Amoebic liver abscess pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*After ingestion of contaminated food and water, ''[[Entamoeba histolytica]]'' trophozoites adhere to epithelial cells of colon, through the galactose/N-acetylgalactosamine specific lectin.<ref name="pmid12049210">{{cite journal| author=Mann BJ| title=Structure and function of the Entamoeba histolytica Gal/GalNAc lectin. | journal=Int Rev Cytol | year= 2002 | volume= 216 | issue= | pages= 59-80 | pmid=12049210 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12049210 }} </ref> | *After ingestion of contaminated food and water, ''[[Entamoeba histolytica]]'' trophozoites adhere to epithelial cells of colon, through the galactose/N-acetylgalactosamine specific lectin.<ref name="pmid12049210">{{cite journal| author=Mann BJ| title=Structure and function of the Entamoeba histolytica Gal/GalNAc lectin. | journal=Int Rev Cytol | year= 2002 | volume= 216 | issue= | pages= 59-80 | pmid=12049210 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12049210 }} </ref> | ||
*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 programme. | *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 programme.<ref name="pmid7715451">{{cite journal| author=Leippe M, Andrä J, Nickel R, Tannich E, Müller-Eberhard HJ| title=Amoebapores, a family of membranolytic peptides from cytoplasmic granules of Entamoeba histolytica: isolation, primary structure, and pore formation in bacterial cytoplasmic membranes. | journal=Mol Microbiol | year= 1994 | volume= 14 | issue= 5 | pages= 895-904 | pmid=7715451 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7715451 }} </ref> | ||
*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. | *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 ''[[Entamoeba histolytica|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. | *Neutrophils transmigrating to the epithelial surface facilitate ''[[Entamoeba histolytica|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. | ||
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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.
Pathophysiology
- Amoebic liver abscess is the most common extraintestinal manifestation of amoebiasis.
- There are two genetically different species of entamoeba.[1] They are
- Mode of transmission of Entamoeba histolytica include
- Fecal-oral route (ingestion of food and water contaminated with feces containing cysts)
- Hepatocyte programmed cell death induced by Entamoeba histolytica causes amoebic liver abscess.
- The infection is transmitted to liver by portal venous system.[2]
- Clinical syndromes associated with Entamoeba histolytica infection
| Entamoeba histolytica | |||||||||||||||||||||||||||||||||||||||||||||||
| Intestinal amoebiasis •Asymptomatic cyst passers •Acute amoebic colitis - Mucosal disease - Transmural disease - Ulcerative postdysentric colitis *Appendicitis *Amoeboma *Amoebic stricture | Extra intestinal amoebiasis *Amoebic Liver abscess *Perforation and peritonitis *Pleuropulmonary amoebiasis *Amoebic pericarditis *Cutaneous Amoebiasis | ||||||||||||||||||||||||||||||||||||||||||||||
Pathogenesis
- After ingestion of contaminated food and water, Entamoeba histolytica trophozoites adhere to epithelial cells of colon, through the galactose/N-acetylgalactosamine specific lectin.[3]
- 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 programme.[4]
- 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.
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.
| Multiple liver abscesses | Left lobe abscess | Compression lesions | Extension of the abscess |
|---|---|---|---|
|
Aspiration + anti-amoebic drugs |
Bilateral pedal edema Ascites Visible veins on anterior and posterior abdominal wall Symptoms disappear after aspiration of abscess |
|
References
- ↑ Gonin P, Trudel L (2003). "Detection and differentiation of Entamoeba histolytica and Entamoeba dispar isolates in clinical samples by PCR and enzyme-linked immunosorbent assay". J Clin Microbiol. 41 (1): 237–41. PMC 149615. PMID 12517854.
- ↑ Aikat BK, Bhusnurmath SR, Pal AK, Chhuttani PN, Datta DV (1979). "The pathology and pathogenesis of fatal hepatic amoebiasis--A study based on 79 autopsy cases". Trans. R. Soc. Trop. Med. Hyg. 73 (2): 188–92. PMID 473308.
- ↑ Mann BJ (2002). "Structure and function of the Entamoeba histolytica Gal/GalNAc lectin". Int Rev Cytol. 216: 59–80. PMID 12049210.
- ↑ Leippe M, Andrä J, Nickel R, Tannich E, Müller-Eberhard HJ (1994). "Amoebapores, a family of membranolytic peptides from cytoplasmic granules of Entamoeba histolytica: isolation, primary structure, and pore formation in bacterial cytoplasmic membranes". Mol Microbiol. 14 (5): 895–904. PMID 7715451.