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Entamoeba histolytica

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Title: Entamoeba histolytica  
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Language: English
Subject: Amoebiasis, Clioquinol, Amoebozoa, Protozoan infection, Amoebic brain abscess
Collection: Amoebozoa, Eukaryotes with Sequenced Genomes, Parasitic Protists
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Entamoeba histolytica

Entamoeba histolytica
Entamoeba histolytica cyst
Scientific classification
Domain: Eukaryota
Kingdom: Amoebozoa
Phylum: Archamoebae
Subphylum: Conosa
Class: Tubulinea
Genus: Entamoeba
Species: E. histolytica
Binomial name
Entamoeba histolytica
Schaudinn, 1903
Life-cycle of Entamoeba histolytica

Entamoeba histolytica is an anaerobic parasitic protozoan, part of the genus Entamoeba.[1] Predominantly infecting humans and other primates, E. histolytica is estimated to infect about 50 million people worldwide. Previously, it was thought that 10% of the world population was infected, but these figures predate the recognition that at least 90% of these infections were due to a second species, E. dispar.[2] Mammals such as dogs and cats can become infected transiently, but are not thought to contribute significantly to transmission.

The word histolytic literally means "Tissue destroyer"


  • Transmission 1
  • Genome 2
  • Pathology 3
  • Pathogen interaction 4
  • Diagnosis 5
  • Treatment 6
  • See also 7
  • References 8
  • External links 9


The active (red blood cells are sometimes seen in the amoeba cell cytoplasm.


The E. histolytica genome was sequenced, assembled, and automatically annotated in 2005.[5] The genome was reassembled and reannotated in 2010.[6] The 20 million basepair genome assembly contains 8,160 predicted genes; known and novel transposable elements have been mapped and characterized, functional assignments have been revised and updated, and additional information has been incorporated, including metabolic pathways, Gene Ontology assignments, curation of transporters, and generation of gene families.[7] The major group of transposable elements in E. histolytica are non-LTR retrotransposons. These have been divided in three families called EhLINEs and EhSINEs (EhLINE1,2,3 and EhSINE1,2,3).[8] EhLINE1 encode an endonuclease (EN) protein (in addition to Reverse Transcriptase and nucleotide-binding ORF1), which have similarity with bacterial Restriction Endonuclease. This similarity with bacterial protein indicates that Transposable Elements have been acquired from prokaryotes by horizontal gene transfer in this protozoan parasite.[9]


In the vast majority of cases, infection is asymptomatic and the carrier is unaware they are infected. However, in an estimated 10% of cases E. histolytica causes disease. Once the trophozoites are excysted they colonise the large bowel, remaining on the surface of the mucus layer and feeding on bacteria and food particles. Occasionally, and in response to unknown stimuli, trophozoites move through the mucus layer where they come in contact with the epithelial cell layer and start the pathological process. E. histolytica has a lectin that binds to galactose and N-acetylgalactosamine sugars on the surface of the epithelial cells, The lectin normally is used to bind bacteria for ingestion. The parasite has several enzymes such as pore forming proteins, lipases, and cysteine proteases, which are normally used to digest bacteria in food vacuoles but which can cause lysis of the epithelial cells by inducing cellular necrosis and apoptosis when the trophozoite comes in contact with them and binds via the lectin. The trophozoites will then ingest these dead cells. This damage to the epithelial cell layer attracts human immune cells and these in turn can be lysed by the trophozoite, which releases the immune cell's own lytic enzymes into the surrounding tissue, creating a type of chain reaction and leading to tissue destruction. This destruction manifests itself in the form of an 'ulcer' in the tissue, typically described as flask shaped because of its appearance in transverse section. this tissue destruction can also involve blood vessels leading to bloody diarrhoea, amebic dysentery. Occasionally, trophozoites enter the bloodstream where they are transported typically to the liver via the portal system. In the liver a similar pathological sequence ensues, leading to amebic liver abscesses. The trophozoites can end up in other organs also, sometimes via the bloodstream, sometimes via liver abscess rupture or fistulas. In all locations similar pathology can occur.

