Amoebic liver abscess

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Synonyms and keywords: Hepatic amoebiasis; Extraintestinal amoebiasis; Abscess-amoebic liver

Amoebic liver abscess is caused by a protozoan Entamoeba histolytica. Is it an inflammatory space occupying lesion in liver.

Amoebiasis was first described as a deadly disease by Hippocrates. ^[1]. The first case of amoebiasis was documented in 1875.

Liver abscess may be classified into 3 types based on etiology into pyogenic, amoebic, and fungal liver abscess.^[2]. Based on duration of symptoms, amoebic liver abscess is classified into acute and chronic.

Ameobic liver abscess is caused by a protozoan Entamoeba histolytica. It is the most common extraintestinal manifestation of amoebiasis. The mode of transmission of Entamoeba histolytica include fecal-oral route (ingestion of food and water contaminated with feces containing cysts), sexual transmission via oral-rectal route in homosexuals, vector transmission via flies, cockroaches, and rodents.^[3][4] Hepatocyte programmed cell death induced by Entamoeba histolytica causes amoebic liver abscess. The infection is transmitted to liver by portal venous system.^[5]

Amoebic liver abscess is caused by a protozoan Entamoeba histolytica.

Amoebic liver abscess must be differentiated from other diseases that cause fever, abdominal pain, cough, jaundice, hepatomegaly, anorexia, nausea, vomiting, and pale or dark stools such as pyogenic liver abscess, fungal liver abscess, echinococcal cyst, and hepatocellular carcinoma.

Amoebiasis is the second leading cause of death worldwide from parasitic disease.^[6][7][8]500 million people are infected with Entamoeba histolytica every year. 50 million individuals develop liver abscess and colitis and results in death in 40,000-100,000 individuals annually. Of all cases of amoebiasis, 3% to 9% of patients reported to have amoebic liver abscess. It most commonly occurs in 20 to 45 years age.

Common risk factors in the development of amoebic liver abscess include alcoholism, pregnancy, malnutrition, old age, immunosupression (including HIV), a recent travel to a tropical region, steroid use, hypoalbuminemia, chronic infection,tuberculosis, syphilis, splenectomy, malignancy, and homosexuality.

^[9][10]

According to the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for Entamoeba histolytica infection.

If left untreated, amoebic liver abscess may disseminate to other organs leading to death.^[11]The complications of amoebic liver abscess develop due to rupture of the abscess into the abdomen or chest cavity. The complications include peritonitis, pericarditis / pneumopericardium / tamponade, pleuropulmonary / pneumothorax (the right lung and pleural space are frequently effected because of their proximity to the liver), obstructive jaundice, bacterial superinfection, cutaneous fistulization of chest and abdominal wall, inferior vena cava obstruction, hemobilia / thoracobilia, internal fistulization, systemic inflammatory response syndrome, Venous and arterial thrombosis.^{[12][13][14][15][16][17][18][19][20][21][22][23]}Prognosis is good with treatment. Patients who are treated have high chance of complete recovery or minor complications.^[24]

Specific areas of focus when obtaining a history from the patient include history of recent travel to or resident of endemic areas, time of onset (duration of symptoms <14 days), history of dysentery within the previous few months, fever and abdominal pain.^[1]Symptoms of amoebic liver abscess include moderate to severe abdominal pain, malaise, loss of appetite, sweating, weight loss, epigastric pain (Commonly seen in left lobe abscesses), fever (high fever with chills is suggestive of secondary bacterial infection), anorexia, pleuritic chest pain, Cough with or without expectoration and chest pain (may be due to abscess rupture into the pleural cavity), jaundice, confusion, abdominal distension, nausea and vomiting, diarrhea and constipation^{[22][10][25][26][27][28]}

Common physical examination findings associated with amoebic liver abscess may include sweating and ill appearing patient with weight loss, fever with chills, tachycardia, yellowish discoloration of skin (jaundice), icteric sclera, reduced breath sounds or crepitations at right lung base may be heard, chest tenderness on palpation and audible pericardial friction rub. Hepatomegaly with point tenderness over the liver, in the intercostal spaces, or below the ribs is a typical finding Epigastric mass if left lobe is involved. Abdominal guarding or rebound tenderness, dullness on percussion, abdominal distension and absent bowel sounds are other findings.^[29][30][31]

Laboratory tests consistent with diagnosis of amoebic liver abscess include complete blood count, ESR, C-reactive protein, liver function tests, and stool examination.^{[1][32][33][34]}

There are no ECG findings associated with amoebic liver abscess.

