups:
I. Asymptomatic amoebiasis.
II. Manifest amoebiasis(with clinical symptoms):
1. Intestinal (amebic dysentery, or amebic dysenteric colitis):
- spicy;
- chronic.
2. Extraintestinal:
- hepatic:
- acute amoebic hepatitis;
- liver abscess.
- pulmonary;
- cerebral;
- urogenital.
Domestic medicine considers extraintestinal and cutaneous forms to be complications of intestinal amebiasis.
Symptoms of amoebiasis
Symptoms of intestinal amoebiasis
Intestinal amoebiasis, as already mentioned, resembles dysentery in its symptoms. The disease begins gradually, the duration of the latent (incubation) period is from one week to four months. Then symptoms begin to appear.The main clinical symptoms of intestinal amoebiasis:
- Frequent bowel movements (from 4-6 times a day at the beginning, to 10-20 times a day at the height of the disease). Gradually, impurities of mucus and blood appear in the stool, and in advanced cases, the stool has the appearance of “raspberry jelly”, i.e. consists of mucus stained with blood.
- Body temperature in the initial stage of the disease is normal or slightly elevated, then fever appears (up to 38.5 o and above).
- Pain in the abdomen (in its lower part), which is cramping or pulling in nature. During defecation, the pain intensifies.
- Painful tenesmus, i.e. false urge to defecate, ending with the release of a completely insignificant amount of feces.
Acute intestinal amebiasis lasts 4-6 weeks, and with timely treatment, it ends in complete recovery. If treatment was not carried out, or was interrupted early, the signs of the disease, however, disappear. A period of remission and well-being begins. The duration of this period can be measured in weeks and even months. Then amebiasis resumes in a chronic form, which, if left untreated, can last for several years.
Chronic intestinal amebiasis is manifested by the following symptoms:
- a feeling of unpleasant taste in the mouth, appetite decreases until it disappears completely - as a result, the patient develops exhaustion;
- fatigue, general weakness;
- liver enlargement;
- development of anemia (decrease in blood hemoglobin), accompanied by pale skin;
- mild pain “in the pit of the stomach” may be noted;
- signs of damage to the cardiovascular system appear (rapid heartbeat, irregular pulse).
- perforation of the intestinal wall;
- internal bleeding;
- peritonitis;
- development of ameboma (intestinal tumor caused by the activity of amoebas);
- gangrene of the colon.
Symptoms of extraintestinal amoebiasis
Symptoms of extraintestinal amebiasis depend on the form of the developed complication. Acute amoebic hepatitis characterized by enlargement and hardening of the liver. Body temperature does not exceed 38 o.
During development amoebic liver abscess, the patient's temperature rises to 39 degrees and above. The liver is enlarged and sharply painful at the site of suppuration. The patient's skin may take on a jaundiced coloration, which is typical for large abscesses and is a bad sign.
Pulmonary (or pleuropulmonary) amoebiasis develops when a liver abscess ruptures into the lungs (through the diaphragm). Less commonly, the cause of this disease can be the introduction of amoebas into the lungs through the bloodstream. Abscesses occur in the lungs, and purulent pleurisy develops (inflammation of the pleura, the lining of the lungs). The patient experiences chest pain, cough with expectoration of sputum containing blood and pus, shortness of breath, fever with chills.
Cerebral amoebiasis occurs when amoebas are carried through the bloodstream into the brain, after which one or more brain abscesses occur. The course of this disease is lightning fast; death develops earlier than the diagnosis is established.
Urogenital amoebiasis develops when the pathogen enters the genitourinary system through ulcers formed in the rectum. Characterized by signs of inflammation of the urinary tract and genital organs.
Symptoms of cutaneous amoebiasis
Skin amebiasis develops as a complication of intestinal amebiasis in patients with reduced immunity.Treatment of amoebiasis
Traditional medicine methods
If amoebiasis is mild, the patient is treated at home. Patients with severe disease are sent for treatment to a hospital or infectious diseases hospital.Treatment of amebiasis is mainly medicinal.
