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 | *After [[adhesion]], the [[parasite]] releases [[proteinase|cysteine proteinases]] which digest [[extracellular]] matrix proteins. This facilitate [[trophozoite]] invasion into [[submucosa|submucosal tissue]] through amoebapore leading to activation of amoebic virulence program.<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><ref name="pmid9284127">{{cite journal| author=Berninghausen O, Leippe M| title=Necrosis versus apoptosis as the mechanism of target cell death induced by Entamoeba histolytica. | journal=Infect Immun | year= 1997 | volume= 65 | issue= 9 | pages= 3615-21 | pmid=9284127 | doi= | pmc=175514 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9284127 }} </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.<ref name="pmid9125540">{{cite journal| author=Seydel KB, Li E, Swanson PE, Stanley SL| title=Human intestinal epithelial cells produce proinflammatory cytokines in response to infection in a SCID mouse-human intestinal xenograft model of amebiasis. | journal=Infect Immun | year= 1997 | volume= 65 | issue= 5 | pages= 1631-9 | pmid=9125540 | doi= | pmc=175187 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9125540 }} </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]].<ref name="pmid9125540">{{cite journal| author=Seydel KB, Li E, Swanson PE, Stanley SL| title=Human intestinal epithelial cells produce proinflammatory cytokines in response to infection in a SCID mouse-human intestinal xenograft model of amebiasis. | journal=Infect Immun | year= 1997 | volume= 65 | issue= 5 | pages= 1631-9 | pmid=9125540 | doi= | pmc=175187 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9125540 }} </ref> | ||
*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.<ref name="pmid10755997">{{cite journal| author=Que X, Reed SL| title=Cysteine proteinases and the pathogenesis of amebiasis. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 196-206 | pmid=10755997 | doi= | pmc=100150 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10755997 }} </ref> | *[[Neutrophils]] transmigrating to the epithelial surface facilitate ''[[Entamoeba histolytica|E histolytica]]'' invasion by creating channels. [[Proteinase|Cysteine proteinases]] digest extracellular matrix protein, causing [[epithelial cells]] to break from the [[villi]], which also aid in the [[parasite's]] direct invasion into [[submucosa|submucosal tissues]].<ref name="pmid10755997">{{cite journal| author=Que X, Reed SL| title=Cysteine proteinases and the pathogenesis of amebiasis. | journal=Clin Microbiol Rev | year= 2000 | volume= 13 | issue= 2 | pages= 196-206 | pmid=10755997 | doi= | pmc=100150 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10755997 }} </ref> | ||
*The mediators released by the neutrophils cause more damage to adjacent intestinal epithelial cells.<ref name="pmid2863284">{{cite journal| author=Salata RA, Pearson RD, Ravdin JI| title=Interaction of human leukocytes and Entamoeba histolytica. Killing of virulent amebae by the activated macrophage. | journal=J Clin Invest | year= 1985 | volume= 76 | issue= 2 | pages= 491-9 | pmid=2863284 | doi=10.1172/JCI111998 | pmc=423849 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2863284 }} </ref> | *The mediators released by the [[neutrophils]] cause more damage to adjacent intestinal epithelial cells.<ref name="pmid2863284">{{cite journal| author=Salata RA, Pearson RD, Ravdin JI| title=Interaction of human leukocytes and Entamoeba histolytica. Killing of virulent amebae by the activated macrophage. | journal=J Clin Invest | year= 1985 | volume= 76 | issue= 2 | pages= 491-9 | pmid=2863284 | doi=10.1172/JCI111998 | pmc=423849 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2863284 }} </ref> | ||
*The trophozoites penetrate the mucosa, submucosal tissues and even into the portal circulation where they encounter additional host defenses, including complement system. | *The trophozoites penetrate the mucosa, submucosal tissues and even into the portal circulation where they encounter additional host defenses, including complement system. | ||
*''[[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 | *''[[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 cross reactivity 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 | *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.<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 | *The [[trophozoites]] which enter the [[liver]] through [[portal circulation]] leading to [[apoptosis]] of [[liver]] cells and [[abscess]] formation. | ||
*Stages of abscess formation include: | *Stages of [[abscess]] formation include: | ||
:*Acute inflammation | :*Acute inflammation | ||
:*Granuloma formation | :*[[Granuloma]] formation | ||
:*Necrosis with necrotic abscess or periportal fibrosis | :*[[Necrosis]] with necrotic [[abscess]] or [[periportal]] [[fibrosis]] | ||
====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]]. | ||
*The right hepatic lobule is most commonly effected due to portal circulatory system of the right colon. | *The right hepatic lobule is most commonly effected due to [[portal]] circulatory system of the [[colon|right colon]]. | ||
{| class="wikitable" style="text-align: Top;" | {| class="wikitable" style="text-align: Top;" | ||
!Multiple liver abscesses | !Multiple liver abscesses | ||
| Line 53: | Line 53: | ||
* 15% of patients have multiple liver abscesses | * 15% of patients have multiple liver abscesses | ||
* Presenting features include: | * Presenting features include: | ||
:*Fever | :*[[Fever]] | ||
:*Toxaemia | :*[[Toxaemia]] | ||
:*Encephalopathy | :*[[Encephalopathy]] | ||
:*Jaundice | :*[[Jaundice]] | ||
*The most common organisms that cause multiple liver abscesses are ''[[E.coli]]'' and ''[[Klebsiella]]'' | *The most common organisms that cause multiple liver abscesses are ''[[E.coli]]'' and ''[[Klebsiella]]'' | ||
*Multiple liver abscesses may cause right hepatic vein occlusion, | *Multiple liver abscesses may cause right hepatic vein occlusion, [[pylephlebitis]], and occlusion of portal vein radicals resulting in [[hepatic failure|acute hepatic failure]] and [[encephalopathy]]. | ||
| | | | ||
* 35% of patients with amoebic liver abscess present with left lobe abscess | *35% of patients with amoebic liver abscess present with left lobe abscess | ||
* Presenting features include: | *Presenting features include: | ||
:*Longer duration of symptoms (3-4 weeks) | :*Longer duration of symptoms (3-4 weeks) | ||
:*Fever | :*[[Fever]] | ||
:*Large epigastric mass (minimal movement with respiration) | :*Large [[epigastric]] mass (minimal movement with respiration) | ||
:*weight loss | :*weight loss | ||
* Complications include: | *Complications include: | ||
:*Peritonitis | :*[[Peritonitis]] | ||
:*Toxaemia | :*[[Toxaemia]] | ||
* Management includes: | * Management includes: | ||
Aspiration + anti-amoebic drugs | Aspiration + anti-amoebic drugs | ||
| | | | ||
* Compression lesions include posteriorly located right lobe abscess which compresses inferior venacava or hepatic vein | *Compression lesions include posteriorly located right lobe abscess which compresses [[inferior venacava]] or [[hepatic vein]] | ||
* Presenting features include: | *Presenting features include: | ||
Bilateral pedal edema | Bilateral pedal edema | ||
Revision as of 16:06, 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
| 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.[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 program.[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 cross reactivity 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 defense against host immune response.[12][13]
- 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 |
|---|---|---|---|
|
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.