Pathogen interaction

E. histolytica may modulate the virulence of certain human viruses and is itself a host for its own viruses.

For example, AIDS accentuates the damage and pathogenicity of E. histolytica.[10] On the other hand, cells infected with HIV are often consumed by E. histolytica. Infective HIV remains viable within the amoeba, although fortunately there has been no proof of human reinfection from amoeba carrying this virus.[11]

A burst of research on viruses of E. histolytica stems from a series of papers published by Diamond et al. from 1972 to 1979. In 1972, they hypothesized two separate polyhedral and filamentous viral strains within E. histolytica that caused cell lysis. Perhaps the most novel observation was that two kinds of viral strains existed, and that within one type of amoeba (strain HB-301) the polyhedral strain had no detrimental effect but led to cell lysis in another (strain HK-9). Although Mattern et al. attempted to explore the possibility that these protozoal viruses could function like bacteriophages, they found no significant changes in Entamoeba histolytica virulence when infected by viruses. However, no newer published research has been conducted on this species since.[12]


It can be diagnosed by stool samples, but it is important to note that certain other species are impossible to distinguish by microscopy alone. Trophozoites may be seen in a fresh fecal smear and cysts in an ordinary stool sample. ELISA or RIA can also be used.


There are many kinds of effective drugs. This is just a short overview of a few of the different methods of treatments.

Intestinal infection: Usually lumen.

Liver abscess: In addition to targeting organisms in solid tissue, primarily with drugs like metronidazole and chloroquine, treatment of liver abscess must include agents that act in the lumen of the intestine (as in the preceding paragraph) to avoid re-invasion. Surgical drainage is usually not necessary except when rupture is imminent.[13]

Asymptomatic patients: For asymptomatic patients (otherwise known as carriers, with no symptoms), non endemic areas should be treated by paromomycin, and other treatments include diloxanide furoate and iodoquinol. There have been problems with the use of iodoquinol and iodochlorhydroxyquin, so their use is not recommended. Diloxanide furoate can also be used by mildly symptomatic persons who are just passing cysts.

Genus and species Entamoeba histolytica
Etiologic agent of: Amoebiasis; amoebic dysentery; extraintestinal amoebiasis, usually amoebic liver abscess; "anchovy sauce"); amoeba cutis; amoebic lung abscess ("liver-colored sputum")
Infective stage Tetranucleated cyst (having 4 nuclei)
Definitive host Human
Portal of entry Mouth
Mode of transmission Ingestion of mature cyst through contaminated food or water
Habitat Colon and cecum
Pathogenic stage Trophozoite
Locomotive apparatus Pseudopodia ("false foot”")
Motility Active, progressive and directional
Nucleus 'Ring and dot' appearance: peripheral chromatin and central karyosome
Mode of reproduction Binary fission
Pathogenesis Lytic necrosis (it looks like “flask-shaped” holes in Gastrointestinal tract sections (GIT)
Type of encystment Protective and Reproductive
Lab diagnosis Most common is direct fecal smear (DFS) and staining (but does not allow identification to species level); enzyme immunoassay (EIA); indirect hemagglutination (IHA); Antigen detection – monoclonal antibody; PCR for species identification. Sometimes only the use of a fixative (formalin) is effective in detecting cysts. Culture: From faecal samples - Robinson's medium, Jones' medium
Treatment Metronidazole for the invasive trophozoites PLUS a lumenal amoebicide for those still in the intestine. Paromomycin (Humatin) is the luminal drug of choice, since Diloxanide furoate (Furamide) is not commercially available in the USA or Canada (being available only from the Centers for Disease Control and Prevention). A direct comparison of efficacy showed that Paromomycin had a higher cure rate.[14] Paromomycin (Humatin) should be used with caution in patients with colitis, as it is both nephrotoxic and ototoxic. Absorption through the damaged wall of the intestinal tract can result in permanent hearing loss and kidney damage. Recommended dosage: Metronidazole 750 mg three times a day orally, for 5 to 10 days FOLLOWED BY Paromomycin 30 mg/kg/day orally in 3 equal doses for 5 to 10 days or Diloxanide furoate 500 mg 3 times a day orally for 10 days, to eradicate lumenal amoebae and prevent relapse.[15][16]
Trophozoite stage
Pathognomonic/diagnostic feature Ingested RBC; distinctive nucleus
Cyst Stage
Chromatoidal body 'Cigar' shaped bodies (made up of crystalline ribosomes)
Number of nuclei 1 in early stages, 4 when mature
Pathognomonic/diagnostic feature 'Ring and dot' nucleus and chromatoid bodies