The most effective and frequently used drugs in the treatment of amoebiasis are:
- trichopolum (metronidazole, flagyl);
- fasigin (tinidazole).
- amoebas residing in the intestinal lumen are affected by intestopan, enteroseptol, quiniophone (yatren), mexaform, etc.;
- amoebas that have penetrated the intestinal wall, liver and other organs are affected by drugs such as ambilgar, emetine hydrochloride, dehydroemetine;
- Tetracycline antibiotics indirectly affect amoebae located in the intestinal wall and in the intestinal lumen.
If the patient has amoebic abscesses of internal organs, it is necessary surgical intervention in combination with the use of antiamoebic drugs.
For cutaneous amebiasis, in addition to taking medications orally, local treatment is prescribed - ointment with yatrene.
Folk remedies
People have long treated amebiasis with the help of medicinal plants. Many of the folk recipes are still used today, in combination with traditional medicines: Infusion of hawthorn or sea buckthorn fruits (Chinese recipe)
100g of dried hawthorn or sea buckthorn fruits are brewed with two glasses of boiling water and, after cooling, drunk throughout the day.
Garlic tincture
To 100 ml of vodka add 40 g of crushed 3.
Sanitary educational work.
The risk group for infection with amoebiasis includes the following persons:
- people suffering from chronic intestinal diseases;
- residents of settlements that do not have sewerage;
- persons who returned from trips to countries with tropical and subtropical climates, where amebiasis is very widespread (India and Mexico share the first place among such countries);
- workers in food trade and food enterprises;
- workers of sewerage and treatment facilities, greenhouses, greenhouses;
- homosexuals.
Patients with chronic diseases of the gastrointestinal tract are examined in clinics or hospitals.
Persons applying for jobs in child care institutions, food factories, sanatoriums, water treatment plants, etc. are also subject to examination for helminth eggs and intestinal protozoa (including amoebas). If amoebic cysts are detected in stool analysis, such people are not hired. until complete recovery.
Those who have recovered from amoebiasis are subject to clinical observation throughout the year.
To break the mechanism of infection transmission, sanitary supervision is carried out over the condition of water supply sources and sewerage systems (in settlements without sewerage systems - over the condition of toilets and cesspools). The purpose of sanitary supervision is to prevent contamination of the external environment with feces.
Sanitary education work is carried out with the aim of teaching the masses the rules of personal hygiene.
An infiltrative-destructive lung disease caused by dysenteric amoeba, one of the forms of extra-intestinal amoebiasis.
Etiology. The causative agent is Entamoeba histolytica, exists in vegetative and cystic forms.
Epidemiology. Sources of infection are cyst excretors. The mechanism of infection is fecal-oral; occurs when amoeba cysts are ingested with food products, water from open sources, and, less often, through contact and household contact. The disease is common in areas with hot climates. In Russia, cases of the disease are registered in the republics of Transcaucasia and Central Asia.
Pathogenesis and pathological anatomy. Under certain conditions, amoebas invade the intestinal wall and, causing ulcerative-necrotic inflammation in it, can hematogenously penetrate the liver, lungs and other organs with the formation of foci of necrosis in them. Pulmonary amebiasis may be a consequence of a rupture of a liver abscess into the pleural cavity.
Clinic. The incubation period is from 1-2 weeks to 3 months or more. There are acute and chronic intestinal, extraintestinal and cutaneous amebiasis. The predominant form is intestinal amebiasis with the development of ulcerative necrotizing colitis. Extraintestinal amebiasis occurs in the form of liver amebiasis, less commonly - amebiasis of the lungs and other organs, and can sometimes develop in the absence of obvious signs of intestinal amebiasis.
Pulmonary amebiasis, which occurs as a result of hematogenous introduction of amoebae, initially occurs in the form of focal pneumonia with moderate fever and pain syndromes, persistent cough with scanty mucous-bloody sputum, and shortness of breath. The hemogram shows moderately pronounced neutrophilic leukocytosis, increased ESR and sometimes eosinophilia. X-rays reveal single or multiple foci of infiltration of lung tissue; with subpleural localization of the process, signs of exudative pleurisy.
