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Amoebiasis of the liver
Medical expert of the article
Last reviewed: 12.07.2025
Liver amebiasis is caused by Entamoeba histolytica, which is capable of parasitizing the lumen of the gastrointestinal tract. In some infected individuals, the amoeba penetrates the intestinal wall or disseminates to other organs, especially the liver.
The causative agent of amebiasis exists in the following forms: cyst, luminal forms (live in the intestinal lumen), a large vegetative form found in the patient's feces, and tissue forms are found in the walls of abscess ulcers. The transition of the amoeba from one form to another depends on the living conditions in the host organism.
A person becomes infected by consuming water and food contaminated with the parasite's cysts.
Pathomorphology
The pathological process in amebiasis develops as a result of the direct cytopathic effect of the parasite's metabolites on the body's cells and the activation of endogenous inflammatory factors secreted by macrophages, lymphocytes, mast cells and intestinal epithelial cells. The vegetative forms of amoeba are aerophiles, their vital activity depends on the parasite's consumption of iron (erythrophagia).
Single or multiple abscesses are formed most often in the right lobe of the liver. The abscess consists of three zones: the central zone - the necrosis zone, containing liquid necrotic masses with an admixture of blood, usually sterile (bacterial infection occurs in 2-3% of cases); the middle zone, consisting of stroma, and the outer zone, containing trophozoites of amoebas and fibrin.
Symptoms of liver amebiasis
Liver amebiasis manifests itself with clinical symptoms in an average of 10% of those infected.
A distinction is made between “invasive” liver amebiasis, in which pathological changes develop, and “non-invasive” - “carriage” of amebic cysts.
The most common clinical manifestations of "invasive" amebiasis are amebic colitis (dysentery) and amebic liver abscess, with amebic colitis occurring 5 to 50 times more often.
In extraintestinal amebiasis, the liver is most often affected. Amebic hepatitis often develops against the background of clinical manifestations of intestinal amebiasis. It is characterized by hepatomegaly and pain in the right hypochondrium. Palpation reveals uniform enlargement and dense consistency of the liver, it is moderately painful. Body temperature is often subfebrile, jaundice rarely develops. In the peripheral blood - moderate leukocytosis.
Liver amebiasis may be acute or chronic. Development of an amebic liver abscess is accompanied by irregular fever, in weakened young children - subfebrile condition. Pain in the right upper quadrant of the abdomen radiating to the right shoulder or right clavicle is more intense with subcapsular localization of the abscess, especially in the subdiaphragmatic region. The liver is moderately enlarged, painful on palpation. The spleen is not enlarged. Neutrophilic leukocytosis up to 20-30x10 9 /l with a band shift is revealed, often eosinophilia up to 7-15%, ESR reaches 30-40 mm/h and higher. Hypoproteinemia (up to 50-60 g/l) with hypoalbuminemia and an increase in the content of a2- and y-globulins are characteristic; activity of serum transaminases and alkaline phosphatase are within normal limits. The latter may increase in case of multiple liver abscesses with cholestasis, jaundice, which is extremely rare in children.
In 10-20% of cases, a long latent or atypical course of the abscess is observed (for example, only fever, pseudocholecystitis, jaundice) with a possible subsequent breakthrough, which can lead to peritonitis and damage to the chest organs.
Amebic abscesses located on the upper surface of the liver, often causing reactive pleurisy through the diaphragm, can open into the pleural cavity with the formation of empyema and/or the development of an abscess of the right lung. Abscesses on the posterior surface of the liver can break through into the retroperitoneal space. Breakthrough of the abscess into the abdominal cavity leads to the development of peritonitis; if the abscess is fused with the abdominal wall, the abscess can break through the abdominal skin. Amebic abscess of the left lobe of the liver can be complicated by breakthrough into the pericardial cavity.
Diagnosis of liver amebiasis
Amebic liver abscesses, single and multiple, are detected by ultrasound. Foci with decreased echogenicity are determined in the liver. Radiologically, when an abscess breaks through the diaphragm from the liver into the right lung, the dome of the diaphragm is immobile during breathing. Computer tomography in liver abscess reveals focal decrease in densimetric density.
Liver abscesses of amoebic etiology are differentiated from bacterial abscesses and deep mycoses. Of decisive importance is the detection of specific antibodies with a diagnosticum for amoebiasis (ELISA). It is important to consider that amoebic abscesses can be the primary manifestation of invasion.
The prognosis for liver amebiasis is favorable only with timely diagnosis and rational treatment.
Treatment of liver amoebiasis
Treatment of liver amebiasis is carried out with agents that act simultaneously on the luminal and tissue forms of the pathogen. Such agents include derivatives of 5-nitroimidazole: metronidazole (trichopolum), tinidazole, ornidazole abroad, as well as tetracycline, oleandomycin.
It is better not to perform surgical interventions in children, limiting the abscess to puncture under ultrasound or CT control with aspiration of the contents and introduction of specific agents into the cavity. Amoebas are rarely found in the center of necrotic masses and are usually localized in the outer walls of the abscess.
Controlled studies have shown no advantage of metronidazole in combination with aspiration over metronidazole alone.
Prevention of liver amoebiasis
The most effective are the neutralization and removal of feces, the prevention of contamination of food and water, and the protection of water bodies from faecal contamination.
Strict adherence to personal hygiene rules is of great importance.