Amoebic liver abscess pathophysiology: Difference between revisions
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==Overview== | ==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]]. | [[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.<ref name="pmid22763633">{{cite journal| author=Fletcher SM, Stark D, Harkness J, Ellis J| title=Enteric protozoa in the developed world: a public health perspective. | journal=Clin Microbiol Rev | year= 2012 | volume= 25 | issue= 3 | pages= 420-49 | pmid=22763633 | doi=10.1128/CMR.05038-11 | pmc=3416492 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22763633 }} </ref><ref name="pmid12660071">{{cite journal| author=Stanley SL| title=Amoebiasis. | journal=Lancet | year= 2003 | volume= 361 | issue= 9362 | pages= 1025-34 | pmid=12660071 | doi=10.1016/S0140-6736(03)12830-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12660071 }} </ref> [[Hepatocyte]] programmed cell death induced by ''[[Entamoeba histolytica]]'' causes [[amoebic liver abscess]]. The [[infection]] is transmitted to [[liver]] by [[portal venous system]].<ref name="pmid473308">{{cite journal |vauthors=Aikat BK, Bhusnurmath SR, Pal AK, Chhuttani PN, Datta DV |title=The pathology and pathogenesis of fatal hepatic amoebiasis--A study based on 79 autopsy cases |journal=Trans. R. Soc. Trop. Med. Hyg. |volume=73 |issue=2 |pages=188–92 |year=1979 |pmid=473308 |doi= |url=}}</ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
*Amoebic liver abscess is the most common extraintestinal manifestation of [[amoebiasis]]. | *[[Amoebic liver abscess]] is the most common [[extraintestinal]] manifestation of [[amoebiasis]]. | ||
*There are two genetically different species of [[entamoeba]].<ref name="pmid12517854">{{cite journal| author=Gonin P, Trudel L| title=Detection and differentiation of Entamoeba histolytica and Entamoeba dispar isolates in clinical samples by PCR and enzyme-linked immunosorbent assay. | journal=J Clin Microbiol | year= 2003 | volume= 41 | issue= 1 | pages= 237-41 | pmid=12517854 | doi= | pmc=149615 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12517854 }} </ref> They are | *There are two genetically different species of [[entamoeba]].<ref name="pmid12517854">{{cite journal| author=Gonin P, Trudel L| title=Detection and differentiation of Entamoeba histolytica and Entamoeba dispar isolates in clinical samples by PCR and enzyme-linked immunosorbent assay. | journal=J Clin Microbiol | year= 2003 | volume= 41 | issue= 1 | pages= 237-41 | pmid=12517854 | doi= | pmc=149615 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12517854 }} </ref> They are | ||
:*''[[Entamoeba histolytica]]'' (the [[pathogen]]) | :*''[[Entamoeba histolytica]]'' (the [[pathogen]]) | ||
:*''[[Entamoeba|Entamoeba dispar]]'' (a [[commensal]]) | :*''[[Entamoeba|Entamoeba dispar]]'' (a [[commensal]]) | ||
*The mode of transmission of ''[[Entamoeba histolytica]]'' include:<ref name="pmid22763633">{{cite journal| author=Fletcher SM, Stark D, Harkness J, Ellis J| title=Enteric protozoa in the developed world: a public health perspective. | journal=Clin Microbiol Rev | year= 2012 | volume= 25 | issue= 3 | pages= 420-49 | pmid=22763633 | doi=10.1128/CMR.05038-11 | pmc=3416492 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22763633 }} </ref><ref name="pmid12660071">{{cite journal| author=Stanley SL| title=Amoebiasis. | journal=Lancet | year= 2003 | volume= 361 | issue= 9362 | pages= 1025-34 | pmid=12660071 | doi=10.1016/S0140-6736(03)12830-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12660071 }} </ref> | *The mode of [[transmission]] of ''[[Entamoeba histolytica]]'' include:<ref name="pmid22763633">{{cite journal| author=Fletcher SM, Stark D, Harkness J, Ellis J| title=Enteric protozoa in the developed world: a public health perspective. | journal=Clin Microbiol Rev | year= 2012 | volume= 25 | issue= 3 | pages= 420-49 | pmid=22763633 | doi=10.1128/CMR.05038-11 | pmc=3416492 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22763633 }} </ref><ref name="pmid12660071">{{cite journal| author=Stanley SL| title=Amoebiasis. | journal=Lancet | year= 2003 | volume= 361 | issue= 9362 | pages= 1025-34 | pmid=12660071 | doi=10.1016/S0140-6736(03)12830-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12660071 }} </ref> | ||
:*[[Fecal-oral route]] (ingestion of food and water contaminated with feces containing [[cysts]]) | :*[[Fecal-oral route]] (ingestion of food and water contaminated with feces containing [[cysts]]) | ||