In untreated cases, abscesses develop, accompanied by hectic fever, severe pain, and symptoms of pulmonary heart failure. The opening of an abscess into the bronchus is manifested by the discharge of a large amount of thick brown (“chocolate”) colored sputum, the occurrence of ulcerative pharyngitis and glossitis. Characterized by anemia, neutrophilic hyperleukocytosis with a shift to the left, and a sharp increase in ESR. X-rays reveal rounded shadows with perifocal infiltration and clearing in the center, and when drained into the bronchus - with a horizontal level of fluid. Opening an abscess into the pleural cavity leads to the development of pyopneumothorax, which is often fatal.
The spread of the pathological process from the liver through the diaphragm to the lungs is manifested initially by signs of subdiaphragmatic abscess, basal pneumonia and reactive pleurisy, and subsequently a lung abscess or pleural empyema develops.
Diagnostics. The diagnosis of amebiasis is confirmed by the detection of a tissue form of amoeba in feces, sputum, pleural fluid and in biopsies of affected organs, as well as using immunoserological tests (skin allergy test, complement fixation reaction, indirect immunofluorescence reaction, enzyme-labeled antibody reaction, etc.). Differential diagnosis is carried out with tuberculosis, tumors and suppurative diseases of the lungs.
Amoebiasis
Amoebiasis (amoebiasis) is a protozoal infection characterized by ulcerative lesions of the colon, the possibility of abscess formation in various organs and a tendency to a protracted and chronic course.
Historical information. The causative agent of amebiasis - dysenteric amoeba - was first discovered by F.A. Lesh in 1875 in St. Petersburg in the feces of a patient who had suffered from bloody diarrhea for a long time.
In 1883, R. Koch in Egypt, conducting a pathological examination of patients who died of dysentery, found amoebas in 4 cases in histological sections of tissue from intestinal ulcers and the walls of liver abscess. He was able to identify amoebas in the feces of two patients with dysentery. This disease was identified as an independent nosological form under the name amoebic dysentery by Councilman and Leffler in 1891. Currently, it is retained to designate amoebic intestinal damage, and the name “amebiasis” means damage to any organ by Entamoeba histolytica.
In 1903, F. Schaudinn presented a detailed description of the dysenteric amoeba, giving it the name Entamoeba histolytica.
In 1912, emetine hydrochloride, characterized by high amoebocidal activity, was introduced into the practice of treating amebiasis.
Etiology. The causative agent of amebiasis, entamoeba histolytica, belongs to the family Entamoebidae, class Sarcodinae (pseudopods), phylum Protozoa. The life cycle of dysentery amoeba includes two stages - vegetative (trophozoite) and dormant (cyst), which can transform into one another depending on the living conditions in the host’s body.
The vegetative form of amoebas is unstable in the external environment; it dies in the patient’s feces after 30 minutes.
The resting stage of dysentery amoeba exists in the form of cysts of varying degrees of maturity. Cysts of a round shape and with a diameter of up to 9-14 microns are found in the feces of convalescents of acute intestinal amebiasis, in patients with chronic recurrent amebiasis in remission and in carriers of amoebae.
When cysts enter the small intestine of a person, their membranes are destroyed, and a quadrinuclear maternal form of amoeba emerges from them, the division of which produces 8 mononuclear amoebas. Under favorable conditions, they multiply, turning into vegetative forms that live in the proximal parts of the colon. Cysts are highly resistant to environmental factors. In moist feces at a temperature of 17-20 ° C and in water free from bacterial saprophytic flora, they do not lose viability for about 1 month, in shaded and moist soil - up to 8 days. In refrigerated foods, on fruits, vegetables, and household items, cysts can live for several days. High temperature has a detrimental effect on cysts. Cysts survive exposure to low temperatures (-20-21 °C) for several months. Drying destroys them almost instantly.
Conventional disinfectants, depending on the chemical composition and concentration, act on cysts differently: a 5% formaldehyde solution and a 1% chloramine solution do not have a noticeable negative effect on them; in a solution of sublimate (1:1000) the cysts die within 4 hours, in a solution of cresol (1:250) - after 5-15 minutes. A low concentration solution of emetine (1:5,000,000) has a detrimental effect on cysts.
