Amoebic liver abscess pathophysiology

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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]

Overview

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. Hepatocyte programmed cell death induced by Entamoeba histolytica causes amoebic liver abscess. The infection is transmitted to liver by portal venous system.

Pathophysiology

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

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

• 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.

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

Pathogenesis

• After ingestion of contaminated food and water, Entamoeba histolytica trophozoites adhere to epithelial cells of colon, through the galactose/N-acetylgalactosamine specific lectin.
• 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.
• 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.
• 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.
• The mediators released by the neutrophils cause more damage to adjacent intestinal epithelial cells.
• 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.
• 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.
• 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

Variants of amoebic liver abscesses

• 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.

Multiple liver abscesses	Left lobe abscess	Compression lesions	Extension of the abscess
15% of patients have multiple liver abscesses Presenting features include: Fever Toxemia Encephalopathy Jaundice The most common organisms that cause multiple liver abscesses are E.coli and Klebsiella Multiple liver abscesses may cause right hepatic vein occlusion, pylephlebitis, and occlusion of portal vein radicals resulting in acute hepatic failure and encephalopathy.	35% of patients with amoebic liver abscess present with left lobe abscess Presenting features include: Longer duration of symptoms (3-4 weeks) Fever Large epigastric mass (minimal movement with respiration) Weight loss Complications include: Peritonitis Toxemia Management includes: Aspiration + anti-amoebic drugs	Compression lesions include posteriorly located right lobe abscess which compresses inferior vena cava or hepatic vein Presenting features include: Bilateral pedal edema Ascites Visible veins on anterior and posterior abdominal wall Symptoms disappear after aspiration of abscess	7% of patients present perforated abscesses Rupture of abscess into the following Perforation of the abscess into pleural cavity causes empyema thoracis Peritoneal cavity causes shock and peritonitis Colon and biliary tree

Gross pathology

• 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).

Microscopic pathology

• 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.