Amoebic liver abscess pathophysiology: Difference between revisions
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*''[[Entameba histolytica|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 crossreactivity with CD59 which protect trophozoites against lysis.<ref name="pmid1381719">{{cite journal| author=Braga LL, Ninomiya H, McCoy JJ, Eacker S, Wiedmer T, Pham C et al.| title=Inhibition of the complement membrane attack complex by the galactose-specific adhesion of Entamoeba histolytica. | journal=J Clin Invest | year= 1992 | volume= 90 | issue= 3 | pages= 1131-7 | pmid=1381719 | doi=10.1172/JCI115931 | pmc=329975 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1381719 }} </ref> | *''[[Entameba histolytica|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 crossreactivity with CD59 which protect trophozoites against lysis.<ref name="pmid1381719">{{cite journal| author=Braga LL, Ninomiya H, McCoy JJ, Eacker S, Wiedmer T, Pham C et al.| title=Inhibition of the complement membrane attack complex by the galactose-specific adhesion of Entamoeba histolytica. | journal=J Clin Invest | year= 1992 | volume= 90 | issue= 3 | pages= 1131-7 | pmid=1381719 | doi=10.1172/JCI115931 | pmc=329975 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1381719 }} </ref> | ||
*The cysteine proteinases cleave and inactivate the anaphylatoxins C3a and C5a along with human IgA and IgG which provides further defence against host immune response.<ref name="pmid8228372">{{cite journal| author=Kelsall BL, Ravdin JI| title=Degradation of human IgA by Entamoeba histolytica. | journal=J Infect Dis | year= 1993 | volume= 168 | issue= 5 | pages= 1319-22 | pmid=8228372 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8228372 }} </ref><ref name="pmid2543700">{{cite journal| author=Reed SL, Keene WE, McKerrow JH, Gigli I| title=Cleavage of C3 by a neutral cysteine proteinase of Entamoeba histolytica. | journal=J Immunol | year= 1989 | volume= 143 | issue= 1 | pages= 189-95 | pmid=2543700 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2543700 }} </ref> | *The cysteine proteinases cleave and inactivate the anaphylatoxins C3a and C5a along with human IgA and IgG which provides further defence against host immune response.<ref name="pmid8228372">{{cite journal| author=Kelsall BL, Ravdin JI| title=Degradation of human IgA by Entamoeba histolytica. | journal=J Infect Dis | year= 1993 | volume= 168 | issue= 5 | pages= 1319-22 | pmid=8228372 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8228372 }} </ref><ref name="pmid2543700">{{cite journal| author=Reed SL, Keene WE, McKerrow JH, Gigli I| title=Cleavage of C3 by a neutral cysteine proteinase of Entamoeba histolytica. | journal=J Immunol | year= 1989 | volume= 143 | issue= 1 | pages= 189-95 | pmid=2543700 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2543700 }} </ref> | ||
*The trophozoites which enter the liver through portal circulations leading to apoptosis of liver cells and abscess formation. | |||
====Variants of amoebic liver abscesses==== | ====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. | *Solitary lesions (30%-70%) are more common amoebic liver abscesses and most commonly seen in right lobe of the liver. | ||
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:* Colon and biliary tree | :* 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=== | |||
*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. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
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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][5]
- 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.[6]
- 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.[7]
- The mediators released by the neutrophils cause more damage to adjacent intestinal epithelial cells.[8]
- 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 crossreactivity with CD59 which protect trophozoites against lysis.[9]
- The cysteine proteinases cleave and inactivate the anaphylatoxins C3a and C5a along with human IgA and IgG which provides further defence against host immune response.[10][11]
- The trophozoites which enter the liver through portal circulations leading to apoptosis of liver cells and abscess formation.
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 |
|
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
- 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.
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.
- ↑ Berninghausen O, Leippe M (1997). "Necrosis versus apoptosis as the mechanism of target cell death induced by Entamoeba histolytica". Infect Immun. 65 (9): 3615–21. PMC 175514. PMID 9284127.
- ↑ Seydel KB, Li E, Swanson PE, Stanley SL (1997). "Human intestinal epithelial cells produce proinflammatory cytokines in response to infection in a SCID mouse-human intestinal xenograft model of amebiasis". Infect Immun. 65 (5): 1631–9. PMC 175187. PMID 9125540.
- ↑ Que X, Reed SL (2000). "Cysteine proteinases and the pathogenesis of amebiasis". Clin Microbiol Rev. 13 (2): 196–206. PMC 100150. PMID 10755997.
- ↑ Salata RA, Pearson RD, Ravdin JI (1985). "Interaction of human leukocytes and Entamoeba histolytica. Killing of virulent amebae by the activated macrophage". J Clin Invest. 76 (2): 491–9. doi:10.1172/JCI111998. PMC 423849. PMID 2863284.
- ↑ Braga LL, Ninomiya H, McCoy JJ, Eacker S, Wiedmer T, Pham C; et al. (1992). "Inhibition of the complement membrane attack complex by the galactose-specific adhesion of Entamoeba histolytica". J Clin Invest. 90 (3): 1131–7. doi:10.1172/JCI115931. PMC 329975. PMID 1381719.
- ↑ Kelsall BL, Ravdin JI (1993). "Degradation of human IgA by Entamoeba histolytica". J Infect Dis. 168 (5): 1319–22. PMID 8228372.
- ↑ Reed SL, Keene WE, McKerrow JH, Gigli I (1989). "Cleavage of C3 by a neutral cysteine proteinase of Entamoeba histolytica". J Immunol. 143 (1): 189–95. PMID 2543700.