Amoebic liver abscess pathophysiology
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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.
- Amoebic liver abscess is the most common extraintestinal manifestation of amoebiasis.
- There are two genetically different species of entamoeba. They are
- 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
• Asymptomatic cyst passers
• Acute amoebic colitis
• Mucosal disease
• Transmural disease
• Ulcerative post dysentric colitis
• Amoebic stricture
|Extra intestinal amoebiasis|
• Amoebic liver abscess
• Perforation and peritonitis
• Pleuropulmonary amoebiasis
• Amoebic pericarditis
• Cutaneous amoebiasis
- 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:
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|
Aspiration + anti-amoebic drugs
- 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.
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