The mechanism of transmission of infection is fecal-oral. There are various possible ways of spreading amoebiasis - food, water, contact and household. Factors of transmission of the pathogen are often food products, especially vegetables and fruits, less often - water, household items, linen, dishes, toys, door handles, etc.
In unsanitary conditions, infection is possible through direct (direct) contact with the cyst excretor. Synanthropic flies and cockroaches contribute to the dispersal of amoeba cysts. In the intestines of these insects, E. histolytica cysts remain viable for up to 48-72 hours.
All age groups of the population of both sexes suffer from amoebiasis, but mainly men aged 20-58 years. Women in the third trimester of pregnancy and the postpartum period are especially susceptible to amebiasis, which is probably due to the characteristics of the cellular immune response in pregnant women, as well as persons who have received immunosuppressive therapy.
Amoebiasis is characterized by sporadic incidence; the possibility of epidemic outbreaks is questioned. Diseases are registered all year round, with a maximum in the hot months, when the transmission mechanism is most fully realized, and the body's resistance is reduced due to overheating, impaired water-electrolyte metabolism, etc.
Amebiasis occurs in all countries of the world, but a particularly high incidence is observed in areas of tropical and subtropical climates, including the countries of Central Asia and Transcaucasia.
The incidence of amoebiasis everywhere is significantly lower than the frequency of carriage of dysenteric amoeba. The ratio between incidence and carriage in endemic areas is 1:7, in the rest – from 1:21 to 1:23.
Pathogenesis and pathological picture. In most infected people, cysts and luminal forms of amoebas can exist in the intestines for a long time without causing disease. Under unfavorable conditions (decreased body resistance, dietary protein deficiency, dysbacteriosis, etc.), amoebas penetrate the intestinal wall, where they multiply. In the pathogenesis of amoebiasis, the degree of virulence of the pathogen strains is of great importance. Strains with higher virulence are more often isolated from patients with intestinal amebiasis than from asymptomatic cyst excretors. The microbial landscape in the intestine also plays a significant role. Some types of bacteria promote the penetration of amoebas into tissues; their presence in the colon is a factor contributing to the onset of the disease. Penetration into the intestinal wall is ensured by the amoeba's own enzymes, which have proteolytic activity.
In the intestine, cytolysis of the epithelium and tissue necrosis occur with the formation of ulcers.
The pathological process in intestinal amebiasis is mainly localized in the cecum and ascending colon. Sometimes the rectum is affected, and even less often, other parts of the intestine.
In typical cases, the early stage of intestinal amebiasis is manifested by hyperemia and swelling of the mucous membrane, the appearance of small erosions and raised nodules with a yellow dot at the top. The nodules are filled with detritus and contain vegetative forms of dysenteric amoeba. Destruction of the nodules due to necrosis leads to the formation of ulcers. The size of the ulcers ranges from a few millimeters to 2-2.5 cm in diameter. Flask-shaped ulcers are distinguished by swollen, undermined edges; they are surrounded by a zone of hyperemia and separated by areas of healthy tissue. The deep bottom of the ulcers, reaching the submucosa, is covered with pus. In the thickness of the tissue and the bottom of the ulcers, amoebas with phagocytosed erythrocytes are found.
In severe cases of intestinal amebiasis, accompanied by tissue breakdown, sinuses appear under the mucous membrane, which, when connected, form extensive ulcers with irregularly shaped edges. Deepening of ulcers to the muscular and serous membranes can cause perforation of the intestinal wall and the development of purulent peritonitis - encysted or, more often, diffuse. Healing and scarring of deep ulcers lead to stenosis of the colon with the development of partial and even complete obstruction. Deep ulcerations of the intestinal wall cause intestinal bleeding.