Chest X ray findings include pleural effusion, elevated right hemidiaphragm, atelectasis, and types of hepatic abscesses.^[10][35]

CT scan findings of amoebic liver abscess include shape of abscess, varying sizes ranging from 4 cm to 12 cm, well defined lesion with attenuation values indicating the presence of complex fluid, wall enhancement, peripheral zone of edema with wall thickness around 3-15 mm, the central abscess cavity with septations and/or fluid-debris levels, and gas in the abscess if associated with hepatobronchial fistula or a hepatocolic fistula.^[35][10]

MRI findings of amoebic liver abscess include T1 weighted images with homogenous low signal intensity (signal homogeneity within the abscess can be present more often on T1– than on T2-weighted images) and T2 images are generally homogeneous with high signal intensity and perilesional edema may be seen in half of the cases.^[35][10]

Ultrasound is the gold standard technique for the diagnosis of amoebic liver abscess. The intrahepatic ultrasound findings include homogenous hypoechoic areas that can be single or multiple with round edges, round or oval in shape and variable size (around 2-6 cm in diameter), an incomplete rim of edema, location near liver capsule, margin of abscess tends to be nodular in around 40% of cases and smooth in 60% of cases, internal septations may be present in 30% of cases, and focal intrahepatic biliary dilatation peripheral to an abscess may be present. The extra hepatic findings include pleural effusion, perihepatic fluid collection, gastric or colonic involvement and retroperitoneal extension.^[35][36]

Other imaging studies include technitium-99m liver scanning, gallium citrate scan and hepatic angiography.^[37][38][39]

Other diagnostic studies include microscopic techniques, culture methods, isoenzyme analysis, antibody detection tests, antigen detection tests, immunochromatographic assays and DNA based diagnostic tests.^{[40][1][9][41][41]}

Indications for medical management of amoebic liver abscess are all non-complicated abscesses, no compression effect, and no features of rupture or impending rupture. Treatment of intraluminal infection include iodoquinol, metronidazole, tinidazole, and paromomycin.^[42]

Surgery is not the mainstay of treatment. Percutaneous needle aspiration and surgical open drainage are the surgical methods used to treat amoebic liver abscess.^[43][44]

Primary prevention of amoebic liver abscess include drinking purified water and eat well-cooked food while traveling in tropical countries with poor sanitation, boiling water before drinking, raw vegetables must be washed with soap and then soaked in vinegar for 15 min before they can be eaten, and screening of family members to prevent spread of disease:^[45]

The secondary prevention of amoebic liver abscess includes long-term follow-up after treatment. Ultrasound is the main imaging technique used during the follow-up period. The mean time for the disappearance of sonographic features (hypoechoic lesions) is 6-9 months.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Amoebiasis was first described as a deadly disease by Hippocrates. ^[1]. The first case of amoebiasis was documented in 1875.

• Amoebiasis was first described as deadly disease by Hippocrates.^[1]
• The first case of amoebiasis was documented in 1875.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Liver abscess may be classified into 3 types based on etiology into pyogenic, amoebic, and fungal liver abscess.^[1]. Based on duration of symptoms, amoebic liver abscess is classified into acute and chronic.

• Amoebic liver abscess may be classified according to international classification of diseases-10 (ICD-10) into:^[2]

• A06.4

• Based on duration of symptoms, amoebic liver abscess is classified into:^[1]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Ameoebic liver abscess is caused by a protozoan Entamoeba histolytica. It is the most common extraintestinal manifestation of amoebiasis. The mode of transmission of Entamoeba histolytica include fecal-oral route (ingestion of food and water contaminated with feces containing cysts), sexual transmission via oral-rectal route in homosexuals, vector transmission via flies, cockroaches, and rodents.^[1][2] Hepatocyte programmed cell death induced by Entamoeba histolytica causes amoebic liver abscess. The infection is transmitted to liver by portal venous system.^[3]

• Amoebic liver abscess is the most common extraintestinal manifestation of amoebiasis.
• There are two genetically different species of entamoeba.^[4] They are

• Entamoeba histolytica (the pathogen)
• Entamoeba dispar (a commensal)

• The mode of transmission of Entamoeba histolytica include:^[1][2]

• Fecal-oral route (ingestion of food and water contaminated with feces containing cysts)
• Sexual transmission via oral-rectal route in homosexuals
• Vector transmission via flies, cockroaches, and rodents.