See also


  1. ^ a b Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 733–8.  
  2. ^ "Amoebiasis" (PDF). Wkly. Epidemiol. Rec. 72 (14): 97–9. April 1997.  
  3. ^ American Water Works Association (June 2006). Waterborne Pathogens.  
  4. ^ Nespola, Benoît; Betz, Valérie; Brunet, Julie; Gagnard, Jean-Charles; Krummel, Yves; Hansmann, Yves; Hannedouche, Thierry; Christmann, Daniel; Pfaff, Alexander W.; Filisetti, Denis; Pesson, Bernard; Abou-Bacar, Ahmed; Candolfi, Ermanno (2015). "First case of amebic liver abscess 22 years after the first occurrence". Parasite 22: 20.  
  5. ^ Loftus B, Anderson I, Davies R, Alsmark UC, Samuelson J, et al. (2005) The genome of the protist parasite Entamoeba histolytica. Nature 433: 865–868. doi: 10.1038/nature03291.
  6. ^ Lorenzi, H. A., Puiu, D., Miller, J. R., Brinkac, L. M., Amedeo, P., Hall, N., & Caler, E. V. (2010). New assembly, reannotation and analysis of the Entamoeba histolytica genome reveal new genomic features and protein content information. PLoS neglected tropical diseases, 4(6), e716.
  7. ^ Caler, E and Lorenzi, H (2010). "Entamoeba histolytica: Genome Status and Web Resources". Anaerobic Parasitic Protozoa: Genomics and Molecular Biology.  
  8. ^ Bakre, Abhijeet A.; Rawal, Kamal; Ramaswamy, Ram; Bhattacharya, Alok; Bhattacharya, Sudha. "The LINEs and SINEs of Entamoeba histolytica: Comparative analysis and genomic distribution". Experimental Parasitology 110 (3): 207–213.  
  9. ^ Yadav, VP; Mandal, PK; Rao, DN; Bhattacharya, S (December 2009). "Characterization of the restriction enzyme-like endonuclease encoded by the Entamoeba histolytica non-long terminal repeat retrotransposon EhLINE1.". The FEBS journal 276 (23): 7070–82.  
  10. ^ Hung CC, Deng HY, Hsiao WH, Hsieh SM, Hsiao CF, Chen MY, Chang SC, Su KE. (Feb 2005). "Invasive amebiasis as an emerging parasitic disease in patients with human immunodeficiency virus type 1 infection in Taiwan.". Arch Intern Med. 165 (4): 409–415.  
  11. ^ Brown M, Reed S, Levy JA, Busch M, McKerrow JH. (Jan 1991). "Detection of HIV-1 in Entamoeba histolytica without evidence of transmission to human cells.". AIDS. 5 (1): 93–6.  
  12. ^ Diamond LS, Mattern CF, Bartgis IL (Feb 1972). "Viruses of Entamoeba histolytica. I. Identification of transmissible virus-like agents.". J Virol. 9 (2): 326–41.  
  13. ^ Kucik, CJ; Martin, GL; Sortor, BV (Mar 1, 2004). "Common intestinal parasites.". American family physician 69 (5): 1161–8.  
  14. ^ Blessmann J, Tannich E (October 2002). "Treatment of asymptomatic intestinal Entamoeba histolytica infection". N. Engl. J. Med. 347 (17): 1384.  
  15. ^ Stanley SL (March 2003). "Amoebiasis". Lancet 361 (9362): 1025–34.  
  16. ^ "Diloxanide (Systemic)". Retrieved 17 November 2011. 

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