Hematogenous dissemination of amoebae causes the development of extraintestinal amebiasis with the formation of abscesses in the liver, lungs, brain and other organs. Long-term, chronic intestinal amebiasis can cause the formation of cysts, polyps and amoebas. Amebomas are tumor-like formations in the wall of the colon, consisting of granulation tissue, fibroblasts and eosinophilic leukocytes.
Intestinal amoebna z, or amoebic dysentery. The main and most common clinical form of invasion. The incubation period lasts from 1-2 weeks to 3 months or longer. The disease can occur in severe, moderate and mild forms. At acute intestinal amebiasis the patients’ state of health remains satisfactory for a long time, intoxication is not expressed, body temperature is normal or subfebrile. Only a small proportion of patients develop general weakness, fatigue, headaches, decreased appetite, a feeling of heaviness in the epigastrium, sometimes short-term pain in the abdominal area, and flatulence. The cardinal symptom of intestinal amebiasis is stool upset. In the initial period, the stool is copious, fecal, with clear mucus, 4-6 times a day, with a pungent odor. Then the frequency of bowel movements increases to 10-20 times a day, the stool loses its fecal character and becomes glassy mucus. Later, blood is mixed in, giving the stool a raspberry jelly appearance. In the acute form of the disease, constant or cramping pain of varying intensity in the abdomen is possible, aggravated by defecation. When the rectum is affected, painful tenesmus appears. The abdomen is soft or slightly swollen, painful on palpation along the colon.
An endoscopic examination of the colon reveals ulcers ranging in size from 2 to 10-20 mm in diameter, most often at the tops of the folds. The ulcers have edematous, swollen, undermined edges; the bottom can reach the submucosa and is covered with pus and necrotic masses. The ulcer is surrounded by a zone (belt) of hyperemia. The mucous membrane, free from ulcers, looks little changed, almost normal, but sometimes slight swelling and hyperemia can be detected.
Irrigoscopy reveals uneven filling of the colon, the presence of spasm and rapid bowel movement.
Acute symptoms of intestinal amebiasis usually persist for no more than 4-6 weeks. Then, without specific treatment, improvement in well-being and relief of colitis syndrome are usually observed. Remission can last from several weeks to several months, followed by a return of all or most of the symptoms of amoebiasis. The disease becomes chronic and without specific treatment continues for many years and even decades.
There are recurrent and continuous courses of chronic intestinal amebiasis. In the recurrent form of the disease, periods of exacerbation alternate with periods of remission, during which the stool is formed and the patient feels good. With a continuous course, there are no periods of remission, the disease proceeds with periodic weakening or intensification of clinical manifestations.
At chronic course of intestinal amebiasis asthenic syndrome, protein and vitamin deficiency, and decreased nutrition gradually develop. Patients complain of an unpleasant taste in the mouth, a burning sensation and soreness of the tongue. Appetite is reduced or absent. During the period of exacerbation, the frequency of bowel movements reaches 20-30 times or more per day. The pain syndrome is not expressed or absent. Facial features become sharper. The tongue is covered with a white or gray coating. The abdomen is usually retracted, painless or slightly painful on palpation in the iliac regions, less often along the entire colon.
Most patients exhibit symptoms of damage to the cardiovascular system; pulse lability, tachycardia, muffled heart sounds and expansion of its boundaries. The liver in uncomplicated intestinal amebiasis is usually of normal size, but sometimes slightly enlarged, and is painless or sensitive on palpation. The size of the spleen remains normal.
With a long course of intestinal amebiasis, the hemogram reveals anemia, eosinophilia, monocytosis, lymphocytosis, and an increase in ESR.
In advanced cases, exhaustion increases and cachexia develops, which leads to death.
The endoscopic picture of chronic intestinal amebiasis is varied. Along with ulcers, cysts, polyps, and amoebomas can be found, which are difficult to differentiate during examination.
During an X-ray examination of a patient with chronic intestinal amebiasis, the same changes are recorded as in the acute phase of the disease, as well as the absence of haustration, sometimes cicatricial changes with intestinal stenosis.)
On fluoroscopy, amoebomas form filling defects and simulate tumors.