• Hepatocyte programmed cell death induced by Entamoeba histolytica causes amoebic liver abscess.
• The infection is transmitted to liver by portal venous system.^[3]
• Clinical syndromes associated with Entamoeba histolytica infection

• After ingestion of contaminated food and water, Entamoeba histolytica trophozoites adhere to epithelial cells of colon, through the galactose/N-acetylgalactosamine specific lectin.^[5]
• After adhesion, the parasite releases cysteine proteinases which digest extracellular matrix proteins. This facilitate trophozoite invasion into submucosal tissue through amoebapore leading to activation of amoebic virulence program.^[6][7]
• The extracellular amoebic cysteine proteinase converts pIL-1β (precursor interleukin 1β) to active IL-1β. The chemokines and cytokines released from epithelial cells attract macrophages and neutrophils to the site of infection.^[8]
• Neutrophils transmigrating to the epithelial surface facilitate E histolytica invasion by creating channels. Cysteine proteinases digest extracellular matrix protein, causing epithelial cells to break from the villi, which also aid in the parasite’s direct invasion into submucosal tissues.^[9]
• The mediators released by the neutrophils cause more damage to adjacent intestinal epithelial cells.^[10]
• The trophozoites penetrate the mucosa, submucosal tissues and even into the portal circulation where they encounter additional host defenses, including complement system.
• E. histolytica are covered by highly glycosylated and phosphorylated lipophosphoglycan which may serve as a physical barrier to complement components. The amoebic Gal/GalNAc lectin has a region with antigenic cross reactivity with CD59 which protect trophozoites against lysis.^[11]
• The cysteine proteinases cleave and inactivate the anaphylatoxins C3a and C5a along with human IgA and IgG which provides further defense against host immune response.^[12][13]
• The trophozoites which enter the liver through portal circulation leading to apoptosis of liver cells and abscess formation.
• Stages of abscess formation include:

• Acute inflammation
• Granuloma formation
• Necrosis with necrotic abscess or periportal fibrosis

• Solitary lesions (30%-70%) are more common amoebic liver abscesses and most commonly seen in right lobe of the liver.
• The right hepatic lobule is most commonly effected due to portal circulatory system of the right colon.

• The amoebic liver abscesses are well circumscribed regions which contain necrotic material (dead hepatocytes, liquefied cells and cellular debris) and the surrounding fibrinous border.
• The adjacent liver parenchyma is usually normal.
• The abscesses are single or multiple.
• The abscess cavity may be filled with chocolate colored pasty material (anchovy sauce-like).

• Multiple neutrophilic abscess with areas of necrosis are seen in the liver parenchyma.
• A rim of connective tissue, with few inflammatory cells and amoebic trophozoites are clustered in the fibrin at the junction of viable and necrotic tissue.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jesus Rosario Hernandez, M.D. [2]

Entamoeba histolytica is a an anaerobic parasitic protozoan that is responsible for the development of amoebiasis.

Cellular organisms; Eukaryota; Protista; Amoebozoa; Archamoebae; Entamoeba

• Usually humans (only)
• Reports of animals as natural reservoirs of E. histolytica have been described.

• The exact number of chromosomes in E. histolytica is still unknown.
• The cysts of E. histolytica contain 4 nuclei with even distribution of chromatin between the nuclei.
• The trophozoites are spherical/oval shaped with a thin cell membrane and a single nucleus.
• E. histolytica is able to move using pseudopods.

• Cysts and trophozoites are passed in human feces. Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool.
• Infection by Entamoeba histolytica occurs by ingestion of mature cysts in fecally contaminated food, water, or hands.
• Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine.
• The trophozoites multiply by binary fission and produce cysts, and both stages are passed in the feces.
• Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission.
• Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment.
• In many cases, the trophozoites remain confined to the intestinal lumen (A: noninvasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool.
• In some patients the trophozoites invade the intestinal mucosa (B: intestinal disease), or, through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (C: extraintestinal disease), with resultant pathologic manifestations.
• It has been established that the invasive and noninvasive forms represent two separate species, respectively E. histolytica and E. dispar. These two species are morphologically indistinguishable unless E. histolytica is observed with ingested red blood cells (erythrophagocystosis).
• Transmission can also occur through exposure to fecal matter during sexual contact (in which case not only cysts, but also trophozoites could prove infective).

Entamoeba histolytica must be differentiated from other causes of viral, bacterial, and parasitic gastroentritis.

8Small bowel diarrhea: watery, voluminous with less than 5 WBC/high power field

Large bowel diarrhea: Mucousy and/or bloody with less volume and more than 10 WBC/high power field
† It could be as high as 1000 based on patient’s immunity system.

The table below summarizes the findings that differentiate inflammatory causes of chronic diarrhea^{[1][2][3][4][4]}

• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]
• 
  Entamoeba histolytica. From Public Health Image Library (PHIL). ^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Amoebic liver abscess must be differentiated from other diseases that cause fever, abdominal pain, cough, jaundice, hepatomegaly, anorexia, nausea, vomiting, and pale or dark stools such as pyogenic liver abscess, fungal liver abscess, echinococcal cyst, and hepatocellular carcinoma.