:*Sexual transmission via [[oral-rectal route]] in [[homosexuals]] | :*Sexual transmission via [[oral-rectal route]] in [[homosexuals]] | ||
:*[[Vector]] transmission via flies, cockroaches, and rodents. | :*[[Vector]] transmission via flies, cockroaches, and rodents. | ||
*[[Hepatocyte]] programmed cell death induced by ''[[Entamoeba histolytica]]'' causes [[amoebic liver abscess]]. | *[[Hepatocyte]] programmed cell death induced by ''[[Entamoeba histolytica]]'' causes [[amoebic liver abscess]]. | ||
*The [[infection]] is transmitted to [[liver]] by [[portal venous system]].<ref name="pmid473308">{{cite journal |vauthors=Aikat BK, Bhusnurmath SR, Pal AK, Chhuttani PN, Datta DV |title=The pathology and pathogenesis of fatal hepatic amoebiasis--A study based on 79 autopsy cases |journal=Trans. R. Soc. Trop. Med. Hyg. |volume=73 |issue=2 |pages=188–92 |year=1979 |pmid=473308 |doi= |url=}}</ref> | *The [[infection]] is [[transmitted]] to [[liver]] by [[portal venous system]].<ref name="pmid473308">{{cite journal |vauthors=Aikat BK, Bhusnurmath SR, Pal AK, Chhuttani PN, Datta DV |title=The pathology and pathogenesis of fatal hepatic amoebiasis--A study based on 79 autopsy cases |journal=Trans. R. Soc. Trop. Med. Hyg. |volume=73 |issue=2 |pages=188–92 |year=1979 |pmid=473308 |doi= |url=}}</ref> | ||
*Clinical syndromes associated with ''[[Entamoeba histolytica]]'' [[infection]] | *Clinical syndromes associated with ''[[Entamoeba histolytica]]'' [[infection]] | ||
{{familytree/start}} | {{familytree/start}} | ||
{{familytree | | | | | | | | | | | A01| | | | | | | | | | | |A01='''Entamoeba histolytica'''}} | {{familytree | | | | | | | | | | | A01| | | | | | | | | | | |A01='''[[Entamoeba histolytica]]'''}} | ||
{{familytree | | | | |,|-|-|-|-|-|-|^|-|-|-|-|-|-|.| }} | {{familytree | | | | |,|-|-|-|-|-|-|^|-|-|-|-|-|-|.| }} | ||
{{familytree | | | | B01 | | | | | | | | | | | | | B02 |B01='''Intestinal amoebiasis'''<br>•Asymptomatic cyst passers<br> | {{familytree | | | | B01 | | | | | | | | | | | | | B02 |B01='''[[Intestinal amoebiasis]]'''<br>•Asymptomatic [[cyst]] passers<br>•[[Acute amoebic colitis]]<br>- [[Mucosal disease]]<br>- [[Transmural disease<br> - [[Ulcerative postdysentric colitis]]<br>*[[Appendicitis]]<br>*[[Amoeboma]]<br>*[[Amoebic stricture]]|B02='''[[Extra intestinal amoebiasis]]'''<br>*[[Amoebic Liver abscess]]<br>*[[Perforation]] and [[peritonitis]]<br>*[[Pleuropulmonary amoebiasis]]<br>*[[Amoebic pericarditis]]<br>*[[Cutaneous amoebiasis]]}} | ||
{{familytree/end}} | {{familytree/end}} | ||
Revision as of 14:43, 14 February 2017
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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.[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]
Pathophysiology
- Amoebic liver abscess is the most common extraintestinal manifestation of amoebiasis.
- There are two genetically different species of entamoeba.[4] They are
- 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
{{familytree | | | | B01 | | | | | | | | | | | | | B02 |B01=Intestinal amoebiasis
•Asymptomatic cyst passers
•Acute amoebic colitis
- Mucosal disease
- [[Transmural disease
- Ulcerative postdysentric colitis
*Appendicitis
*Amoeboma
*Amoebic stricture|B02=Extra intestinal amoebiasis
*Amoebic Liver abscess
*Perforation and peritonitis
*Pleuropulmonary amoebiasis
*Amoebic pericarditis
*Cutaneous amoebiasis}}
| Entamoeba histolytica | |||||||||||||||||||||||||||||||||||||||||||||||
Pathogenesis
- 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 programme.[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 crossreactivity 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 defence against host immune response.[12][13]
- The trophozoites which enter the liver through portal circulations 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 |
|---|---|---|---|
|
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
- Multiple neutrophilic abscess with areas of necrosis are seen in the liver parencyma.
- 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
- ↑ 1.0 1.1 Fletcher SM, Stark D, Harkness J, Ellis J (2012). "Enteric protozoa in the developed world: a public health perspective". Clin Microbiol Rev. 25 (3): 420–49. doi:10.1128/CMR.05038-11. PMC 3416492. PMID 22763633.
- ↑ 2.0 2.1 Stanley SL (2003). "Amoebiasis". Lancet. 361 (9362): 1025–34. doi:10.1016/S0140-6736(03)12830-9. PMID 12660071.
- ↑ 3.0 3.1 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.
- ↑ 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.
- ↑ 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.