With intestinal amebiasis, numerous complications can develop, among which the most common are pericolitis, perforation of the intestinal wall followed by peritonitis, gangrene of the mucous membrane, its detachment (dissecting colitis), bleeding, acute specific appendicitis, amoebomas, intestinal strictures, rectal prolapse, etc.
Extraintestinal amoebiasis. This is one of the clinical forms of invasion. Liver amoebiasis is the most common. It can occur during acute manifestations of intestinal amoebiasis or several months or even years later. It is known, however, that in 30-40% of patients it is not possible to identify intestinal signs in the anamnesis. Men are more often affected than women (ratio 96:4).
Liver amebiasis occurs acutely, subacutely and chronically. It is observed in two clinical forms: amoebic hepatitis and liver abscess.
Acute amoebic hepatitis develops most often against the background of symptoms of intestinal amebiasis. Over the course of several days, a uniform enlargement of the liver occurs, sometimes significant, which is accompanied by pain in the right hypochondrium, usually without irradiation. On palpation, the liver is somewhat compacted and moderately painful. Jaundice rarely develops. Body temperature is often subfebrile with periodic rises to high numbers, but can remain normal. The hemogram shows moderate leukocytosis.
Constant symptoms liver abscess are enlarged liver and often pain localized at the site of development of the pathological process. The pain can be of varying intensity, radiating to the right shoulder, intensifying with deep breathing, palpation of the liver, or changing the patient’s position in bed. The temperature rises to 39 °C and above, the temperature curves acquire a remitting, hectic or constant type. Fever is accompanied by chills. As the temperature drops, increased sweating is observed.
Signs of intoxication are evident. The appearance of patients is characteristic: emaciation, sunken cheeks and eyes, pointed facial features, depression. Skin turgor is reduced, sometimes the skin acquires an earthy tint. In severe cases, swelling of the skin, feet and legs appears.
In patients with amoebic liver abscess, damage to the cardiovascular system is noted. Heart sounds are muffled or dull, the maximum and minimum pressure is reduced. The pulse is increased. Sometimes jaundice develops. The abdomen is usually swollen, weakly involved in the act of breathing, and muscle tension is often detected in the right hypochondrium. Pastosity of the subcutaneous tissue of the skin of the chest on the right is often detected. An X-ray examination reveals a high position of the diaphragm with a decrease in the mobility of the right dome; with subphrenic localization of the abscess, effusion in the right pleural sinus can be detected.
At chronic course of amoebic liver abscess the fever becomes abnormal, weakness and exhaustion increase, and there is constant pressing pain in the right hypochondrium. The liver is enlarged, painful, and when the abscess is localized on its anterior surface, it can be palpated in the form of a tumor-like formation (up to 10 cm in diameter). Abscesses can be single or multiple; they are usually localized in the right lobe of the liver.
In the hemogram of an amoebic liver abscess, neutrophilic leukocytosis (15.0-50.0 * 10^9 /l) is found with a shift in the leukocyte formula to the left, the ESR is increased. With prolonged course, hypochromic anemia develops.
Liver abscesses are complicated by perihepatitis, subphrenic abscess, and when they rupture – purulent peritonitis, pleurisy, pericarditis, mediastinitis.
Mortality in amoebic liver abscesses without specific treatment reaches 25% or higher.
When amoebae are hematogenously introduced into the lungs or when a liver abscess ruptures into the pleural cavity, pulmonary amoebiasis develops. Clinically, it occurs as specific pleuropneumonia or lung abscess.
At pneumonia chest pain, cough, dry or with scanty sputum, sometimes mixed with blood, appear. Body temperature is normal or subfebrile. Percussion reveals dullness, auscultation reveals fine bubbling rales. X-ray examination reveals infiltrative changes in the lungs without signs of cavity formation. In the peripheral blood, a slight neutrophilic leukocytosis is sometimes detected, and the ESR is increased. Pneumonia has a sluggish course and without specific treatment can develop into lung abscesses.