Amoebic liver abscess must be differentiated from:^{[1][2][3][4][5][6][7][8][9][10]}

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Amoebiasis is the second leading cause of death worldwide from parasitic disease.^[1][2][3]500 million people are infected with Entamoeba histolytica every year. 50 million individuals develop liver abscess and colitis and results in death in 40,000-100,000 individuals annually. Of all cases of amoebiasis, 3% to 9% of patients reported to have amoebic liver abscess. It most commonly occurs in 20 to 45 years age.

Incidence and Prevalence

• Amoebiasis is the second leading cause of death worldwide from parasitic disease.^[4][2][3][5]
• 500 million people are infected with Entamoeba histolytica every year.
• 50 million individuals develop liver abscess and colitis, and results in death in 40,000-100,000 individuals annually.
• Of all cases of amoebiasis, 3% to 9% of patients reported to have amoebic liver abscess.

Age

• Amoebic liver abscess most commonly occurs in 20 to 45 years age.

Gender

• Amoebic liver abscess is more common among men compared to women.^[6][7][8]

Developed and Developing Countries

• Entamoeba histolytica infection is more common in tropical and sub tropical areas.^[9]
• Infection rates are higher in temperate regions with poor sanitation.
• In the United States most cases of amoebiasis occur in immigrants from endemic areas and HIV infected patients.^[10]
• Amoebic liver abscess is the most common extra intestinal manifestation of Entamoeba histolytica infection. It is endemic in the following countries^[11]

• Mexico
• The Indian subcontinent
• Indonesia
• Sub saharan and tropical regions of Africa
• Parts of central and south America

• In developed countries, amoebiasis occurs usually in^[12]

• Homosexual men
• Immigrants
• Recent travel to endemic areas
• Institutionalized persons
• HIV positive individuals

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Common risk factors in the development of amoebic liver abscess include alcoholism, pregnancy, malnutrition, old age, immunosupression (including HIV), a recent travel to a tropical region, steroid use, hypoalbuminemia, chronic infection,tuberculosis, syphilis, splenectomy, malignancy, and homosexual.^[1][2]

Common risk factors in the development of amoebic liver abscess include:^[1][2]

• Alcoholism
• Pregnancy
• Malnutrition
• Old age
• Immunosupression (including HIV)
• Recent travel to a tropical region
• Steroid use
• Hypoalbuminemia
• Chronic infection
• Tuberculosis
• Syphilis
• Splenectomy
• Malignancy
• Homosexual

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

According to the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for Entamoeba histolytica infection.

According to the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for Entamoeba histolytica infection.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

If left untreated, amoebic liver abscess may disseminate to other organs leading to death.^[1]The complications of amoebic liver abscess develop due to rupture of the abscess into the abdomen or chest cavity. The complications include peritonitis, pericarditis / pneumopericardium / tamponade, pleuropulmonary / pneumothorax (the right lung and pleural space are frequently effected because of their proximity to the liver), obstructive jaundice, bacterial superinfection, cutaneous fistulization of chest and abdominal wall, inferior vena cava obstruction, hemobilia / thoracobilia, internal fistulization, systemic inflammatory response syndrome, Venous and arterial thrombosis.^{[2][3][4][5][6][7][8][9][10][11][12][13]}Prognosis is good with treatment. Patients who are treated have high chance of complete recovery or minor complications.^[14]

If left untreated, amoebic liver abscess may disseminate to other organs leading to death.^[1]

The complications of amoebic liver abscess develop due to rupture of the abscess into the abdomen or chest cavity. The complications include:^{[2][3][4][5][6][7][8][9][10][11][12][13]}

• Peritonitis
• Pericarditis / pneumopericardium / tamponade
• Pleuropulmonary/pneumothorax (the right lung and pleural space are frequently effected because of their proximity to the liver)
• Obstructive jaundice
• Bacterial superinfection
• Cutaneous fistulization of chest and abdominal wall
• Inferior vena cava obstruction
• Hemobilia/thoracobilia
• Internal fistulization
• Systemic inflammatory response syndrome
• Venous and arterial thrombosis

• Prognosis is good with treatment. Patients who are treated have the high chance of complete recovery or minor complications.
• If left untreated, abscess ruptures leading to death.

Poor prognostic factors include:^[14]

• Multiple abscesses
• Abscess volume greater than 500 ml
• Elevated right hemidiaphragm
• Pleural effusion on chest radiography
• Anemia (hemoglobin <10g/dl)
• Albumin <2g/dl
• Bilirubin level >3.5mg/dl
• Hypoalbuminemia (serum albumin <2.0g/dl)
• Diabetes
• Encephalopathy