Amoebic lung abscesses, As a rule, they take a chronic course. The temperature is low-grade with periodic high rises. Patients produce a large amount of sputum with blood (“chocolate” sputum, “anchovy sauce”), in which amoebas can be found. Ulcerative laryngitis and tracheitis develop. X-ray reveals a cavity in the affected lung with a horizontal level of fluid contained in it. Lung abscesses sometimes lead to purulent pleurisy, empyema, pyopneumothorax, pericarditis, hepatopulmonary fistulas, etc.
Amoebas from the intestines can hematogenously penetrate into the brain, where amebic abscesses may occur with the development of focal and cerebral symptoms. Patients experience severe headaches, nausea, and vomiting; body temperature is subfebrile or normal. Neurological symptoms depend on the location of abscesses and the degree of damage to the brain centers. Lifetime diagnosis is difficult.
Amoebic abscesses of the spleen, kidneys, and female genital organs with corresponding symptoms have been described.
Skin amoebiasis in the vast majority of cases is a secondary process. Erosions and/or ulcers form on the skin mainly of the perianal area, perineum and buttocks. Amoebic ulcers can occur around purulent fistulas of the liver or near surgical sutures after opening of amoebic abscesses.
The ulcers are deep, slightly painful, with blackened edges and an unpleasant odor. In scrapings from ulcers, vegetative forms of amoebas are revealed.
Forecast. In the absence of specific therapy, it is serious; if the diagnosis is untimely, extraintestinal amebiasis is bad. With early recognition and proper treatment of amebiasis, the prognosis is favorable.
Diagnostics. In the diagnosis of amebiasis, a carefully collected epidemiological history, medical history, and data from a clinical examination of patients are important. Sigmoidoscopy and biopsy of the intestinal mucosa, and x-ray examination help in recognition. In case of liver damage, for diagnostic purposes they resort to scanning, ultrasound, hepatolienography, laparoscopy, laparotomy with abscess puncture.
Decisive for the diagnosis is the detection of a large vegetative form of amoeba in feces, a tissue form in sputum, the contents of abscesses, material from the bottom of ulcers obtained by scraping, sampling with a curette, aspiration, etc. Detection of luminal forms and cysts of amoebae in stool is not enough for a final diagnosis.
If it is not possible to examine fresh feces on site, they are sent to the laboratory in a preservative.
The main method for detecting amoebas is microscopy of native stool preparations. The study of smears stained with Lugol's solution and Heidenhain iron hematoxylin, which can be stored indefinitely, is widely used.
Valuable data for recognizing all forms of amebiasis, but especially extraintestinal and amoebae, can be obtained by performing immunological (serological) reactions. Thus, with intestinal amebiasis, immunological methods are positive in 60-70% of patients, with amoebic liver abscess - in no less than 95%. The most sensitive are RNGA, IFM, VIEF, the least sensitive are RNIF and RSK. In some cases, in order to diagnose amebiasis, laboratory animals (kittens, rat pups, hamsters, etc.) are infected with the test material.
Differential diagnosis. Intestinal amebiasis is differentiated from other protozoal infections, dysentery, ulcerative colitis, intestinal cancer, and in case of amoebic liver abscess - from purulent angiocholitis, biliary tract cancer, sometimes from malaria, visceral leishmaniasis. In case of abscesses in the lungs, one should keep in mind the presence of tuberculosis and abscess pneumonia of other etiologies.
Treatment. A large number of effective drugs have been proposed for the specific treatment of amoebiasis. All of them are divided into 3 groups.
Group I – drugs of direct contact action (direct amebocides), which include quiniophone (Yatren) and diiodoquine, which have a detrimental effect on the luminal forms of pathogens. They are used for the rehabilitation of amoeba carriers and the treatment of chronic intestinal amebiasis in remission.
Quiniophone is prescribed 0.5 g 3 times a day for 10 days. If necessary, after a 10-day break, another course of treatment is carried out for 10 days in the same doses. At the same time, quiniophone can be used in the form of enemas (1-2 g of the drug per glass of warm water).
Diiodoquine (diiodohydroxyquinoline) is also used for 10 days, 0.25-0.3 g 3-4 times a day.
Group II - drugs acting on amoebae in the mucous membrane (tissue amoebicides). Effective against tissue and luminal forms of amoebae, which is used in the treatment of acute intestinal and sometimes extraintestinal amebiasis.
Emetine hydrochloride is used in a daily dose of 1 mg/kg (maximum daily dose 60 mg) intramuscularly or subcutaneously. Treatment is carried out in a hospital under ECG monitoring.
Dihydroemetine is prescribed intramuscularly or subcutaneously at 1.5 mg/kg per day (maximum daily dose 90 mg) or 1 mg/kg per day orally in the form of dihydroemetine resinate. The drug is less toxic, but is also effective, like emetine, and is quickly excreted from the body in the urine.
For the treatment of patients with intestinal amebiasis, emetine and dihydroemetine are used for 5 days; for the treatment of amoebic liver abscess, the course is doubled - up to 10 days.
Ambilgar is superior to emetine and dihydroemetine in its amoebicidal effect. Used orally - 25 mg/kg per day (but not more than 1.5 mg/kg per day) for 7-10 days.
Chingamine (delagil) has a pronounced antiprotozoal effect. It is used to treat patients with amoebic liver abscesses, as it is quickly absorbed from the intestine and concentrated in the liver unchanged.
Chingamine therapy is carried out for 3 weeks. The drug is prescribed in the first two days of treatment, 1 g, and in all subsequent 19 days - 0.5 g per day. The drug is often combined with tetracycline.
Group III – drugs with universal action, which are successfully used for all forms of amoebiasis. The most important representative of the group at present is metronidazole (Trichopol). It is used 0.4-0.8 g 3 times a day for 5-8 days. Tinidazole (Fasigin) is prescribed at a dose of 2 g per day for 3 days (children 50-60 mg/kg per day).
Furamide is used in the same cases as metronidazole, and also (due to its lower toxicity) for chemoprophylaxis of amoebiasis in foci. The course of treatment is 5 days. The drug is taken 1-2 tablets 3 times a day.
Broad-spectrum antibiotics are used as adjuncts to change the microbial biocenosis in the intestine.
Abscesses of the liver, lungs, brain and other organs are treated surgically in combination with antiamoebic agents (usually a combination of tissue and general-purpose amoebicides).
For skin amebiasis, ointment with quiniophone is used.
Broad pathogenetic and symptomatic therapy is required.
Prevention. Measures aimed at the source of infection include identifying and treating cyst excretors and amoeba carriers. Measures aimed at interrupting the transmission of infection coincide with those for acute intestinal infections.
From the book Children's Infectious Diseases. Complete guide author author unknown From the book Pathological Anatomy author Marina Aleksandrovna Kolesnikova56. Malaria, amoebiasis Malaria is an acute or chronic recurrent infectious disease, which has various clinical forms depending on the period of maturation of the pathogen, is characterized by febrile paroxysms, hypochromic anemia, increased
From the book Infectious Diseases: Lecture Notes author N.V. GavrilovaLECTURE No. 11. Amebiasis. Balantidiasis. Etiology, epidemiology, clinical picture, diagnosis, treatment 1. Amebiasis Amebiasis is a protozoal disease characterized by ulcerative lesions of the large intestine, with the formation of abscesses in the liver, lungs and other organs and
From the book Seasonal Diseases. Summer author Lev Vadimovich Shilnikov1. Amebiasis Amebiasis is a protozoal disease characterized by ulcerative lesions of the large intestine, with the formation of abscesses in the liver, lungs and other organs and a tendency to a protracted and chronic course. Etiology. The causative agent is dysenteric amoeba,
From the book Your Family Doctor. Interpretation of tests without consulting a doctor by D. V. Nesterov From the book Intestinal Diseases author S. Trofimov (ed.)Amoebiasis Amoebiasis is a serious disease caused by dysenteric amoeba (Entamoeba histolytica), which affects the intestinal mucosa. The presence of ANTI - ENTAMOEBA HYSTOLITICA in the blood indicates
From the book Home Directory of Diseases author Y. V. Vasilyeva (comp.)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
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 inflammation of the nerves.
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.
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